www.perpetualcommotion.com
"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The
Children of Hurin
- The Distillery -
(In
other words, "I found it interesting, but haven't had the time
to research and categorize it
yet.")
Potential treatment for Parkinson's disease discovered
Date: July 16, 2015
Source: Nanyang Technological University
Summary: Scientists have found that existing anti-malaria drugs
could be a potential treatment for Parkinson's disease.
Parkinson's disease is a degenerative disorder of the central
nervous system that causes a person to lose control of motor
movements, such as the ability to move his or her hands, arms,
and legs.
...two anti-malaria drugs which worked:
Chloroquine and Amodiaquine...
http://www.sciencedaily.com/releases/2015/07/150716091710.htm
Journal Reference:
Nuclear receptor Nurr1 agonists
enhance its dual functions and improve behavioral deficits in an
animal model of Parkinson’s disease.
Chun-Hyung Kim, Baek-Soo Han,
Jisook Moon, Deog-Joong Kim, Joon Shin, Sreekanth Rajan, Quoc
Toan Nguyen, Mijin Sohn, Won-Gon Kim, Minjoon Han, Inhye Jeong,
Kyoung-Shim Kim, Eun-Hye Lee, Yupeng Tu, Jacqueline L.
Naffin-Olivos, Chang-Hwan Park, Dagmar Ringe, Ho Sup Yoon,
Gregory A. Petsko, Kwang-Soo Kim.
Proceedings of the National Academy of Sciences, 2015; 112 (28):
8756 DOI: 10.1073/pnas.1509742112
http://dx.doi.org/10.1073/pnas.1509742112
Cancer-fighting spices offer flavorful way to eat healthy
Published June 30, 2015
FoxNews.com
“Turmeric..." Adding freshly
ground black pepper can strengthen the benefits of turmeric in
some dishes, and even help prevent breast cancer tumors from
growing, according to a study from the University of Michigan
Comprehensive Cancer Center.
... Fennel... contains anethole
which restricts the adhesive properties of cancer cells. Ginger,
another cancer-fighting spice, consists of not one, but two
anti-cancer compounds called gingerol and zingerol which
complement each other in the body... capsaicin
in chili peppers ignites the body’s fight against potential
cancer cells. Studies have shown it can also dramatically reduce
leukemia cells. Garlic, onions, shallots and leeks can also act
as cancer preventers, while adding flavor to many everyday
dishes.
http://www.foxnews.com/health/2015/06/30/cancer-fighting-spices-offer-flavorful-way-to-eat-healthy/?intcmp=obnetwork
Hay fever and sleeping tablets 'can increase risk of
Alzheimer's and dementia'
Jan 26, 2015 21:26
By Ben Rossington
...The drugs have an “anticholinergic” effect, which
blocks a chemical transmitter that people with Alzheimer’s
lack... at higher risk if they took at least 10mg a day of
antidepressant doxepin, 4mg a day of antihistamine
diphenhydramine, or 5mg a day of oxybutynin for more than three
years...
http://www.mirror.co.uk/news/uk-news/hay-fever-sleeping-tablets-can-5048128
teixobactin: If this new antibiotic
will treat tough "chronic infections", and if (many cases
of)AD is caused by spirochetes (neurospirochetosis), then
maybe this would work on AD too.
Newly discovered antibiotic kills pathogens without
resistance
Date: January 8, 2015
Source: Northeastern University
Summary: For years, pathogens' resistance to antibiotics has
put them one step ahead of researchers, which is causing a
public health crisis. But now scientists have discovered a new
antibiotic that eliminates pathogens without encountering
any detectable resistance -- a finding that challenges
long-held scientific beliefs and holds great promise for
treating chronic infections like tuberculosis and those
caused by MRSA.
http://www.sciencedaily.com/releases/2015/01/150108124854.htm
A new antibiotic kills
pathogens without detectable resistance.
Nature. 2015 Jan 7. doi:
10.1038/nature14098. [Epub ahead of print]
Ling LL1, Schneider T2, Peoples AJ1, Spoering AL1, Engels I2,
Conlon BP3, Mueller A2, Schäberle TF4, Hughes DE1, Epstein S5,
Jones M6, Lazarides L6, Steadman VA6, Cohen DR1, Felix CR1,
Fetterman KA1, Millett WP1, Nitti AG1, Zullo AM1, Chen C3, Lewis
K3.
Abstract: Antibiotic resistance is spreading faster than the
introduction of new compounds into clinical practice, causing a
public health crisis. Most antibiotics were produced by
screening soil microorganisms, but this limited resource of
cultivable bacteria was overmined by the 1960s. Synthetic
approaches to produce antibiotics have been unable to replace
this platform. Uncultured bacteria make up approximately 99% of
all species in external environments, and are an untapped source
of new antibiotics. We developed several methods to grow
uncultured organisms by cultivation in situ or by using specific
growth factors. Here we report a new antibiotic that we term teixobactin,
discovered in a screen of uncultured bacteria. Teixobactin
inhibits cell wall synthesis by binding to a highly conserved
motif of lipid II (precursor of peptidoglycan) and lipid III
(precursor of cell wall teichoic acid). We did not obtain any
mutants of Staphylococcus aureus or Mycobacterium tuberculosis
resistant to teixobactin. The properties of this compound
suggest a path towards developing antibiotics that are likely to
avoid development of resistance.
PMID: 25561178 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/25561178
Blueberries may help reduce blood pressure and arterial
stiffness
Date: January 8, 2015
Source: Florida State University
Summary: Just one cup of blueberries per day could be the key to
reducing blood pressure and arterial stiffness, both of which
are associated with cardiovascular disease.
...22 grams of freeze-dried blueberry
powder -- the equivalent to one cup of fresh blueberries...
http://www.sciencedaily.com/releases/2015/01/150108113525.htm
Journal Reference:
Daily Blueberry Consumption Improves
Blood Pressure and Arterial Stiffness in Postmenopausal
Women with Pre- and Stage 1-Hypertension: A Randomized,
Double-Blind, Placebo-Controlled Clinical Trial.
Sarah A. Johnson, Arturo Figueroa, Negin
Navaei, Alexei Wong, Roy Kalfon, Lauren T. Ormsbee, Rafaela G.
Feresin, Marcus L. Elam, Shirin Hooshmand, Mark E. Payton,
Bahram H. Arjmandi. Journal of the Academy of Nutrition
and Dietetics, 2015; DOI: 10.1016/j.jand.2014.11.001
Could gut microbes help treat brain disorders? Mounting
research tightens their connection with the brain
Date: January 8, 2015
Source: Kavli Foundation
Summary: The community of microbes that inhabits the body, known
as the microbiome, has a powerful influence on the brain and may
offer a pathway to new therapies for psychiatric and
neurological disorders, according to researchers.
...exploring whether the microbiome
plays a role in neurodegenerative diseases such as Alzheimer's
and Parkinson's. "There are flash bulbs going off in the dark,
suggesting that very complex neurodegenerative disorders may
be linked to the microbiome. But once again this is very
speculative. These seminal findings, the flash bulbs, are only
just beginning to illuminate our vision of the
gut-microbiome-brain connection,"...
http://www.sciencedaily.com/releases/2015/01/150108125953.htm
Nasal spray with insulin equivalent shows promise as
treatment for adults with mild cognitive impairment,
Alzheimer’s dementia
Date: January 8, 2015
Source: Wake Forest Baptist Medical Center
Summary: A human-made form of insulin delivered by nasal spray
may improve working memory and other mental capabilities in
adults with mild cognitive impairment and Alzheimer's disease
dementia, according to a pilot study. The researchers also
sought to determine if the insulin detemir doses would
cause any negative side effects, and found only minor adverse
reactions among the subjects.
http://www.sciencedaily.com/releases/2015/01/150108141315.htm
[NOTE: People with type-2 diabetes have found through
personal experience that cinnamon helps control their blood sugar levels. So this may be why some
people with AD respond positively to adding cinnamon capsule
supplements to their diet. Also, adding medium chain
triglycerides (medium chain fatty acids) may help because the
liver converts the MCTs directly to ketones, and cells not
able to use sugar apparently often are still able to use the
ketones.]
Long-Acting Intranasal Insulin Detemir
Improves Cognition for Adults with Mild Cognitive Impairment
or Early-Stage Alzheimer's Disease Dementia.
J Alzheimers Dis. 2014 Nov 5. [Epub ahead of print]
Claxton A1, Baker LD2, Hanson A1, Trittschuh EH1, Cholerton
B3, Morgan A1, Callaghan M1, Arbuckle M4, Behl C1, Craft S2.
Abstract: Previous trials have shown promising effects of
intranasally administered insulin for adults with Alzheimer's
disease dementia (AD) or amnestic mild cognitive impairment
(MCI). These trials used regular insulin, which has a shorter
half-life compared to long-lasting insulin analogues such as insulin
detemir. The current trial examined whether intranasal
insulin detemir improves cognition or daily functioning for
adults with MCI or AD. Sixty adults diagnosed with MCI or mild
to moderate AD received placebo (n = 20), 20 IU of insulin
detemir (n = 21), or 40 IU of insulin detemir (n = 19) for 21
days, administered with a nasal drug delivery device. Results
revealed a treatment effect for the memory composite for the
40 IU group compared with placebo (p < 0.05). This effect
was moderated by APOE status (p < 0.05), reflecting
improvement for APOE-ε4 carriers (p < 0.02), and worsening
for non-carriers (p < 0.02). Higher insulin resistance at
baseline predicted greater improvement with the 40 IU dose (r
= 0.54, p < 0.02). Significant treatment effects were also
apparent for verbal working memory (p < 0.03) and
visuospatial working memory (p < 0.04), reflecting
improvement for subjects who received the high dose of
intranasal insulin detemir. No significant differences were
found for daily functioning or executive functioning. In
conclusion, daily treatment with 40 IU insulin detemir
modulated cognition for adults with AD or MCI, with
APOE-related differences in treatment response for the primary
memory composite. Future research is needed to examine the
mechanistic basis of APOE-related treatment differences, and
to further assess the efficacy and safety of insulin detemir.
PMID: 25374101 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/25374101
Blocking receptor in brain's immune cells counters
Alzheimer's in mice
Date: December 9, 2014
Source: Stanford University
Medical Center
Summary: The mass die-off of nerve cells in the brains of people
with Alzheimer's disease may largely occur because an entirely
different class of brain cells, called microglia, begin to fall
down on the job, according to a new study. The researchers found
that, in mice, blocking the action of a single molecule on the
surface of microglia restored the cells' ability to get the job
done -- and reversed memory loss and myriad other
Alzheimer's-like features in the animals.
http://www.sciencedaily.com/releases/2014/12/141209082149.htm
Prostaglandin
signaling suppresses beneficial microglial function in
Alzheimer's disease models.
J Clin Invest. 2014 Dec 8. pii: 77487. doi:
10.1172/JCI77487. [Epub ahead of print]
Johansson JU, Woodling NS, Wang Q, Panchal M, Liang X,
Trueba-Saiz A, Brown HD, Mhatre SD, Loui T, Andreasson KI.
Abstract
Microglia, the innate immune cells of the CNS, perform
critical inflammatory and noninflammatory functions that
maintain normal neural function. For example, microglia clear
misfolded proteins, elaborate trophic factors, and regulate
and terminate toxic inflammation. In Alzheimer's disease (AD),
however, beneficial microglial functions become impaired,
accelerating synaptic and neuronal loss. Better understanding
of the molecular mechanisms that contribute to microglial
dysfunction is an important objective for identifying
potential strategies to delay progression to AD. The
inflammatory cyclooxygenase/prostaglandin E2 (COX/PGE2)
pathway has been implicated in preclinical AD development,
both in human epidemiology studies and in transgenic rodent
models of AD. Here, we evaluated murine models that
recapitulate microglial responses to Aβ peptides and
determined that microglia-specific deletion of the gene
encoding the PGE2 receptor EP2 restores microglial chemotaxis
and Aβ clearance, suppresses toxic inflammation, increases
cytoprotective insulin-like growth factor 1 (IGF1) signaling,
and prevents synaptic injury and memory deficits. Our findings
indicate that EP2 signaling suppresses beneficial microglia
functions that falter during AD development and suggest that
inhibition of the COX/PGE2/EP2 immune pathway has potential as
a strategy to restore healthy microglial function and prevent
progression to AD.
PMID: 25485684 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/25485684
Interesting things about canola
(rapeseed) oil to investigate:
"Use "medium
chain triglycerides" (MCTs) to supply the ailing neurons
with an alternative energy source, since they are having a
problem with using the sugar glucose, which is their normal
energy source."
Yes. The
brain is 60 % fat. Myelin sheets 75 %.
http://www.kellydorfman.com/images/Fat-_A_Moment_in_the_Mouth.pdf
The opposite
"snack" for the brain would be canola oil, when I learned
this a few years ago I saved my eye sight.
A few others
found out about it too;
"My
cholesterol level was 150. After a year using Canola oil I
tested 260. I switched back to pure olive oil and it has
taken 5 years to get it down to 160. Thus began this project
to find answers since most Doctors will say that Canola oil
is O.K.
http://curezone.org/forums/am.asp?i=2145367
Treat and Prevent UTIs Without Drugs
by Chris Kresser
The typical dose of D-mannose for UTI treatment is 500 mg, in
capsule or powder form, taken in a glass of water or juice every
two to three hours for five days… supplements that help disrupt
biofilms can be useful in treating and preventing UTIs...
[bromelain???]
http://chriskresser.com/treat-and-prevent-utis-without-drugs
Antibiot Khimioter. 2010;55(9-10):11-3.
[Bactericidal activity of colloidal silver against
grampositive and gramnegative bacteria].
[Article in Russian]
Afonina IA, Kraeva LA, Tseneva GIa.
Abstract
It was shown that colloidal silver solution prepared in
cooperation with the A. F. Ioffe Physical Technical Institute of
the Russian Academy of Sciences, had significant bactericidal
activity. Stable bactericidal effect on gramnegative
microorganisms was observed after their 2-hour exposition in the
solution of colloidal silver at a concentration of 10 ppm.
Grampositive capsule-forming microorganisms were less
susceptible to the colloidal silver solution: their death was
observed after the 4-hour exposition in the solution.
PMID: 21400747 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/21400747
Silver Makes Antibiotics Thousands of Times More Effective
The antimicrobial treatment could help to solve modern bacterial
resistance
Jun 20, 2013 |By Brian Owens and Nature magazine
Stenotrophomonas maltophilia
Like werewolves and vampires, bacteria have a weakness: silver.
The precious metal has been used to fight infection for
thousands of years — Hippocrates first described its
antimicrobial properties in 400 bc — but how it works has been a
mystery. Now, a team led by James Collins, a biomedical engineer
at Boston University in Massachusetts, has described how silver
can disrupt bacteria, and shown that the ancient treatment could
help to deal with the thoroughly modern scourge of antibiotic
resistance. The work is published today in Science Translational
Medicine.
http://www.scientificamerican.com/article/silver-makes-antibiotics-thousands-of-times-more-effective/
A shot in the arm for old antibiotics
Date: June 19, 2013
Source: Wyss Institute for Biologically Inspired Engineering at
Harvard
Summary: Slipping bacteria some silver could give old
antibiotics new life, scientists report. This could pave the way
for new therapies for drug-resistant and recurrent infections.
http://www.sciencedaily.com/releases/2013/06/130619164754.htm
Journal Reference: 1.J. R. Morones-Ramirez, J. A. Winkler, C. S.
Spina, J. J. Collins. Silver Enhances Antibiotic Activity
Against Gram-Negative Bacteria. Science Translational Medicine,
2013; 5 (190): 190ra81 DOI: 10.1126/scitranslmed.3006276
Certain gut bacteria may induce metabolic changes following
exposure to artificial sweeteners
Date: September 17, 2014
Source: Weizmann Institute of Science
Summary: Artificial sweeteners have long been promoted as diet
and health aids. But breaking research shows that these products
may be leading to the very diseases they were said to help
prevent: scientists have discovered that, after exposure to
artificial sweeteners, our gut bacteria may be triggering
harmful metabolic changes.
http://www.sciencedaily.com/releases/2014/09/140917131634.htm
Jotham Suez, Tal Korem, David Zeevi, Gili Zilberman-Schapira,
Christoph A. Thaiss, Ori Maza, David Israeli, Niv Zmora, Shlomit
Gilad, Adina Weinberger, Yael Kuperman, Alon Harmelin, Ilana
Kolodkin-Gal, Hagit Shapiro, Zamir Halpern, Eran Segal, Eran
Elinav. Artificial sweeteners induce glucose intolerance by
altering the gut microbiota. Nature, 2014; DOI:
10.1038/nature13793
Asian Americans lower insulin resistance on traditional diet
Date: September 17, 2014
Source: Joslin Diabetes Center
Summary: Asian Americans have been shown to lower insulin
resistance on a traditional diet, researchers report. One part
of this puzzle may lie in the transition from traditional
high-fiber, low-fat Asian diets to current westernized diets,
which may pose extra risks for those of Asian heritage, says the
senior author of the study.
http://www.sciencedaily.com/releases/2014/09/140917151935.htm
William C. Hsu, Ka Hei Karen Lau, Motonobu Matsumoto, Dalia
Moghazy, Hillary Keenan, George L. King. Improvement of Insulin
Sensitivity by Isoenergy High Carbohydrate Traditional Asian
Diet: A Randomized Controlled Pilot Feasibility Study. PLoS ONE,
2014; 9 (9): e106851 DOI: 10.1371/journal.pone.0106851
How stress tears us apart: Enzyme attacks synaptic molecule,
leading to cognitive impairment
Date: September 18, 2014
Source: Ecole Polytechnique Fédérale de Lausanne
Summary: Why is it that when people are too stressed they are
often grouchy, grumpy, nasty, distracted or forgetful?
Researchers have just highlighted a fundamental synaptic
mechanism that explains the relationship between chronic stress
and the loss of social skills and cognitive impairment. When
triggered by stress, an enzyme attacks a synaptic regulatory
molecule in the brain, leading to these problems.
http://www.sciencedaily.com/releases/2014/09/140918091418.htm
Michael A. van der Kooij, Martina Fantin, Emilia Rejmak, Jocelyn
Grosse, Olivia Zanoletti, Celine Fournier, Krishnendu Ganguly,
Katarzyna Kalita, Leszek Kaczmarek, Carmen Sandi. Role for MMP-9
in stress-induced downregulation of nectin-3 in hippocampal CA1
and associated behavioural alterations. Nature Communications,
2014; 5: 4995 DOI: 10.1038/ncomms5995
A heart-felt need for dairy food: Small serving beneficial,
large not necessary
Date: September 16, 2014
Source: Monash University
Summary: A daily small serve of dairy food may reduce the risk
of heart disease or stroke, even in communities where such foods
have not traditionally formed part of the diet according to new
research.
http://www.sciencedaily.com/releases/2014/09/140916102226.htm
More cheese, please! News study shows dairy is good for your
metabolic health
Date: September 16, 2014
Source: Canadian Science Publishing (NRC Research Press)
Summary: Researchers studied the dairy-eating habits of healthy
French-Canadians' and monitored how dairy consumption may have
an effect on their overall metabolic health. It's well known
that dairy products contain calcium and minerals good for bones,
but new research has shown that dairy consumption may also have
beneficial effects on metabolic health and can reduce risk of
metabolic diseases such as obesity and type 2 diabetes.
http://www.sciencedaily.com/releases/2014/09/140916092737.htm
Marine S. Da Silva, Pierre Julien, Patrick Couture, Simone
Lemieux, Marie-Claude Vohl, Iwona Rudkowska. Associations
between dairy intake and metabolic risk parameters in a healthy
French-Canadian population. Applied Physiology, Nutrition, and
Metabolism, 2014; 1 DOI: 10.1139/apnm-2014-0154
Consumption of high-fat dairy products associated with lower
risk of developing diabetes
Date: September 15, 2014
Source: Diabetologia
Summary: People with the highest consumption of high-fat dairy
products -- eight or more portions per day -- have a 23 percent
lower risk of developing type 2 diabetes than those with the
lowest consumption -- one or less per day, a new study shows.
http://www.sciencedaily.com/releases/2014/09/140915202955.htm
Small, fast, and crowded: Mammal traits amplify tick-borne
illness
Date:September 18, 2014
Source:Cary Institute of Ecosystem Studies
Summary:In the U.S., some 300,000 people are diagnosed with Lyme
disease annually. Thousands also suffer from babesiosis and
anaplasmosis, tick-borne ailments that can occur alone or as
co-infections with Lyme disease. In our struggle to manage the
ever-growing list of tick-borne diseases, we need to understand
which animals magnify human disease risk. New results suggest
when generalist pathogens emerge, small mammals with large
populations and a fast pace of life warrant careful monitoring.
http://www.sciencedaily.com/releases/2014/09/140918141550.htm
Fasting triggers stem cell regeneration of damaged, old
immune system
Date: June 5, 2014
Source: University of Southern California
Summary: In the first evidence of a natural intervention
triggering
stem cell-based regeneration of an organ or system, a study
shows that
cycles of prolonged fasting not only protect against immune
system
damage -- a major side effect of chemotherapy -- but also induce
immune system regeneration, shifting stem cells from a dormant
state
to a state of self-renewal.
http://www.sciencedaily.com/releases/2014/06/140605141507.htm
Journal Reference:
Prolonged Fasting Reduces IGF-1/PKA to Promote Hematopoietic-Stem-Cell-Based
Regeneration and Reverse Immunosuppression.
Chia-Wei Cheng, Gregor B. Adams, Laura Perin, Min Wei, Xiaoying
Zhou,
Ben S. Lam, Stefano Da Sacco, Mario Mirisola, David I. Quinn,
Tanya B.
Dorff, John J. Kopchick, Valter D. Longo.
Cell Stem Cell, 2014; 14 (6): 810 DOI:
10.1016/j.stem.2014.04.014
Bacteria help explain why stress, fear trigger heart attacks
Date: June 10, 2014
Source: American Society for Microbiology
Summary: The axiom that stress, emotional shock, or overexertion
may
trigger heart attacks in vulnerable people may now be
explainable,
researchers say. Hormones released during these events appear to
cause
bacterial biofilms on arterial walls to disperse, allowing
plaque
deposits to rupture into the bloodstream, according to research.
http://www.sciencedaily.com/releases/2014/06/140610102010.htm
Journal Reference:
Bacteria Present in Carotid Arterial Plaques Are Found as
Biofilm Deposits Which May Contribute to Enhanced Risk of
Plaque Rupture.
Bernard B. Lanter, Karin Sauer and David G. Davies.
mBio, June 2014 DOI: 10.1128/mBio.01206-14
Findings point toward one of first therapies for Lou Gehrig's
disease
Date: June 12, 2014
Source: Oregon State University
Summary: Researchers have determined that a copper compound
[CuII(atsm)] known for decades may form the basis for a therapy
for amyotrophic lateral sclerosis (ALS), or Lou Gehrig's
disease. In humans, prior to this, no therapy for ALS has ever
been discovered that could extend lifespan more than a few
additional months.
http://www.sciencedaily.com/releases/2014/06/140612142352.htm
Journal Reference:
Oral Treatment with CuII(atsm) Increases Mutant SOD1 In Vivo
but Protects Motor Neurons and Improves the Phenotype of a
Transgenic Mouse Model of Amyotrophic Lateral Sclerosis.
B. R. Roberts, N. K. H. Lim, E. J. McAllum, P. S. Donnelly, D.
J.
Hare, P. A. Doble, B. J. Turner, K. A. Price, S. Chun Lim, B. M.
Paterson, J. L. Hickey, T. W. Rhoads, J. R. Williams, K. M.
Kanninen,
L. W. Hung, J. R. Liddell, A. Grubman, J.-F. Monty, R. M.
Llanos, D.
R. Kramer, J. F. B. Mercer, A. I. Bush, C. L. Masters, J. A.
Duce,
Q.-X. Li, J. S. Beckman, K. J. Barnham, A. R. White, P. J.
Crouch.
Journal of Neuroscience, 2014; 34 (23): 8021 DOI:
10.1523/JNEUROSCI.4196-13.2014
Immune response affects sleep and memory
Date: June 12, 2014
Source: University of Leicester
Summary: Sickness-induced insomnia is common because of the link
between the brain and the immune system. Fighting off illness-
rather
than the illness itself- causes sleep deprivation and affects
memory,
a new study has found. Biologists said a common perception is
that if
you are sick, you sleep more. But the study, carried out in
flies,
found that sickness induced insomnia is quite common.
http://www.sciencedaily.com/releases/2014/06/140612085130.htm
Journal Reference:
Immune stimulation reduces sleep and memory ability
inDrosophila melanogaster.
Eamonn B. Mallon, Akram Alghamdi, Robert T.K. Holdbrook, Ezio
Rosato.
PeerJ, 2014; 2: e434 DOI: 10.7717/peerj.434
'Tomato pill' improves function of blood vessels in patients
with cardiovascular disease
Date: June 9, 2014
Source: University of Cambridge
Summary: A daily supplement of an extract found in tomatoes may
improve the function of blood vessels in patients with
cardiovascular
disease, according to new research. The incidence of
cardiovascular is
notably reduced in southern Europe where a 'Mediterranean diet'
consisting of a larger consumption of fruit, vegetables and
olive oil
predominates. Recent dietary studies suggest that this diet
reduces
the incidence of events related to the disease, including heart
attack
and stroke, in patients at high cardiovascular risk, or those
who have
previously had the disease.
http://www.sciencedaily.com/releases/2014/06/140609205652.htm
Journal Reference:
Effects of Oral Lycopene Supplementation on Vascular Function in
Patients with Cardiovascular Disease and Healthy Volunteers: A
Randomised Controlled Trial.
Parag R. Gajendragadkar, Annette Hubsch, Kaisa M. Mäki-Petäjä,
Martin
Serg, Ian B. Wilkinson, Joseph Cheriyan.
PLoS ONE, 2014; 9 (6): e99070 DOI: 10.1371/journal.pone.0099070
LRRK2 inhibitors may be key to combating parkinson's disease
Date: June 10, 2014
Source: University of Alabama at Birmingham
Summary: An enzyme closely associated with genetic forms of
Parkinson’s disease appears to play a larger role in its
progression
than previously thought, say investigators. The new research
offers
encouraging evidence that drugs to block this enzyme, known as
leucine-rich repeat kinase 2 or LRRK2, could slow -- or even
prevent
-- Parkinson's from developing.
Journal Reference:
Abrogation of -synuclein-mediated dopaminergic
neurodegeneration in LRRK2-deficient rats.
J. P. L. Daher, L. A. Volpicelli-Daley, J. P. Blackburn, M. S.
Moehle,
A. B. West.
Proceedings of the National Academy of Sciences, 2014; DOI:
10.1073/pnas.1403215111
New sensor could light the way forward in low-cost medical
imaging
Date: May 23, 2014
Source: University of Surrey
Summary: A new type of light sensor that could allow medical and
security imaging via low cost cameras has been developed by
researchers. Near infrared light can be used to perform
non-invasive
medical procedures, such as measuring the oxygen level in tissue
and
detecting tumors. It is also already commonly used in security
camera
systems and for quality control in the agriculture and food
industry.
http://www.sciencedaily.com/releases/2014/05/140523082928.htm
Journal Reference:
Ultrahigh Performance C60 Nanorod Large Area Flexible
Photoconductor Devices via Ultralow Organic and Inorganic
Photodoping.
Rinku Saran, Vlad Stolojan, Richard J. Curry.
Scientific Reports, 2014; 4 DOI: 10.1038/srep05041
http://www.nature.com/srep/2014/140523/srep05041/full/srep05041.html
Anti-diabetic drug slows aging and lengthens lifespan, animal
study suggests
Date: June 2, 2014
Source: KU Leuven
Summary: Researchers have provided new evidence that metformin,
the
world’s most widely used anti-diabetic drug, slows aging and
increases
lifespan. Scientists teased out the mechanism behind metformin's
age-slowing effects: the drug causes an increase in the number
of
toxic oxygen molecules released in the cell and this,
surprisingly,
increases cell robustness and longevity in the long term.
http://www.sciencedaily.com/releases/2014/06/140602150724.htm
Journal Reference:
Metformin promotes lifespan through mitohormesis via the
peroxiredoxin PRDX-2.
Wouter De Haes, Lotte Frooninckx, Roel Van Assche, Arne
Smolders,
Geert Depuydt, Johan Billen, Bart P. Braeckman, Liliane Schoofs,
and
Liesbet Temmerman.
PNAS, 2014 DOI: 10.1073/pnas.1321776111
New amyloid-reducing compound could be a preventive measure
against Alzheimer's
Date: June 3, 2014
Source: NYU Langone Medical Center
Summary: Scientists have identified a compound, called 2-PMAP,
in
animal studies that reduced by more than half levels of amyloid
proteins in the brain associated with Alzheimer’s disease.
http://www.sciencedaily.com/releases/2014/06/140603092006.htm
Journal Reference:
Modulation of amyloid precursor protein expression reduces
β-amyloid deposition in a mouse model.
Ayodeji A. Asuni, Maitea Guridi, Joanna E.
Pankiewicz, Sandrine Sanchez, Martin J. Sadowski.
Annals of Neurology, 2014; DOI: 10.1002/ana.24149
Newborns exposed to dirt, dander, germs may have lower
allergy, asthma risk
Date: June 6, 2014
Source: Johns Hopkins Medicine
Summary: Infants exposed to rodent and pet dander, roach
allergens and
a wide variety of household bacteria in the first year of life
appear
less likely to suffer from allergies, wheezing and asthma,
according
to results of a recent study. Those who encounter such
substances
before their first birthdays seem to benefit rather than suffer
from
them. Importantly, the protective effects of both allergen and
bacterial exposure were not seen if a child's first encounter
with
these substances occurred after age 1, the research found.
http://www.sciencedaily.com/releases/2014/06/140606091157.htm
Journal Reference:
Effects of early-life exposure to allergens and bacteria on
recurrent wheeze and atopy in urban children.
Susan V. Lynch, Robert A. Wood, Homer Boushey, Leonard B.
Bacharier,
Gordon R. Bloomberg, Meyer Kattan, George T. O’Connor, Megan T.
Sandel, Agustin Calatroni, Elizabeth Matsui, Christine C.
Johnson,
Henry Lynn, Cynthia M. Visness, Katy F. Jaffee, Peter J. Gergen,
Diane
R. Gold, Rosalind J. Wright, Kei Fujimura, Marcus Rauch, William
W.
Busse, James E. Gern.
Journal of Allergy and Clinical Immunology, 2014; DOI:
10.1016/j.jaci.2014.04.018
Sleep after learning strengthens connections between brain
cells and enhances memory
Date: June 5, 2014
Source: NYU Langone Medical Center / New York University School
of Medicine
Summary: Researchers show for the first time that sleep after
learning
encourages the growth of dendritic spines, the tiny protrusions
from
brain cells that connect to other brain cells and facilitate the
passage of information across synapses, the junctions at which
brain
cells meet.
http://www.sciencedaily.com/releases/2014/06/140605141849.htm
Journal Reference:
Sleep promotes branch-specific formation of dendritic spines
after learning.
G. Yang, C. S. W. Lai, J. Cichon, L. Ma, W. Li, W.-B. Gan.
Science, 2014; 344 (6188): 1173 DOI: 10.1126/science.1249098
New cause of high blood pressure, heart disease discovered:
Phosphate-rich foods
Date: May 5, 2014
Source: Veterinärmedizinische Universität Wien
Summary: Phosphate-rich foods
include processed cheese, Parmesan, cola, baking
powder and most processed foods. Phosphates are widely used in
the
food industry as preservatives and pH stabilizers. When large
quantities of phosphates are consumed, production of the FGF23
hormone
is stimulated, which has a negative effect on the cardiovascular
system. One expert warns that “our phosphate consumption
is relevant
for our state of health.”
http://www.sciencedaily.com/releases/2014/05/140505104229.htm
Journal References:
Olena Andrukhova, Svetlana Slavic, Alina Smorodchenko, Ute
Zeitz,
Victoria Shalhoub, Beate Lanske, Elena E. Pohl and Reinhold G.
Erben.
FGF23 Regulates Renal Sodium Handling and Blood Pressure. EMBO
Molecular Medicine, May 2014 DOI: 10.1002/emmm.201303716
Olena Andrukhova, Alina Smorodchenko, Monika Egerbacher, Carmen
Streicher, Ute Zeitz, Regina Goetz, Victoria Shalhoub, Moosa
Mohammadi, Elena E Pohl, Beate Lanske, Reinhold G Erben. FGF23
promotes renal calcium reabsorption through the TRPV5 channel.
The
EMBO Journal, 2014; DOI: 10.1002/embj.201284188
Novel antioxidant makes old arteries seem young again, study
shows
Date: May 6, 2014
Source: University of Colorado at Boulder
Summary: An antioxidant that targets specific cell structures --
mitochondria -- may be able to reverse some of the negative
effects of
aging on arteries, reducing the risk of heart disease, according
to a
new study. When the research team gave old mice -- the
equivalent of
70- to 80-year-old humans -- water containing an antioxidant
known as
MitoQ for four weeks, their arteries functioned as well as the
arteries of mice with an equivalent human age of just 25 to 35
years.
http://www.sciencedaily.com/releases/2014/05/140506094940.htm
Scientists discover a natural molecule to treat type 2
diabetes: Molecule mimics some effect of physical exercise
Date: May 12, 2014
Source: Université Laval
Summary: Researchers have discovered a natural molecule that
could be
used to treat insulin resistance and type 2 diabetes. The
molecule, a
derivative of omega-3 fatty acids, mimics some of the effects of
physical exercise on blood glucose regulation.
http://www.sciencedaily.com/releases/2014/05/140512112547.htm
Diets rich in antioxidant resveratrol fail to reduce deaths,
heart disease or cancer
Date: May 12, 2014
Source: Johns Hopkins Medicine
Summary: A study of Italians who consume a diet rich in
resveratrol --
the compound found in red wine, dark chocolate and berries --
finds
they live no longer than and are just as likely to develop
cardiovascular disease or cancer as those who eat or drink
smaller
amounts of the antioxidant.
http://www.sciencedaily.com/releases/2014/05/140512214128.htm
Journal Reference:
Mortality
in Older Community-Dwelling Adults.
Richard D. Semba, Luigi Ferrucci, Benedetta
Bartali, Mireia
Urpí-Sarda, Raul Zamora-Ros, Kai Sun, Antonio Cherubini,
Stefania
Bandinelli, Cristina Andres-Lacueva. Resveratrol Levels and
All-Cause
JAMA Internal Medicine,
2014; DOI: 10.1001/jamainternmed.2014.1582
Herpes-loaded stem cells used to kill brain tumors
Date: May 16, 2014
Source: Harvard University
Summary: A potential solution for how to more effectively kill
tumor
cells using cancer-killing viruses has been discovered by
researchers.
The investigators report that trapping virus-loaded stem cells
in a
gel and applying them to tumors significantly improved survival
in
mice with glioblastoma multiform, the most common brain tumor in
human
adults and also the most difficult to treat.
http://www.sciencedaily.com/releases/2014/05/140516203342.htm
Journal Reference:
Matthias Duebgen, Jordi Martinez-Quintanilla, Kaoru Tamura,
Shawn
Hingtgen, Navid Redjal, Hiroaki Wakimoto And Khalid Shah.
Stem Cells Loaded With Multimechanistic Oncolytic Herpes
Simplex Virus Variants for Brain Tumor Therapy.
Journal of the National Cancer Institute, May
2014 DOI: 10.1093/jnci/dju090
Gum disease bacteria may cause heart disease
Date: May 18, 2014
Source: American Society for Microbiology
Summary: The same bacteria that cause gum disease also promotes
heart
disease -- a discovery that could change the way heart disease
is
diagnosed and treated. Heart disease is the leading cause of
death in
the North America. Gum disease affects 46 percent of the U.S.
population and is caused by bacteria that grow on the teeth
under the
gums. Although doctors know that patients with gum disease are
at
higher risk for heart disease, gum disease isn't viewed as a
traditional risk factor for heart disease.
... four specific bacteria (Porphyromonas gingivalis, Treponema
denticola [a spirochete], Tannerella forsythia, Fusobacterium
nucleatum)
http://www.sciencedaily.com/releases/2014/05/140518164339.htm
American Society for Microbiology. "Gum disease bacteria may
cause
heart disease." ScienceDaily. ScienceDaily, 18 May 2014.
<www.sciencedaily.com/releases/2014/05/140518164339.htm>.
Update Wikipedia entry for teponema denticola for
neurospirochetosis.
Create Wikipedia page for neurospirochetosis???
Bacteria in mouth may diagnose pancreatic cancer
Date: May 18, 2014
Source: American Society for Microbiology
Summary: Patients with pancreatic cancer have a different and
distinct
profile of specific bacteria in their saliva compared to healthy
controls and even patients with other cancers or pancreatic
diseases,
according to new research. These findings could form the basis
for a
test to diagnose the disease in its early stages.
http://www.sciencedaily.com/releases/2014/05/140518164419.htm
[Bacteria is maybe the CAUSE???? not just a symptom.]
American Society for Microbiology.
"Bacteria in mouth may diagnose pancreatic cancer."
ScienceDaily. ScienceDaily, 18 May 2014.
<www.sciencedaily.com/releases/2014/05/140518164419.htm>.
Pine bark substance could be potent melanoma drug
Date: May 20, 2014
Source: Penn State
Summary: A substance that comes from pine bark is a potential
source
for a new treatment of melanoma, according to researchers.
Current
melanoma drugs targeting single proteins can initially be
effective,
but resistance develops relatively quickly and the disease
recurs. In
those instances, resistance usually develops when the cancer
cell's
circuitry bypasses the protein that the drug acts on, or when
the cell
uses other pathways to avoid the point on which the drug acts.
http://www.sciencedaily.com/releases/2014/05/140520120041.htm
Journal References:
R. Gowda, S. V. Madhanupantula, O. F. Kuzu, A. Sharma, G. P.
Robertson. Targeting Multiple Key Signaling Pathways in Melanoma
using
Leelamine. Molecular Cancer Therapeutics, 2014; DOI:
10.1158/1535-7163.MCT-13-0867
O. F. Kuzu, R. Gowda, A. Sharma, G. P. Robertson.
Leelamine mediates cancer cell death through inhibition of
intracellular cholesterol transport.
Molecular Cancer Therapeutics, 2014; DOI:
10.1158/1535-7163.MCT-13-0868
Research explains action of drug that may slow aging, related
disease
Date: May 20, 2014
Source: Oregon State University
Summary: A proven approach to slow the aging process is dietary
restriction, but new research helps explain the action of a drug
that
appears to mimic that process -- rapamycin. The advance
moves science
closer to a compound that might slow aging and reduce
age-related
disease. The lead researcher said that this study "could provide
a way
not only to increase lifespan but to address some age-related
diseases
and improve general health."
...the combined use of rapamycin and metformin prevented the
unwanted
side effect....
http://www.sciencedaily.com/releases/2014/05/140520142416.htm
[wasn't there another article saying rapamycin may be useful
for treating autism?]
Journal Reference:
Z. Yu, R. Wang, W. C. Fok, A. Coles, A. B. Salmon, V. I. Perez.
Rapamycin and Dietary Restriction Induce Metabolically
Distinctive Changes in Mouse Liver.
The Journals of Gerontology Series A: Biological Sciences and
Medical Sciences, 2014; DOI:
10.1093/gerona/glu053
Some pancreatic cancer treatments may be going after wrong
targets
Date: May 22, 2014
Source: University of Michigan Health System
Summary: New research represents a significant change in the
understanding of how pancreatic cancer grows – and how it might
be
defeated. Unlike other types of cancer, pancreatic cancer
produces a
lot of scar tissue and inflammation. For years, researchers
believed
that this scar tissue, called desmoplasia, helped the tumor
grow, and
they’ve designed treatments to attack this. But new research
finds
that when you eliminate desmoplasia, tumors grow even more
quickly and
aggressively. In the study, mice in which the desmoplasia was
eliminated developed tumors earlier and died sooner.
...What they found in this study was that a drug designed to
attack
blood vessels, called an angiogenesis inhibitor, significantly
improved overall survival in the mice who had desmoplasia
blocked.
Angiogenesis inhibitors already exist on the market with
approval from
the U.S. Food and Drug Administration...
[Curcumin is an anti-angiogenesis agent. Myricetin?]
http://www.sciencedaily.com/releases/2014/05/140522123352.htm
Journal Reference:
Stromal Elements Act to Restrain, Rather Than Support,
Pancreatic Ductal Adenocarcinoma.
Andrew D. Rhim, Paul E. Oberstein, Dafydd H. Thomas, Emily T.
Mirek,
Carmine F. Palermo, Stephen A. Sastra, Erin N. Dekleva, Tyler
Saunders, Claudia P. Becerra, Ian W. Tattersall, C. Benedikt
Westphalen, Jan Kitajewski, Maite G. Fernandez-Barrena, Martin
E.
Fernandez-Zapico, Christine Iacobuzio-Donahue, Kenneth P. Olive,
Ben
Z. Stanger.
Cancer Cell, 2014; DOI: 10.1016/j.ccr.2014.04.021
Functioning of aged brains and muscles in mice made younger:
More progress with GDF 11, anti-aging protein
Date: May 4, 2014
Source: Harvard University
Summary: Scientists have shown that a protein they previously
demonstrated can make the failing hearts in aging mice appear
more
like those of young health mice, similarly improves brain and
skeletal
muscle function in aging mice. In two separate articles
scientists
report that injections of a protein known as GDF11, which is
found in
humans as well as mice, improved the exercise capability of mice
equivalent in age to that of about a 70-year-old human.
http://www.sciencedaily.com/releases/2014/05/140504133205.htm
Infusion of young blood recharges brains of old mice
Date: May 5, 2014
Source: Stanford University Medical Center
Summary: Something -- or some things -- in the blood of young
mice has
the ability to restore mental capabilities in old mice, a new
study
has found. If the same goes for humans, it could spell a new
paradigm
for recharging our aging brains, and it might mean new
therapeutic
approaches for treating dementias such as Alzheimer's disease.
http://www.sciencedaily.com/releases/2014/05/140505094906.htm
Journal Reference:
Saul A Villeda, Kristopher E Plambeck, Jinte Middeldorp, Joseph
M
Castellano, Kira I Mosher, Jian Luo, Lucas K Smith, Gregor
Bieri,
Karin Lin, Daniela Berdnik, Rafael Wabl, Joe Udeochu, Elizabeth
G
Wheatley, Bende Zou, Danielle A Simmons, Xinmin S Xie, Frank M
Longo,
Tony Wyss-Coray.
Young blood reverses age-related impairments in cognitive
function and synaptic plasticity in mice.
Nature Medicine,
2014; DOI: 10.1038/nm.3569
Brain may never fully recover from exposure to paint, glue,
degreasers
Date: May 12, 2014
Source:
American Academy of Neurology (AAN)
Summary: People who are exposed to paint, glue or degreaser
fumes at
work may experience memory and thinking problems in retirement,
decades after their exposure, according to a new study.
Researchers
assessed the workers' lifetime exposure to chlorinated solvents,
petroleum solvents, and benzene, including the timing of last
exposure
and lifetime dosage. Benzene is used to make plastics, rubber,
dye,
detergents and other synthetic materials. Chlorinated solvents
can be
found in dry cleaning solutions, engine cleaners, paint removers
and
degreasers. Petroleum solvents are used in carpet glue,
furniture
polishes, paint, paint thinner and varnish.
http://www.sciencedaily.com/releases/2014/05/140512213734.htm
Journal Reference:
E. L. Sabbath, L.-A. Gutierrez, C. A. Okechukwu, A.
Singh-Manoux, H.
Amieva, M. Goldberg, M. Zins, C. Berr. Time may not fully
attenuate
solvent-associated cognitive deficits in highly exposed workers.
Neurology, 2014; 82 (19): 1716 DOI: 10.1212/WNL.0000000000000413
NAP (Davuentide)
Novel protein fragments may protect against Alzheimer's
Date: May 13, 2014
Source: American Friends of Tel Aviv University
Summary: Alzheimer's research has centered on trying to
understand the
protective or regenerative properties of brain cells as an
avenue for
treating the widespread disease. Now a researcher has discovered
novel
protein fragments that have proven protective properties for
cognitive
functioning. Her findings have the potential to serve as a
pipeline
for new drug candidates to treat the disease.
http://www.sciencedaily.com/releases/2014/05/140513152955.htm
Herpes-loaded stem cells used to kill brain tumors
Date: May 16, 2014
Source: Harvard University
Summary: A potential solution for how to more effectively kill
tumor
cells using cancer-killing viruses has been discovered by
researchers.
The investigators report that trapping virus-loaded stem cells
in a
gel and applying them to tumors significantly improved survival
in
mice with glioblastoma multiform, the most common brain tumor in
human
adults and also the most difficult to treat.
http://www.sciencedaily.com/releases/2014/05/140516203342.htm
Journal Reference:
Matthias Duebgen, Jordi Martinez-Quintanilla, Kaoru Tamura,
Shawn
Hingtgen, Navid Redjal, Hiroaki Wakimoto And Khalid Shah.
Stem Cells Loaded With Multimechanistic Oncolytic Herpes
Simplex Virus Variants for
Brain Tumor Therapy.
Journal of the National Cancer Institute, May
2014 DOI: 10.1093/jnci/dju090
Research explains action of drug that may slow aging, related
disease
Date: May 20, 2014
Source: Oregon State University
Summary: A proven approach to slow the aging process is dietary
restriction, but new research helps explain the action of a drug
that
appears to mimic that process -- rapamycin. The advance moves
science
closer to a compound that might slow aging and reduce
age-related
disease. The lead researcher said that this study "could provide
a way
not only to increase lifespan but to address some age-related
diseases
and improve general health."
http://www.sciencedaily.com/releases/2014/05/140520142416.htm
Journal Reference:
Z. Yu, R. Wang, W. C. Fok, A. Coles, A. B. Salmon, V. I. Perez.
Rapamycin and Dietary Restriction Induce Metabolically
Distinctive Changes in Mouse Liver.
The Journals of Gerontology Series A:
Biological Sciences and Medical Sciences, 2014; DOI:
10.1093/gerona/glu053
Compound reverses symptoms of Alzheimer's disease in mice
Date: May 20, 2014
Source: Saint Louis University Medical Center
Summary: Research in an animal model supports the potential
therapeutic value of an antisense compound to treat Alzheimer's
disease. The molecule also reduced inflammation in the part of
the
brain responsible for learning and memory. The article is the
second
mouse study that supports the potential therapeutic value of an
antisense compound in treating Alzheimer's disease in humans.
antisense oligonucleotide (OL-1)
http://www.sciencedaily.com/releases/2014/05/140520184640.htm
Take notes by hand for better long-term comprehension
Date: April 24, 2014
Source: Association for Psychological Science
Summary: Dust off those Bic ballpoints and college-ruled
notebooks:
research shows that taking notes by hand is better than taking
notes
on a laptop for remembering conceptual information over the long
term.
"Our new findings suggest that even when laptops are used as
intended
-- and not for buying things on Amazon during class -- they may
still
be harming academic performance," says a psychological scientist
involved in the study.
http://www.sciencedaily.com/releases/2014/04/140424102837.htm
Journal Reference:
The Pen Is Mightier Than the Keyboard: Advantages of Longhand
Over Laptop Note Taking.
P. A. Mueller, D. M. Oppenheimer.
Psychological Science, 2014; DOI: 10.1177/0956797614524581
Young Blood May Hold Key to Reversing Aging
By CARL ZIMMERMAY 4, 2014
...a protein called GDF11 was abundant in young mice and scarce
in old ones.
http://www.nytimes.com/2014/05/05/science/young-blood-may-hold-key-to-reversing-aging.html?_r=0
Infusion of young blood recharges brains of old mice
Date: May 5, 2014
Source: Stanford University Medical Center
Summary: Something -- or some things -- in the blood of young
mice has
the ability to restore mental capabilities in old mice, a new
study
has found. If the same goes for humans, it could spell a new
paradigm
for recharging our aging brains, and it might mean new
therapeutic
approaches for treating dementias such as Alzheimer's disease.
http://www.sciencedaily.com/releases/2014/05/140505094906.htm
Journal Reference:
Young blood reverses age-related impairments in cognitive
function and synaptic plasticity in mice.
Saul A Villeda, Kristopher E Plambeck, Jinte Middeldorp, Joseph
M
Castellano, Kira I Mosher, Jian Luo, Lucas K Smith, Gregor
Bieri,
Karin Lin, Daniela Berdnik, Rafael Wabl, Joe Udeochu, Elizabeth
G
Wheatley, Bende Zou, Danielle A Simmons, Xinmin S Xie, Frank M
Longo,
Tony Wyss-Coray.
Nature Medicine, 2014; DOI: 10.1038/nm.3569
Functioning of aged brains and muscles in mice made younger:
More progress with GDF 11, anti-aging protein
Date: May 4, 2014
Source: Harvard University
Summary: Scientists have shown that a protein they previously
demonstrated can make the failing hearts in aging mice appear
more
like those of young health mice, similarly improves brain and
skeletal
muscle function in aging mice. In two separate articles
scientists
report that injections of a protein known as GDF11, which is
found in
humans as well as mice, improved the exercise capability of mice
equivalent in age to that of about a 70-year-old human.
http://www.sciencedaily.com/releases/2014/05/140504133205.htm
Vitamin D deficiency, cognition appear to be linked in older
adults
Date: April 15, 2014
Source: Wake Forest Baptist Medical Center
Summary:
A study that looks at Vitamin D deficiency and cognition
relationship
in older adults adds to the existing literature on the subject.
"This
study provides increasing evidence that suggests there is an
association between low vitamin D levels and cognitive decline
over
time," said the lead author. "Although this study cannot
establish a
direct cause and effect relationship, it would have a huge
public
health implication if vitamin D supplementation could be shown
to
improve cognitive performance over time because deficiency is so
common in the population."
http://www.sciencedaily.com/releases/2014/04/140415111314.htm
Journal Reference:
Relationship Between 25-Hydroxyvitamin D and Cognitive
Function in Older Adults: The Health, Aging and Body
Composition Study.
Valerie K. Wilson, Denise K. Houston, Laurel Kilpatrick, James
Lovato,
Kristine Yaffe, Jane A. Cauley, Tamara B. Harris, Eleanor M.
Simonsick, Hilsa N. Ayonayon, Stephen B. Kritchevsky, Kaycee M.
Sink.
Journal of the American Geriatrics Society, 2014; 62 (4): 636
DOI:
10.1111/jgs.12765
Obesity: Are lipids hard drugs for the brain?
Date: April 15, 2014
Source: CNRS (Délégation Paris Michel-Ange)
Summary:
Why can we get up for a piece of chocolate, but never because we
fancy
a carrot? Research has demonstrated part of the answer:
triglycerides,
fatty substances from food, may act in our brains directly on
the
reward circuit, the same circuit that is involved in drug
addiction.
These results show a strong link in mice between fluctuations in
triglyceride concentration and brain reward development.
Identifying
the action of nutritional lipids on motivation and the search
for
pleasure in dietary intake will help us better understand the
causes
of some compulsive behaviors and obesity.
http://www.sciencedaily.com/releases/2014/04/140415084200.htm
Cancer drugs block dementia-linked brain inflammation, study
finds
Date: April 16, 2014
Source: University of California - Irvine
Summary:
A class of drugs developed to treat immune-related conditions
and
cancer -- including one currently in clinical trials for
glioblastoma
and other tumors -- eliminates neural inflammation associated
with
dementia-linked diseases and brain injuries, according to
researchers.
In their study, the researchers discovered that the drugs, which
can
be delivered orally, eradicated microglia, the primary immune
cells of
the brain. These cells exacerbate many neural diseases,
including
Alzheimer's and Parkinson's, as well as brain injury.
http://www.sciencedaily.com/releases/2014/04/140416133343.htm
Journal Reference:
Colony-Stimulating Factor 1 Receptor Signaling Is Necessary for
Microglia Viability, Unmasking a Microglia Progenitor Cell in
the
Adult Brain.
Monica R.P. Elmore, Allison R. Najafi, Maya A. Koike, Nabil N.
Dagher,
Elizabeth E. Spangenberg, Rachel A. Rice, Masashi Kitazawa,
Bernice
Matusow, Hoa Nguyen, Brian L. West, Kim N. Green.
Neuron, 2014; 82 (2): 380 DOI: 10.1016/j.neuron.2014.02.040
Fat metabolism in animals altered to prevent most common type
of heart disease
Date: April 22, 2014
Source: Johns Hopkins Medicine
Summary:
Working with mice and rabbits, scientists have found a way to
block
abnormal cholesterol production, transport and breakdown,
successfully
preventing the development of atherosclerosis, the main cause of
heart
attacks and strokes and the number-one cause of death among
humans.
The condition develops when fat builds inside blood vessels over
time
and renders them stiff, narrowed and hardened, greatly reducing
their
ability to feed oxygen-rich blood to the heart muscle and the
brain.
http://www.sciencedaily.com/releases/2014/04/140422121001.htm
"The Johns Hopkins team used an existing human-made compound
called
D-PDMP to block the synthesis of the GSL molecule, and by doing
so,
prevented the development of heart disease in mice and rabbits
fed a
high-fat, cholesterol-laden diet."
Journal Reference:
Inhibition of Glycosphingolipid Synthesis Ameliorates
Atherosclerosis and Arterial Stiffness in Apo E-/- Mice and
Rabbits Fed a High Fat and Cholesterol Diet.
S. Chatterjee, D. Bedja, S. Mishra, C. Amuzie, A. Avolio, D.
Kass, D.
Berkowitz, M. Renehan.
Circulation, 2014; DOI: 10.1161/%u200BCIRCULATIONAHA.113.007559
Proposal: Managing most troubling symptoms of dementia,
lessen use of drugs
Date: April 21, 2014
Source: University of Michigan Health System
Summary:
A new approach to handling agitation, aggression and other
unwanted
behaviors by people with dementia may help reduce the use of
antipsychotics and other psychiatric drugs in this population,
and
make life easier for them and their caregivers. A panel of
specialists
in senior mental health hope to spark better teamwork among
those who
care for dementia patients at home, in residential facilities
and in
hospitals and clinics.
http://www.sciencedaily.com/releases/2014/04/140421093734.htm
Journal Reference:
Management of Neuropsychiatric Symptoms of Dementia in
Clinical Settings: Recommendations from a Multidisciplinary
Expert Panel.
Helen C. Kales, Laura N. Gitlin, Constantine G. Lyketsos.
Journal of the American Geriatrics Society, 2014; 62 (4): 762
DOI:
10.1111/jgs.12730
Ginseng can treat, prevent influenza, RSV, researcher
finds
Date: April 21, 2014
Source: Georgia State University
Summary: Ginseng can help treat and prevent influenza and
respiratory
syncytial virus, a respiratory virus that infects the lungs and
breathing passages, according to research findings. Seasonal
influenza
is a serious respiratory disease that causes annual epidemics in
humans worldwide, resulting in about three to five million cases
of
severe illness and about 250,000 to 500,000 deaths, according to
the
World Health Organization.
http://www.sciencedaily.com/releases/2014/04/140421102346.htm
Journal Reference:
Immunomodulatory Activity of Red Ginseng against Influenza A
Virus Infection.
Jong Lee, Hye Hwang, Eun-Ju Ko, Yu-Na Lee, Young-Man Kwon,
Min-Chul
Kim, Sang-Moo Kang.
Nutrients, 2014; 6 (2): 517 DOI: 10.3390/nu6020517
Regular exercise can keep dementia at bay - even if it's in your
genes: Being active three times a week stops the brain from
shrinking
Study found being active at least three times a week stops brain
shrinking
Experts recommend swimming, jogging, cycling and even mundane
chores
US researchers measured brain activity in pensioners over 18
months
By FIONA MACRAE
PUBLISHED: 17:51 EST, 23 April 2014 | UPDATED: 07:45 EST, 24
April 2014
http://www.dailymail.co.uk/health/article-2611693/Regular-exercise-dementia-bay-genes-Being-active-three-times-week-stops-brain-shrinking.html
Physical activity keeps hippocampus healthy in people at
risk for Alzheimer's disease
Date: April 23, 2014
Source: University of Maryland
Summary: Moderate physical activity may preserve the hippocampus
--
the brain region responsible for memory and spatial orientation
that
is attacked first in Alzheimer's disease, a study of older
adults at
increased risk for Alzheimer's disease shows. It is the first
evidence
that physical activity may protect against cognitive decline and
the
onset of dementia symptoms in those who carry the genetic marker
for
Alzheimer's.
http://www.sciencedaily.com/releases/2014/04/140423102746.htm
Journal Reference:
Physical activity reduces hippocampal atrophy in elders at
genetic risk for Alzheimer's disease.
J. Carson Smith, Kristy A. Nielson, John L. Woodard, Michael
Seidenberg, Sally Durgerian, Kathleen E. Hazlett, Christina M.
Figueroa, Cassandra C. Kandah, Christina D. Kay, Monica A.
Matthews,
Stephen M. Rao.
Frontiers in Aging Neuroscience, 2014; 6 DOI:
10.3389/fnagi.2014.00061
Taking a walk may lead to more creativity than sitting, study
finds
PUBLIC RELEASE DATE:
24-Apr-2014
Contact: Lisa Bowen
lbowen@apa.org
202-336-5707
American Psychological Association
Free-flowing thought more likely while walking indoors or
outdoors,research reveals
WASHINGTON -- When the task at hand requires some imagination,
taking
a walk may lead to more creative thinking than sitting,
according to
research published by the American Psychological Association.
http://www.eurekalert.org/pub_releases/2014-04/apa-taw042414.php
Is Sitting For Long Hours At Work The New Smoking?
April 22, 2014 10:52 AM
http://pittsburgh.cbslocal.com/2014/04/22/is-sitting-for-long-hours-at-work-the-new-smoking/
Moderate exercise not only treats, but prevents depression
Date:October 28, 2013
http://www.sciencedaily.com/releases/2013/10/131028163003.htm
Taking a walk 'makes your brain grow': Energetic stroll three
times a week can increase size of organ's memory hub
By Fiona Macrae Science
Correspondent In Chicago
PUBLISHED: 19:51 EST, 17 February 2014 | UPDATED: 03:28 EST, 18
February 2014
http://www.dailymail.co.uk/health/article-2561708/Taking-walk-makes-brain-grow-Energetic-stroll-three-times-week-increase-size-organs-memory-hub.html
Walking can lower risk of heart-related conditions as much as
running
Date:April 4, 2013
http://www.sciencedaily.com/releases/2013/04/130404170225.htm
High blood caffeine levels in older adults linked to
avoidance of Alzheimer’s disease
Date:June 4, 2012
http://www.sciencedaily.com/releases/2012/06/120604142615.htm
Iron is at core of Alzheimer's disease, study suggests
Date:August 20, 2013
http://www.sciencedaily.com/releases/2013/08/130820135032.htm
CPAP therapy restores brain tissue in adults with sleep
apnea, study finds
Date:June 9, 2010
Source:American Academy of Sleep Medicine
Summary:Obstructive sleep apnea patients had reductions of
grey-matter
volume at baseline but showed significant grey-matter volume
increase
after three months of CPAP therapy, according to new research.
http://www.sciencedaily.com/releases/2010/06/100607065550.htm
Strawberries lower cholesterol, study suggests
Date:February 25, 2014
Source:Plataforma SINC
Summary:A team of volunteers ate half a kilo of strawberries a
day for
a month to see whether it altered their blood parameters in any
way.
At the end of this unusual treatment, their levels of bad
cholesterol
and triglycerides were significantly reduced, according to the
analyses conducted by Italian and Spanish scientists. Several
studies
had already demonstrated the antioxidant capacity of
strawberries, but
now researchers conducted an analysis that revealed that these
fruits
also help to reduce cholesterol.
http://www.sciencedaily.com/releases/2014/02/140225101256.htm
Poor sleep quality linked to cognitive decline in older men
Date:March 31, 2014
Source:American Academy of Sleep Medicine
Summary:A link between poor sleep quality and the development of
cognitive decline over three to four years was found in a new
study of
older men. Results show that higher levels of fragmented sleep
and
lower sleep efficiency were associated with a 40 to 50 percent
increase in the odds of clinically significant decline in
executive
function, which was similar in magnitude to the effect of a
five-year
increase in age. In contrast, sleep duration was not related to
subsequent cognitive decline.
http://www.sciencedaily.com/releases/2014/03/140331170557.htm
Chowing down on watermelon could lower blood pressure, study
suggests
April 3, 2014
Florida State University
Summary:
Watermelon could significantly reduce blood pressure in
overweight
individuals both at rest and while under stress. "The pressure
on the
aorta and on the heart decreased after consuming watermelon
extract,"
the small study concludes.
http://www.sciencedaily.com/releases/2014/04/140403095457.htm
Morning rays keep off pounds
April 2, 2014
Northwestern University
Summary:
A surprising new strategy for managing your weight? Bright
morning
light. People who had most of their daily exposure to bright
light in
the morning had a significantly lower body mass index (BMI) than
those
who had most of their light exposure later in the day, reports a
new
study. The earlier light exposure occurred, the lower the BMI.
The
influence of morning light on weight was independent of physical
activity, caloric intake, sleep timing, age or season.
http://www.sciencedaily.com/releases/2014/04/140402212531.htm
Key chocolate ingredients could help prevent obesity,
diabetes
April 2, 2014
American Chemical Society
Summary:
Improved thinking. Decreased appetite. Lowered blood pressure.
The
potential health benefits of dark chocolate keep piling up, and
scientists are now homing in on what ingredients in chocolate
might
help prevent obesity, as well as type-2 diabetes. They found
that one
particular type of antioxidant in cocoa prevented laboratory
mice from
gaining excess weight and lowered their blood sugar levels.
http://www.sciencedaily.com/releases/2014/04/140402110000.htm
Levels of sodium intake recommended by CDC associated with
harmful
health outcomes, study finds
April 2, 2014
Oxford University Press USA
Summary:
A new study finds evidence that the average daily sodium intake
of
most Americans is actually associated with better health
outcomes than
intake levels currently recommended by the CDC and major health
departments, which are now being viewed by many in the
scientific
community as excessively and unrealistically low.
http://www.sciencedaily.com/releases/2014/04/140402095848.htm
Coffee consumption reduces mortality risk from liver
cirrhosis
April 2, 2014
Wiley
Summary:
Consuming two or more cups of coffee each day reduces the risk
of
death from liver cirrhosis by 66%, specifically cirrhosis caused
by
non-viral hepatitis, new research reveals. Findings show that
tea,
fruit juice, and soft drink consumption are not linked to
cirrhosis
mortality risk. As with previous studies, heavy alcohol use was
found
to increase risk of death from cirrhosis.
http://www.sciencedaily.com/releases/2014/04/140402095656.htm
Article
Potential anticancer activity of myricetin in human T24
bladder cancer cells both in vitro and in vivo.
Fang Sun, Xiang Yi Zheng, Jia Ye, Ting Ting Wu, Jian li Wang,
Weilin Chen
Institute of Immunology, Zhejiang University School of Medicine,
Hangzhou, China.
Nutrition and Cancer (Impact Factor: 2.7). 04/2012;
64(4):599-606.
DOI:10.1080/01635581.2012.665564
Source: PubMed
ABSTRACT Myricetin, a naturally occurring phytochemical, has
potent
anticancer-promoting activity and contributes to the
chemopreventive
potential of several foods. In this preliminary study, we
evaluate the
chemopreventive potential of myricetin against
Outcome of stroke worse for people with infection
Date: April 15, 2014
Source: Manchester University
Summary:
Infection is bad news for all of us - but it can be really
serious to
people who have had a stroke. Evidence is mounting that
infection
makes things much worse after a stroke. The researchers show
that
rodents with pneumonia fared worse after having a stroke than
those
without the bacterial infection. This study builds on previous
research demonstrating that an anti-inflammatory drug, called
'interleukin-1 receptor antagonist', could dramatically limit
the
amount of brain damage in experimental stroke.
http://www.sciencedaily.com/releases/2014/04/140415084150.htm
[how about UTI or spirochete infection?]
5/8/2013
Experts Call for Research On Prevalence of Delayed
Neurological Dysfunction After Head Injury
Apr. 5, 2013 —
http://www.sciencedaily.com/releases/2013/04/130405171430.htm
New Light Shed On Traumatic Brain Injuries
Apr. 15, 2013 — Even a mild injury to the brain can have long
lasting consequences, including increased risk of cognitive
impairment later in life. While it is not yet known how brain
injury increases risk for dementia, there are indications that
chronic, long-lasting, inflammation in the brain may be
important. A new paper by researchers at the University of
Kentucky Sanders-Brown Center on Aging (SBCoA), appearing in
the Journal of Neuroscience, offers the latest information
concerning a "switch" that turns "on" and "off" inflammation
in the brain after trauma
http://www.sciencedaily.com/releases/2013/04/130415151444.htm
Mild Blast Injury Causes Molecular Changes in Brain Akin to
Alzheimer
Apr. 24, 2013 — A multicenter study led by scientists at the
University of Pittsburgh School of Medicine shows that mild
traumatic brain injury after blast exposure produces
inflammation, oxidative stress and gene activation patterns
akin to disorders of memory processing such as Alzheimer's
disease.
http://www.sciencedaily.com/releases/2013/04/130424103128.htm
The Power of Cocoa Polyphenols Against Neurodegenerative
Diseases
Apr. 12, 2013 — Epidemiological studies have indicated that
dietary habits and antioxidants from diet can influence the
incidence of neurodegenerative disorders such as Alzheimer's
and Parkinson's diseases. In the recent years, a number of
papers have reported on neuroprotective effects of polyphenols
in cell and animal models. However, the majority of these
studies have focused only on the anti-oxidant properties of
these compounds and less on the mechanism/s of action at
cellular and molecular levels.
http://www.sciencedaily.com/releases/2013/04/130412132229.htm
Bursts of Brain Activity May Protect Against Alzheimer's
Disease
Apr. 18, 2013 — ...This represents a major advance in
understanding that brain circuits regulate composition of
amyloid-beta proteins, showing that the disease is not just
driven by genetic mutations, but by physiological mechanisms
as well. ...
http://www.sciencedaily.com/releases/2013/04/130418125742.htm
No Evidence Drugs, Vitamins, Supplements Help Prevent
Cognitive Decline in Healthy Older Adults
Apr. 15, 2013 — ...They found no strong evidence for
pharmacologic treatments such as cholinesterase inhibitors
that were developed to improve the effectiveness of
acetylcholine, a chemical messenger that assists memory,
thought and judgment.
Nor was there strong evidence that herbal supplements such as
gingko improved cognitive functions or vitamins and fatty
acids such as vitamin B6 or omega-3 fatty acids... [ Note what
was NOT studied: The supplements included in Dale's List]
http://www.sciencedaily.com/releases/2013/04/130415151439.htm
No Link Between Anesthesia, Dementia in Elderly
May 1, 2013 — Elderly patients who receive anesthesia are no
more likely to develop long-term dementia or Alzheimer's
disease than other seniors, according to new Mayo Clinic
research. The study analyzed thousands of patients using the
Rochester Epidemiology Project -- which allows researchers
access to medical records of nearly all residents of Olmsted
County, Minn. -- and found that receiving general anesthesia
for procedures after age 45 is not a risk factor for
developing dementia. The findings were published Wednesday,
May 1, online in Mayo Clinic Proceedings.
http://www.sciencedaily.com/releases/2013/05/130501090720.htm
[Of course they would come to this
conclusion... Tobacco companies would come to the
conclusion that smoking is harmless, and pharmaceutical
comanies would find that all drugs they make are benign
while those of their compentition are deadly.]
Neurodegenerative Disease
Advance: Study Details How Brain Enzyme Interacts With
Drug-Like Lead Compound for Huntington's
Apr. 10, 2013 —
...Professor Nigel Scrutton who led the study said: "UPF 648
works very well as an inhibitor of enzyme activity. However,
in its current form it does not pass into the brain from the
blood. The search is now on for related compounds that can
both inhibit the enzyme and pass into the brain."
He continues: "Our research detailing the molecular structure
of the enzyme now enables a search for new KMO inhibitors that
are able to cross the blood-brain barrier. This provides real
hope for developing drug therapies to target neurodegenerative
diseases such as Huntington's, Alzheimer's and Parkinson's
diseases."...
http://www.sciencedaily.com/releases/2013/04/130410131219.htm
Potential Therapy for Human Prion Disease
Apr. 3, 2013 —...The two compounds are already marketed as the
drugs tacrolimus and astemizole. Tacrolimus is an immune
suppressant widely used in organ transplantation. Tacrolimus
could prove problematic as an anti-prion drug, however,
because of issues including possible neurotoxicity.
However, astemizole is an antihistamine that has
potential for use as an anti-prion drug. While withdrawn
voluntarily from the U.S. over-the-counter market in 1999
because of rare cardiac arrhythmias when used in high doses,
it has been available in generic form in more than 30
countries and has a well-established safety profile.
Astemizole not only crosses the blood-brain barrier, but works
effectively at a relatively low concentration.
http://www.sciencedaily.com/releases/2013/04/130403154305.htm
Accused of Complicity in Alzheimer's, Amyloid Proteins May
Be Getting a Bad Rap
Apr. 3, 2013 —
http://www.sciencedaily.com/releases/2013/04/130403141438.htm
Alzheimer's Discovery: Amyloid Beta Triggers Increased
Levels of Protein That Appears to Cause Neuronal Dysfunction
Mar. 19, 2013 —
http://www.sciencedaily.com/releases/2013/03/130319202323.htm
Feeling Hungry May Protect the Brain Against Alzheimer's
Disease
Apr. 2, 2013 — The feeling of hunger itself may protect
against Alzheimer's disease, according to study published
today in the journal PLOS ONE. Interestingly, the results of
this study in mice suggest that mild hunger pangs, and related
hormonal pathways, may be as important to the much-discussed
value of "caloric restriction" as actually eating less...
'synthetic ghrelin' (ghrelin agonist), a second that underwent
caloric restriction (20 percent less food) ...
http://www.sciencedaily.com/releases/2013/04/130402182457.htm
Neurodegenerative Diseases: Transmission Routes of
Spreading Protein Particles
Mar. 27, 2013 — ...Now, a new laboratory study by scientists
from Germany and the US shows that certain protein particles
are indeed capable of multiplying and spreading from one cell
to the next....
http://www.sciencedaily.com/releases/2013/03/130327104156.htm
Carmustine Decreases Amyloid Beta Plaques
Mar. 26, 2013 — Long term treatment by carmustine, a chemical
relative of mustard gas and already used to treat some types
of brain cancer, can decrease the amount of amyloid ß and
number of amyloid plaques in a mouse model of Alzheimer's
disease. The research is published in Biomed Central's open
access journal BMC Medicine.
http://www.sciencedaily.com/releases/2013/03/130325202526.htm
May 10, 2013 ***********************
Rejuvenating Hormone Found to Reverse Symptoms of Heart
Failure
May 9, 2013 — Heart failure is one of the most debilitating
conditions linked to old age, and there are no specific
therapies for the most common form of this condition in the
elderly. A study published by Cell Press May 9th in the
journal Cell reveals that a blood hormone known as growth
differentiation factor 11 (GDF11) declines with age, and old
mice injected with this hormone experience a reversal in signs
of cardiac aging.
http://www.sciencedaily.com/releases/2013/05/130509123416.htm
Could Eating Peppers Prevent Parkinson's? Dietary
Nicotine May Hold Protective Key
May 9, 2013 — New research reveals that Solanaceae -- a
flowering plant family with some species producing foods that
are edible sources of nicotine -- may provide a protective
effect against Parkinson's disease.
1.Susan Searles Nielsen, Gary M. Franklin, W.T. Longstreth Jr,
Phillip D. Swanson and Harvey Checkoway. Nicotine from Edible
Solanaceae and Risk of Parkinson Disease. Annals of Neurology,
May 9, 2013 DOI: 10.1002/ana.23884
[ The story does not mention that Anatabine was studied. ]
http://www.sciencedaily.com/releases/2013/05/130509091215.htm
Study: Using anticholinergics for as few as 60 days causes
memory problems in older adults
INDIANAPOLIS -- Research from the Regenstrief Institute, the
Indiana University Center for Aging Research and
Wishard-Eskenazi Health on medications commonly taken by older
adults has found that drugs with strong anticholinergic
effects cause cognitive impairment when taken continuously for
as few as 60 days. A similar impact can be seen with 90 days
of continuous use when taking multiple drugs with weak
anticholinergic effect.
http://www.eurekalert.org/pub_releases/2013-05/iu-sua050713.php
http://www.agingbraincare.org/tools/abc-anticholinergic-cognitive-burden-scale/
May 14, 2013 *************
New Drug Reverses Memory Deficits and Slows Alzheimer's in
Mice
May 13, 2013 — A drug developed by scientists at the Salk
Institute for Biological Studies, known as J147, reverses
memory deficits and slows Alzheimer's disease in aged mice
following short-term treatment.
..the Salk team used living neurons grown in laboratory dishes
to test whether their new synthetic compounds, which are based
upon natural products derived from plants,.. [ Which plant
compounds???? Fisetin? Myricetin? Curcumin???]
...Prior and her colleagues say that several cellular
processes known to be associated with Alzheimer's pathology
are affected by J147, including an increase in a protein
called brain-derived neurotrophic factor (BDNF), which
protects neurons from toxic insults, helps new neurons grow
and connect with other brain cells, and is involved in memory
formation. Postmortem studies show lower than normal levels of
BDNF in the brains of people with Alzheimer's.
http://www.sciencedaily.com/releases/2013/05/130513202449.htm
The neurotrophic compound J147 reverses cognitive impairment
in aged Alzheimer's disease mice.
Marguerite Prior, Richard Dargusch, Jennifer L Ehren,
Chandramouli Chiruta and Dave Schubert.
Alzheimer's Research & Therapy, 2013 (in press)
The neurotrophic compound J147 reverses cognitive impairment
in aged Alzheimer's disease mice.
Prior M, Dargusch R, Ehren JL, Chiruta C, Schubert D.
Alzheimers Res Ther. 2013 May 14;5(3):25.
Abstract
INTRODUCTION: Despite years of research, there are no
disease-modifying drugs for Alzheimer's disease (AD), a fatal,
age-related neurodegenerative disorder. Screening for
potential therapeutics in rodent models of AD has generally
relied on testing compounds before pathology is present,
thereby modeling disease prevention rather than disease
modification. Furthermore, this approach to screening does not
reflect the clinical presentation of AD patients which could
explain the failure to translate compounds identified as
beneficial in animal models to disease modifying compounds in
clinical trials. Clearly a better approach to pre-clinical
drug screening for AD is required.
METHODS: To more accurately reflect the clinical setting, we
used an alternative screening strategy involving the treatment
of AD mice at a stage in the disease when pathology is already
advanced. Aged (20-month-old) transgenic AD mice
(APP/swePS1[increment]E9) were fed an exceptionally potent,
orally active, memory enhancing and neurotrophic molecule
called J147. Cognitive behavioral assays, histology, ELISA and
Western blotting were used to assay the effect of J147 on
memory, amyloid metabolism and neuroprotective pathways. J147
was also investigated in a scopolamine-induced model of memory
impairment in C57Bl/6J mice and compared to donepezil. Details
on the pharmacology and safety of J147 are also included.
RESULTS: Data presented here demonstrate that J147 has the
ability to rescue cognitive deficits when administered at a
late stage in the disease. The ability of J147 to improve
memory in aged AD mice is correlated with its induction of the
neurotrophic factors NGF (nerve growth factor) and BDNF (brain
derived neurotrophic factor) as well as several
BDNF-responsive proteins which are important for learning and
memory. The comparison between J147 and donepezil in the
scopolamine model showed that while both compounds were
comparable at rescuing short term memory, J147 was superior at
rescuing spatial memory and a combination of the two worked
best for contextual and cued memory.
CONCLUSION: J147 is an exciting new compound that is extremely
potent, safe in animal studies and orally active. J147 is a
potential AD therapeutic due to its ability to provide
immediate cognition benefits, and it also has the potential to
halt and perhaps reverse disease progression in symptomatic
animals as demonstrated in these studies.
PMID:23673233[PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/23673233
Science News...
Possible Reason for Cholesterol-Drug Side Effects Such as
Memory Loss
May 10, 2013 — The U.S. Food and Drug Administration and
physicians continue to document that some patients experience
fuzzy thinking and memory loss while taking statins, a class
of global top-selling cholesterol-lowering drugs.
http://www.sciencedaily.com/releases/2013/05/130510150143.htm
Cancer Drug Prevents Build-Up of Toxic Brain Protein
May 10, 2013 — Researchers at Georgetown University Medical
Center ...
"The doses used to treat CML are high enough that the drug
pushes cells to chew up their own internal organelles, causing
self-cannibalization and cell death," Moussa says. "We
reasoned that small doses -- for these mice, an equivalent to
one percent of the dose used in humans -- would turn on just
enough autophagy in neurons that the cells would clear
malfunctioning proteins, and nothing else."...They discovered
two candidates -- nilotinib and bosutinib, which is also
approved to treat CML...
http://www.sciencedaily.com/releases/2013/05/130510075623.htm
[ NOTE: Autophagy isn't necessarily destructive to a
cell... it is the method a cell uses to repair itself.
See the Wikipedia entry for Autophagy: http://en.wikipedia.org/wiki/Autophagy
The sugar trehalose may promote
autophagy... a little bit of repair may be beneficial, but too
much is destructive? ]
May 20, 2013
********************************************************
Sleep Apnea Linked to Alzheimer's
May 19, 2013 — A new study looking at sleep-disordered
breathing (SDB) and markers for Alzheimer's disease (AD) risk
in cerebrospinal fluid (CSF) and neuroimaging adds to the
growing body of research linking the two... "Our study did not
determine the direction of the causality,.."
http://www.sciencedaily.com/releases/2013/05/130519145635.htm
[amyloid beta] Molecular Trigger for Alzheimer's Disease
Identified
May 20, 2013 — Researchers have pinpointed a catalytic trigger
for the onset of Alzheimer’s disease – when the fundamental
structure of a protein molecule changes to cause a chain
reaction that leads to the death of neurons in the brain...
“There are no disease modifying therapies for Alzheimer’s and
dementia at the moment, only limited treatment for symptoms.”
said Dr Tuomas Knowles, lead author of the study and long-time
collaborator of Professor Dobson... [They always say this...
but I don't think it's true.]
...Small and highly diffusible, these are the ‘toxic
oligomers’ that careen dangerously around the brain cells,
killing neurons and ultimately causing loss of memory and
other symptoms of dementia...
http://www.sciencedaily.com/releases/2013/05/130520154217.htm
May 24, 2013
********************************************************
Cinnamon Compound Has Potential Ability to Prevent
Alzheimer's
May 23, 2013
...cinnamaldehyde and epicatechin...
http://www.sciencedaily.com/releases/2013/05/130523143737.htm
Interaction of Cinnamaldehyde and Epicatechin with Tau:
Implications of Beneficial Effects in Modulating Alzheimer's
Disease Pathogenesis.
Roshni C. George, John Lew, Donald J. Graves.
Journal of Alzheimer's Disease, 2013 DOI: 10.3233/JAD-122113
Interaction of Cinnamaldehyde and Epicatechin with Tau:
Implications of Beneficial Effects in Modulating Alzheimer's
Disease Pathogenesis.
George RC, Lew J, Graves DJ.
J Alzheimers Dis. 2013 Mar 26. [Epub ahead of print]
Source: Department of Molecular, Cellular and Developmental
Biology, University of California, CA, USA.
Abstract
Abnormal modifications in tau such as hyperphosphorylation,
oxidation, and glycation interfere with its interaction with
microtubules leading to its dissociation and self-aggregation
into neurofibrillary tangles, a hallmark of Alzheimer's
disease (AD). Previously we reported that an aqueous extract
of cinnamon has the ability to inhibit tau aggregation in
vitro and can even induce dissociation of tangles isolated
from AD brain. In the present study, we carried out
investigations with cinnamaldehyde (CA) and epicatechin (EC),
two components of active cinnamon extract. We found that CA
and the oxidized form of EC (ECox) inhibited tau aggregation
in vitro and the activity was due to their interaction with
the two cysteine residues in tau. Mass spectrometry of a
synthetic peptide, SKCGS, representing the actual tau
sequence, identified the thiol as reacting with CA and ECox.
Use of a cysteine double mutant of tau showed the necessity of
cysteine for aggregation inhibition by CA. The interaction of
CA with tau cysteines was reversible and the presence of CA
did not impair the biological function of tau in tubulin
assembly in vitro. Further, these compounds protected tau from
oxidation caused by the reactive oxygen species, H2O2, and
prevented subsequent formation of high molecular weight
species that are considered to stimulate tangle formation.
Finally, we observed that EC can sequester highly reactive and
toxic byproducts of oxidation such as acrolein. Our results
suggest that small molecules that form a reversible
interaction with cysteines have the potential to protect tau
from abnormal modifications.
PMID:23531502[PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/23531502
[This is a very interesting example of an academic squabble
leaving us wondering what are the motives? The first
group thinks they have found a remarkable side effect of the
cancer drug bexarotene. Their study showed that the drug
would improve the cognitive abilities of genetically
engineered "Alzheimer mice". After the report was
published, some physicians decided to try bexarotene on their
patients. They can use drugs tested and approved by the
FDA for one purpose "off-label" to treat other conditions that
the drug was not tested for. The second group of
researchers could not replicate the results of the reduction
of amyloid beta plaques, but I don't read anything about not
being able to reduce the improvement in cognitive
abilities. They seem mostly concerned with convincing
physicians from using bexarotene "off-label"]
Drug Reverses Alzheimer's Disease Deficits in Mice
May 23, 2013
Dr. Koldamova and her colleagues were studying mice expressing
human Apolipoprotein E4 (APOE4), the only established genetic
risk factor for late-onset Alzheimer's disease, or APOE3,
which is known not to increase the risk for Alzheimer's
disease, when a Case Western Reserve University study was
published last year stating that bexarotene improved memory
and rapidly cleared amyloid plaques from the brains of
Alzheimer's model mice expressing mouse Apolipoprotein E
(APOE)... The Pitt Public Health researchers were able to
verify that the drug does significantly improve cognitive
deficits in mice expressing gene mutations linked to human
Alzheimer's disease, but could not confirm the effect on
amyloid plaques... ..."We believe these findings make a solid
case for continued exploration of bexarotene as a therapeutic
treatment for Alzheimer's disease,"... "We did find a
significant decrease in soluble oligomers,"...
http://www.sciencedaily.com/releases/2013/05/130523143541.htm
ApoE-directed therapeutics rapidly clear ß-amyloid and
reverse deficits in AD mouse models.
Cramer PE, Cirrito JR, Wesson DW, Lee CY, Karlo JC, Zinn AE,
Casali BT, Restivo JL, Goebel WD, James MJ, Brunden KR, Wilson
DA, Landreth GE.
Science. 2012 Mar 23;335(6075):1503-6. doi:
10.1126/science.1217697. Epub 2012 Feb 9.
Source: Department of Neurosciences, Case Western Reserve
University School of Medicine, Cleveland, OH 44106, USA.
Abstract
Alzheimer's disease (AD) is associated with impaired clearance
of ß-amyloid (Aß) from the brain, a process normally
facilitated by apolipoprotein E (apoE). ApoE expression is
transcriptionally induced through the action of the nuclear
receptors peroxisome proliferator-activated receptor gamma and
liver X receptors in coordination with retinoid X receptors
(RXRs). Oral administration of the RXR agonist bexarotene to a
mouse model of AD resulted in enhanced clearance of soluble Aß
within hours in an apoE-dependent manner. Aß plaque area was
reduced more than 50% within just 72 hours. Furthermore,
bexarotene stimulated the rapid reversal of cognitive, social,
and olfactory deficits and improved neural circuit function.
Thus, RXR activation stimulates physiological Aß clearance
mechanisms, resulting in the rapid reversal of a broad range
of Aß-induced deficits.
Comment in
Neurodegenerative disease: RXR agonist reverses Alzheimer's
disease. [Nat Rev Drug Discov. 2012]
Neurodegenerative disease: RXR agonist reverses Alzheimer's
disease.Crunkhorn S. Nat Rev Drug Discov. 2012 Mar 30;
11(4):271. Epub 2012 Mar 30.
Medicine. Old drug, new hope for Alzheimer's disease.
[Science. 2012]
Medicine. Old drug, new hope for Alzheimer's
disease.Strittmatter WJ. Science. 2012 Mar 23;
335(6075):1447-8.
PMID:22323736[PubMed] PMCID:PMC3651582
http://www.ncbi.nlm.nih.gov/pubmed/22323736
Free article:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3651582/
Multiple Research Teams Unable to Confirm High-Profile
Alzheimer's Study
May 23, 2013
"We repeated the initial experiments -- a standard process in
science. Combined results are really important in this field.
None of us found anything like what they described in the 2012
paper."
http://www.sciencedaily.com/releases/2013/05/130523143004.htm
Memory enhancement....
Mediterranean Diet Seems to Boost Aging Brain Power
May 20, 2013 — A Mediterranean diet with added extra virgin
olive oil or mixed nuts seems to improve the brain power of
older people better than advising them to follow a low-fat
diet, indicates research published online in the Journal of
Neurology Neurosurgery and Psychiatry.
http://www.sciencedaily.com/releases/2013/05/130520185428.htm
NOTE: Need section on Niacinamide. See also Autophagy
page.
NOTE: Reduce text from sciencedaily references in "memory
enhancemen" page
NOTE: Need a link to a Cinnamaldehyde section of the Cinnamon
page, and on the Grand Index
NOTE: Cinnamon page, "Known sources" has a link to myricetin?
5/29/2013***********************************************
Changing Gut Bacteria Through Diet Affects Brain Function
May 28, 2013 — UCLA researchers now have the first evidence
that bacteria ingested in food can affect brain function in
humans. In an early proof-of-concept study of healthy women,
they found that women who regularly consumed beneficial
bacteria known as probiotics through yogurt showed altered
brain function, both while in a resting state and in response
to an emotion-recognition task.
http://www.sciencedaily.com/releases/2013/05/130528180900.htm
5/29/2013***********************************************
Exposure to General Anaesthesia Could Increase the Risk of
Dementia in Elderly by 35 Percent
June 1, 2013 — Exposure to general anaesthesia increases the
risk of dementia in the elderly by 35%, says new research
presented at Euroanaesthesia, the annual congress of the
European Society of Anaesthesiology (ESA). The research is by
Dr Francois Sztark, INSERM and University of Bordeaux, France,
and colleagues.
http://www.sciencedaily.com/releases/2013/06/130601133925.htm
6/10/2013***********************************************
Diabetes Drug Shows Promise in Treatment of
Neurodegenerative Disease
June 7, 2013 — Researchers in Spain have found that a drug
used to control Type II diabetes can help repair the spinal
cords of mice suffering from the inherited disease
adrenoleukodystrophy which, untreated, leads eventually to a
paralysis, a vegetative state and death. They believe that
their findings may be relevant to other neurodegenerative
diseases. A Phase II trial will be starting shortly... "We
also knew that the pathway involved in the mitochondrial loss
could be treated by the use of the diabetes drug pioglitazone"...
multiple sclerosis, and many others where impaired
bioenergetics combined with oxidative stress and degeneration
of axons are known to be involved. The latter category of
disease includes Parkinson's, Huntington's, and Alzheimer's.
"It is possible that our findings may be relevant to these
conditions as well,"...
http://www.sciencedaily.com/releases/2013/06/130607222510.htm
Pioglitazone halts axonal degeneration in a mouse model of
X-linked adrenoleukodystrophy.
Laia Morato´ , Jorge Galino, Montserrat Ruiz, Noel Ylagan
Calingasan, Anatoly A. Starkov, Magali Dumont, Alba Naudi´,
Juan Jose´ Marti´nez, Patrick Aubourg, Manuel Portero-Oti´n,
Reinald Pamplona, Elena Galea, M. Flint Beal,3 Isidre Ferrer,
Ste´phane Fourcade and Aurora Pujol.
Brain, 2013 DOI: 10.1093/brain/awt143
Wikipedia: http://en.wikipedia.org/wiki/Pioglitazone
Pioglitazone, Actos (USA, Canada, the UK and Germany), Glustin
(Europe), Glizone and Pioz (India), Zactos (Mexico)
Pioglitazone is a prescription drug of the class
thiazolidinedione (TZD) with hypoglycemic (antihyperglycemic,
antidiabetic) action to treat diabetes. It is used to improve
glucose control in adults over the age of 18 with type 2
diabetes. Pioglitazone is marketed as trademarks Actos in the
USA, Canada, the UK and Germany, Glustin in Europe, Glizone
and Pioz in India by Zydus Cadila and USV Limited,
respectively and Zactos in Mexico by Takeda Pharmaceuticals.
Actos was the tenth-best selling drug in the U.S. in 2008,
with sales exceeding $2.4 billion.[1] Its cardiovascular
safety profile compares favorably with rosiglitazone
(Avandia), which was withdrawn after concerns about an
increased risk of cardiac events. However, pioglitazone has
subsequently been found to be associated with bladder tumors
and has been withdrawn in some countries.
[NOTE: One would think that those treated with this
drug for Type II diabetes would have a lower incidence of
the neurodegenerative diseases if this indeed is effective.]
6/13/2013***********************************************
Carvedilol
http://www.sciencedaily.com/releases/2013/13/130612132535.htm
"Unintended Effects of Cardiovascular Drugs on the
Pathogenesis of Alzheimer's Disease"
A Peptide to Protect Brain Function
June 13, 2013 — A structure called "the microtubule network"
is a crucial part of our nervous system. It acts as a
transportation system within nerve cells, carrying essential
proteins and enabling cell-to-cell communications. But in
neurodegenerative diseases like Alzheimer's, ALS, and
Parkinson's, this network breaks down, hindering motor
abilities and cognitive function... a new peptide in her lab,
called NAP or Davunetide, that has the capacity to both
protect and restore microtubule function. The peptide is a
compound derived from the protein ADNP, which regulates more
than 400 genes and is essential for brain formation, memory,
and behavior...
http://www.sciencedaily.com/releases/2013/06/130613112230.htm
6/18/2013***********************************************
New Drug Reverses Loss of Brain Connections in Alzheimer's
June 17, 2013 — The first experimental drug to boost brain
synapses lost in Alzheimer's disease has been developed by
researchers at Sanford-Burnham Medical Research Institute. The
drug, called NitroMemantine, combines two FDA-approved
medicines to stop the destructive cascade of changes in the
brain that destroys the connections between neurons, leading
to memory loss and cognitive decline.
http://www.sciencedaily.com/releases/2013/06/130617160849.htm
Aß induces astrocytic glutamate release, extrasynaptic NMDA
receptor activation, and synaptic loss.
Maria Talantova, Sara Sanz-Blasco, Xiaofei Zhang, Peng Xia,
Mohd Waseem Akhtar, Shu-ichi Okamoto, Gustavo Dziewczapolski,
Tomohiro Nakamura, Gang Cao, Alexander E. Pratt, Yeon-Joo
Kang, Shichun Tu, Elena Molokanova, Scott R. McKercher, Samuel
Andrew Hires, Hagit Sason, David G. Stouffer, Matthew W.
Buczynski, James P. Solomon, Sarah Michael, Evan T. Powers,
Jeffery W. Kelly, Amanda Roberts, Gary Tong, Traci
Fang-Newmeyer, James Parker, Emily A. Holland, Dongxian Zhang,
Nobuki Nakanishi, H.-S. Vincent Chen, Herman Wolosker, Yuqiang
Wang, Loren H. Parsons, Rajesh Ambasudhan, Eliezer Masliah,
Stephen F. Heinemann, Juan C. Piña-Crespo, and Stuart A.
Lipton
PNAS, June 17, 2013 DOI: 10.1073/pnas.1306832110
Blocking Overactive Receptor in Alzheimer's Recovers Memory
Loss and More, Mouse Study Suggests
June 17, 2013 — A new study shows that memory pathology in
older mice with Alzheimer's disease can be reversed with
treatment.
The researchers found an increased level of a receptor known
as bradykinin B1 receptor (B1R) in the brain of mice with AD,
a receptor involved in inflammation. "By administering a
molecule that selectively blocks the action of this receptor,
we observed important improvements in both cognitive and
cerebrovascular function," says Dr. Baptiste Lacoste, research
fellow who conducted the study at The Neuro and now pursuing
his training at Harvard Medical School in Boston. "Alzheimer's
disease destroys nerve cells and also compromises the function
of blood vessels in the brain. Not only were there
improvements in learning and memory, but also marked recovery
in blood flow and vascular reactivity, i.e. the ability of
cerebral vessels to dilate or constrict when necessary."
Proper functioning of blood vessels in the brain is vital to
providing nutrients and oxygen to nerve cells, and vascular
diseases represent important risk factors for developing AD at
an advanced age.
"Another interesting result that has not been seen before in
our mouse model is a reduction by over 50% of toxic
amyloid-beta peptide," adds Dr. Hamel. "In Alzheimer's
disease, protein fragments called amyloid-beta have a
deleterious effect on the blood and nervous systems. Normally,
these protein fragments are broken down and removed. In
Alzheimer's disease, the protein fragments clump together -- a
factor believed to contribute to neuronal and vascular
dysfunction. We are not sure if these decreases contribute to
the functional recovery, but we hope that our findings will
aid in clarifying this issue and identifying new targets for
therapeutic approaches."
http://www.sciencedaily.com/releases/2013/06/130617122357.htm
[Are there substances found in foods (i.e. supplements)
that also block this bradykinin B1 receptor (B1R)?]
6/20/2013***********************************************
Chemical That Makes Naked Mole Rats Cancer-Proof Discovered
June 19, 2013 — Two researchers at the University of Rochester
have discovered the chemical that makes naked mole rats
cancer-proof... "There's indirect evidence that HMW-HA
would work in people," said Seluanov. "It's used in
anti-wrinkle injections and to relieve pain from arthritis in
knee joints, without any adverse effects. Our hope is that it
can also induce an anti-cancer response."...
http://www.sciencedaily.com/releases/2013/06/130619132444.htm
How Underground Rodent Wards Off Cancer: Second Mole Rat
Species Has Different Mechanism for Resisting Cancer
Nov. 5, 2012
...Gorbunova and Seluanov say they next want to find out
exactly what triggers the secretion of interferon beta...
http://www.sciencedaily.com/releases/2012/11/121105200058.htm
Stress Hormone Could Trigger Mechanism for the Onset of
Alzheimer's
June 19, 2013 — A chemical hormone released in the body as a
reaction to stress could be a key trigger of the mechanism for
the late onset of Alzheimer's disease, according to a study by
researchers at Temple University.
"Corticosteroid uses the 5-lipoxygenase as a mechanism to
damage the synapse, which results in memory and learning
impairment, both key symptoms for Alzheimer's," said Pratico.
"So that is strong support for the hypothesis that if you
block 5-lipoxygenase, you can probably block the negative
effects of corticosteroid in the brain."
http://www.sciencedaily.com/releases/2013/06/130619102605.htm
[Can a chronic infection either of the brain or in some
remote location in the body (helicobacter, etc.) cause a
"stress" reaction even if there is no environmental
"stress"?]
Antioxidant Shows Promise in Parkinson's Disease
June 19, 2013 — Diapocynin, a synthetic molecule derived from
a naturally occurring compound (apocynin), has been found to
protect neurobehavioral function in mice with Parkinson's
Disease symptoms by preventing deficits in motor coordination.
http://www.sciencedaily.com/releases/2013/06/130619122131.htm
Virus Combination Effective Against Deadly Brain Tumor
June 20, 2013 — A combination of the myxoma virus and the
immune suppressant rapamycin can kill glioblastoma multiforme,
the most common and deadliest malignant brain tumor,
http://www.sciencedaily.com/releases/2013/06/130620100739.htm
"leuko form" of methylene blue... see Tauopathies forum on
Yahoo.
Source: Cape Apothacary http://capedrugs.com
6/21/2013 ***********************************************
Concussion Patients Show Alzheimer's-Like Brain
Abnormalities
June 18, 2013 — The distribution of white matter brain
abnormalities in some patients after mild traumatic brain
injury (MTBI) closely resembles that found in early
Alzheimer's dementia, according to a new study published
online in the journal Radiology.
http://www.sciencedaily.com/releases/2013/06/130618101727.htm
New Alzheimer's Research Suggests Possible Cause: Interaction
of Proteins in Brain
June 19, 2013 — For years, Alzheimer's researchers have
focused on two proteins that accumulate in the brains of
people with Alzheimer's and may contribute to the disease:
plaques made up of the protein amyloid-beta, and tangles of
another protein, called tau...
"So much Alzheimer's research has been done to look at
amyloid-beta and tau," Reddy said. "But ours is the first
paper to strongly demonstrate that yes, there is an
amyloid-beta/phosphorylated tau interaction. And that
interaction might be causing the synaptic damage and cognitive
decline in persons with Alzheimer's disease."
http://www.sciencedaily.com/releases/2013/06/130619102806.htm
6/25/2013 ***********************************************
Protein That Contributes to Cognitive Decline in
Alzheimer's Identified
June 25, 2013 — Researchers at Columbia University Medical
Center (CUMC) have demonstrated that a protein called
caspase-2 is a key regulator of a signaling pathway that leads
to cognitive decline in Alzheimer's disease. The findings,
made in a mouse model of Alzheimer's, suggest that inhibiting
this protein could prevent the neuronal damage and subsequent
cognitive decline associated with the disease.
http://www.sciencedaily.com/releases/2013/06/130625120933.htm
7/3/2013 ***********************************************
New Way Discovered to Block Inflammation
July 1, 2013 — Researchers at NYU Langone Medical Center have
discovered a mechanism that triggers chronic inflammation in
Alzheimer's, atherosclerosisand type-2 diabetes. The results,
published today in Nature Immunology, suggest a common
biochemical thread to multiple diseases and point the way to a
new class of therapies that could treat chronic inflammation
in these non-infectious diseases without crippling the immune
system. Alzheimer's, atherosclerosis and type-2 diabetes --
diseases associated with aging and inflammation -- affect more
than 100 million Americans.
http://www.sciencedaily.com/releases/2013/07/130701135556.htm
Promising Alzheimer's 'Drug' Halts Memory Loss
June 26, 2013 — A new class of experimental drug-like small
molecules is showing great promise in targeting a brain enzyme
to prevent early memory loss in Alzheimer's disease, according
to Northwestern Medicine® research.
The target is a stress-related protein kinase, p38alpha MAPK.
"We think this protein kinase target is one of the key players
in the early to mid-stage of several diseases of the central
nervous system and cancer,"
http://www.sciencedaily.com/releases/2013/06/130626184019.htm
Development of Novel In Vivo Chemical Probes to Address CNS
Protein Kinase Involvement in Synaptic Dysfunction.
D. Martin Watterson, Valerie L. Grum-Tokars, Saktimayee M.
Roy, James P. Schavocky, Brinda Desai Bradaric, Adam D.
Bachstetter, Bin Xing, Edgardo Dimayuga, Faisal Saeed, Hong
Zhang, Agnieszka Staniszewski, Jeffrey C. Pelletier, George
Minasov, Wayne F. Anderson, Ottavio Arancio, Linda J. Van
Eldik.
PLoS ONE, 2013; 8 (6): e66226 DOI:
10.1371/journal.pone.0066226
A Second Amyloid May Play a Role in Alzheimer's Disease
June 27, 2013 — A second amyloid may play a role in
Alzheimer's disease, UC Davis researchers find.
A protein secreted with insulin travels through the
bloodstream and accumulates in the brains of individuals with
type 2 diabetes and dementia, in the same manner as the
amyloid beta (?ß) plaques that are associated with Alzheimer's
disease...
Amylin, or islet amyloid polypeptide, is a hormone produced by
the pancreas that circulates in the bloodstream with insulin
and plays a critical role in glycemic regulation by slowing
gastric emptying, promoting satiety and preventing
post-prandial spikes in blood glucose levels.
http://www.sciencedaily.com/releases/2013/06/130627141812.htm
Amylin deposition in the brain: A second amyloid in
Alzheimer's disease?
Kaleena Jackson, Gustavo A. Barisone, Elva Diaz, Lee-way Jin,
Charles DeCarli, Florin Despa.
Annals of Neurology, 2013; DOI: 10.1002/ana.23956
Discovery Sheds Light On Why Alzheimer's Drugs Rarely Help
July 1, 2013
UCLA scientists discovered that Aß has a vastly different
organization in oligomers than in amyloid plaques
http://www.sciencedaily.com/releases/2013/07/130701100602.htm
Building on research published eight years ago in the journal
Chemistry and Biology, Kenneth S. Kosik, Harriman Professor in
Neuroscience and co-director of the Neuroscience Research
Institute (NRI) at UC Santa Barbara, and his team have now
applied their findings to two distinct, well-known mouse
models, demonstrating a new potential target in the fight
against Alzheimer's and other neurodegenerative diseases.
...Treatments for hyperphosphorylated tau, one of the main
causes of Alzheimer's disease, do not exist...
...the possibility that a small class of molecules called
diaminothiazoles can act as inhibitors of kinase enzymes that
phosphorylate tau. Kosik's team studied the toxicity and
immunoreactivity of several diaminothiazoles that targeted two
key kinases, CDK5/p25 and GSK3ß, in two Alzheimer's disease
mouse models. The investigators found that the compounds can
efficiently inhibit the enzymes with hardly any toxic effects
in the therapeutic dose range.
http://www.sciencedaily.com/releases/2013/06/130626143114.htm
[Donald Graves, the man researching cinnamon
proanthrocyanidins and cinnameldahyde works at UC Santa
Barbara. Don't these people talk?]
3/17/2013
Green Tea and Red Wine
Extracts Interrupt Alzheimer's Disease Pathway in Cells
Feb. 5, 2013 — Natural chemicals found in green tea and red wine
may disrupt a key step of the Alzheimer's disease pathway,
according to new research from the University of Leeds.
Lightning may affect headache, migraines
UPI 1/28/2013 12:53:59 AM
CINCINNATI, Jan. 27 Dr. Vincent Martin-- professor in the
division of general internal medicine and University of
Cincinnati Health physician -- and his son, Geoffrey Martin
...The study published in the journal Cephalalgia, found
new-onset headache and migraine increased by 24 percent and 23
percent in participants when lightning occurred...
http://www.sciencedaily.com/releases/2013/02/130205200241.htm
Prion protein-mediated
toxicity of amyloid-β oligomers requires lipid rafts and the
transmembrane LRP1.
Rushworth JV, Griffiths HH, Watt NT, Hooper NM.
J Biol Chem. 2013 Feb 5. [Epub
ahead of print]
Source: University of Leeds, United
Kingdom.
Abstract
Soluble oligomers of the amyloid-β (Aβ) peptide cause
neurotoxicity, synaptic dysfunction and memory impairments which
underlie Alzheimers disease (AD). The cellular prion protein
(PrPC) was recently identified as a high-affinity neuronal
receptor for Aβ oligomers. We report that fibrillar Aβ oligomers
recognised by the OC antibody, which have been shown to
correlate with the onset and severity of AD, bind preferentially
to cells and neurons expressing PrPC. The binding of Aβ
oligomers to cell surface PrPC, as well as their downstream
activation of Fyn kinase, was dependent on the integrity of
cholesterol-rich lipid rafts. In SH-SY5Y cells, fluorescence
microscopy and co-localisation with sub-cellular markers
revealed that the Aβ oligomers co-internalised with PrPC,
accumulated in endosomes and subsequently trafficked to
lysosomes. The cell surface binding, internalisation and
downstream toxicity of Aβ oligomers was dependent on the
transmembrane low density lipoprotein receptor-related protein-1
(LRP1). The binding of Aβ oligomers to cell surface PrPC
impaired its ability to inhibit the activity of the β-secretase
BACE1 which cleaves the amyloid precursor protein to produce Aβ.
The green tea polyphenol (-)-epigallocatechin gallate (EGCG) and
the red wine extract resveratrol both re-modelled the fibrillar
conformation of Aβ oligomers. The resulting non-fibrillar
oligomers displayed significantly reduced binding to
PrPC-expressing cells and were no longer cytotoxic. These data
indicate that soluble, fibrillar Aβ oligomers bind to PrPC in a
conformation-dependent manner and require the integrity of lipid
rafts and the transmembrane LRP1 for their cytotoxicity, thus
revealing potential targets to alleviate the neurotoxic
properties of Aβ oligomers in AD.
PMID: 23386614 [PubMed] http://www.ncbi.nlm.nih.gov/pubmed/23386614
Vitamin D, Omega-3 May Help
Clear Amyloid Plaques Found in Alzheimer's
Feb. 5, 2013 — A team of academic researchers has pinpointed how
vitamin D3 and omega-3 fatty acids may enhance the immune
system's ability to clear the brain of amyloid plaques, one of
the hallmarks of Alzheimer's disease...
http://www.sciencedaily.com/releases/2013/02/130205131629.htm
1α,25-Dihydroxyvitamin D3 and
Resolvin D1 Retune the Balance between Amyloid-β Phagocytosis
and Inflammation in Alzheimer's Disease Patients.
Mizwicki MT, Liu G, Fiala M, Magpantay L, Sayre J, Siani A,
Mahanian M, Weitzman R, Hayden EY, Rosenthal MJ, Nemere I,
Ringman J, Teplow DB.
J Alzheimers Dis. 2013 Jan 1;34(1):155-70. doi:
10.3233/JAD-121735.
Source: Department of Surgery, David
Geffen School of Medicine at UCLA, Los Angeles, CA, USA.
Abstract
As immune defects in amyloid-β (Aβ) phagocytosis and degradation
underlie Aβ deposition and inflammation in Alzheimer's disease
(AD) brain, better understanding of the relation between Aβ
phagocytosis and inflammation could lead to promising preventive
strategies. We tested two immune modulators in peripheral blood
mononuclear cells (PBMCs) of AD patients and controls:
1α,25(OH)2-vitamin D3 (1,25D3) and resolvin D1 (RvD1). Both
1,25D3 and RvD1 improved phagocytosis of FAM-Aβ by AD
macrophages and inhibited fibrillar Aβ-induced apoptosis. The
action of 1,25D3 depended on the nuclear vitamin D and the
protein disulfide isomerase A3 receptors, whereas RvD1 required
the chemokine receptor, GPR32. The activities of 1,25D3 and RvD1
commonly required intracellular calcium, MEK1/2, PKA, and PI3K
signaling; however, the effect of RvD1 was more sensitive to
pertussis toxin. In this case study, the AD patients: a) showed
significant transcriptional up regulation of IL1RN, ITGB2, and
NFκB; and b) revealed two distinct groups when compared to
controls: group 1 decreased and group 2 increased transcription
of TLRs, IL-1, IL1R1 and chemokines. In the PBMCs/macrophages of
both groups, soluble Aβ (sAβ) increased the
transcription/secretion of cytokines (e.g., IL1 and IL6) and
chemokines (e.g., CCLs and CXCLs) and 1,25D3/RvD1 reversed most
of the sAβ effects. However, they both further increased the
expression of IL1 in the group 1, sβ-treated cells. We conclude
that in vitro, 1,25D3 and RvD1 rebalance inflammation to promote
Aβ phagocytosis, and suggest that low vitamin D3 and
docosahexaenoic acid intake and/or poor anabolic production of
1,25D3/RvD1 in PBMCs could contribute to AD onset/pathology.
PMID: 23186989 [PubMed] http://www.ncbi.nlm.nih.gov/pubmed/23186989
Study Confirms No Transmission
of Alzheimer's Proteins Between Humans
Feb. 4, 2013 — Mounting evidence demonstrates that the
pathological proteins linked to the onset and progression of
neurodegenerative disorders are capable of spreading from
cell-to-cell within the brains of affected individuals and
thereby "spread" disease from one interconnected brain region to
another. A new study found no evidence to support concerns that
these abnormal disease proteins are "infectious" or transmitted
from animals to humans or from one person to another...
http://www.sciencedaily.com/releases/2013/02/130204184537.htm
Chemical Reaction Keeps
Stroke-Damaged Brain from Repairing Itself
Feb. 4, 2013 — Nitric oxide, a gaseous molecule produced in the
brain, can damage neurons. When the brain produces too much
nitric oxide, it contributes to the severity and progression of
stroke and neurodegenerative diseases such as Alzheimer's.
http://www.sciencedaily.com/releases/2013/02/130204153910.htm
Oxygen Chamber Can Boost Brain
Repair Years After Stroke or Trauma
Jan. 23, 2013 — Stroke, traumatic injury, and metabolic disorder
are major causes of brain damage and permanent disabilities,
including motor dysfunction, psychological disorders, memory
loss, and more. Current therapy and rehab programs aim to help
patients heal, but they often have limited success.
http://www.sciencedaily.com/releases/2013/01/130123144218.htm
Type II Diabetes and
Alzheimer's Connection
Feb. 1, 2013 — A research team in Israel has devised a novel
approach to identifying the molecular basis for designing a drug
that might one day decrease the risk diabetes patients face of
developing Alzheimer's disease.
http://www.sciencedaily.com/releases/2013/02/130201095945.htm
10/11/12
7/6/2012
Ginkgo PMC2254622
7/1/2012
*****
http://www.j-alz.com/issues/16/vol16-1.html
[from the J Alz.com link above…]
Pages 15-27
Review
Accumulated Amyloid-β Peptide
and Hyperphosphorylated Tau Protein: Relationship and Links in
Alzheimer’s Disease
Han-chang Huang, Zhao-feng Jiang
Abstract: The neuropathology associated
with Alzheimer’s disease (AD) is characterized by the presence
of extracellularly neuritic plaques, intracellularly
neurofibrillary tangles and the loss of basal forebrain
cholinergic neurons. The neuritic plaque is composed of a core
of amyloid-β peptide (Aβ) while the neurofibrillary tangles
contain phosphorylated tau protein, and, as such, both Aβ and
tau are important molecules associated with AD. In healthy human
bodies, clearance mechanisms for Aβ are available; yet if
clearance fails, Aβ accumulates, increasing the risk of
neurotoxicity in the brain. Tau, one of the main
microtubule-associated proteins, will be hyperphosphorylated and
lose the ability to bind microtubules when the homeostasis of
phosphorylation and dephosphorylation is disturbed in neurons.
Accumulated Aβ and hyperphosphorylated tau are thought to be
coexistent. Research on the pathological changes in AD indicates
that accumulated Aβ in vivo may initiate the
hyperphosphorylation of tau. Also, the signal transduction
pathways of tau hyperphosphorylation may be related to
accumulated Aβ. In this review, we will discuss how Aβ
accumulates, how tau protein is hyperphosphorylated, and how
accumulated Aβ initiates hyperphosphorylation of tau protein in
AD.
***
Epo-D About a year ago in the Alzheimer's Research Forum
reported:
"In a study performed on three-month-old mice with tauopathy,
one of these compounds, epothilone D, when given at the
relatively low dose of 1 mg/kg body weight for three months,
decreased axon degeneration and improved cognition in treated
animals (see Brunden et al., 2010). [ NEED LINK ]
This month, in the Journal of Neuroscience, Brunden and his
colleagues report positive results in older tauopathy mice using
1/30th to 1/100th of the dose used with cancer patients. Here is
the website for the original press release http://www.uphs.upenn.edu/news/News_Releases/2012/03/alzheimer/
This drug is now in human trials with Alzheimer's patients that
ends in 2014.
Methylene Blue/2nd gen Rember. TauRx.com's website states: "…the
clinical tolerability profile of LMTX, one of TauRx's second
generation TAIs, is currently being investigated clinically in
trials conducted under an open US IND. TauRx is now preparing to
advance LMTX into pivotal international phase 3 trials in mild
and moderate AD and related neurodegenerative diseases." [ NEED
TO FIND LINK ]
In the meantime, two OTC low toxicity agents with established
neuroprotective and neuro-repair properties merit review:
bio-available curcumin (Longvida) and a new product that comes
from research done at the Salk Institute, fisetin (Swanson). Both are
strong anti-oxidants and anti-inflammatories that protect and
help neurons repair damage from tauopathy.
San Francisco: Tau—Time to
Shine as Therapeutic Target?
17 May 2011. At the “Tau and Tauopathies: Pathogenic Mechanisms”
workshop held 28-30 March 2011 at the Gladstone Institute of
Neurological Disease (GIND) in San Francisco... The researchers
found that tau pathology correlated with increased serum IL-1β
in the transgenic mice, and wondered whether blocking signals
through this inflammatory cytokine could possibly help...
epothilone D—a brain-penetrant, microtubule-stabilizing compound
that slowed axon degeneration and improved cognition...
hyperphosphorylated tau... “If you express c-Abl in the
forebrain, you get tau phosphorylation, cell death, and gliosis
accompanying the cell loss,”... The results are reminiscent of
the cognitive recovery seen in tangle-bearing Tg4510 mice after
tau transgene inhibition with doxycycline (ARF related news
story on Santacruz et al., 2005), Cole wrote in an e-mail to
ARF. The data “support tau oligomers as a target and curcumin as
a pleiotropic drug capable of targeting pure tauopathy with late
intervention,” he noted. Investigators at Jaslok Hospital and
Research Centre in Mumbai, India, are recruiting AD patients for
a Phase 2 trial of a highly absorbed, lipophilic curcumin
formulation. Manufactured as a food supplement called LongVida
by Verdure Sciences... eight-week treatment with the
autophagy-promoting compound trehalose cleared tau aggregates
and improved behavior in tauopathy mouse models with primarily
motor...
http://www.alzforum.org/new/detail.asp?id=2792
This excerpt is from a 2010 case description (LaBuzetta, et.al.
2010):
"Signs and symptoms of hyperammonemia are usually neurological
in nature and range from mild cognitive and psychomotor changes
to impaired intellectual functioning, personality changes,
altered levels of consciousness, and neuromuscular dysfunction.
At high enough concentrations, coma or death can be observed."
*****
Human Cytomegalovirus Essential
hypertension:
Virus can cause high blood
pressure
2011/08/15
BEIJING: High blood pressure could be caused by a common virus,
according to a study carried out by a team of Chinese doctors
which has possible implications for millions of people around
the world.
The human cytomegalovirus (HCMV) infects most adults but is
repressed by the body’s immune system and rarely causes any
symptoms.
But a team from Beijing Chaoyang Hospital’s cardiology centre
has found the first evidence of a link between HCMV and
essential hypertension, according to a report published on the
website of the US medical journal Circulation.
http://www.nst.com.my/nst/articles/Viruscancausehighbloodpressure/Article/
Virus can cause high blood
pressure: Chinese study
Agence France-Presse
Posted at 08/15/2011
http://www.abs-cbnnews.com/lifestyle/08/15/11/virus-can-cause-high-blood-pressure-chinese-study
Virus can cause high blood
pressure: Chinese study
Relaxnews – Wed, Aug 17, 2011
http://news.yahoo.com/virus-cause-high-blood-pressure-chinese-study-153649965.html
Virus can cause high blood
pressure: Chinese study
AFP NewsBy Philip Lim | AFP News – Mon, Aug 15, 2011
http://my.news.yahoo.com/virus-cause-high-blood-pressure-chinese-study-095735139.html
Treatment With Vitamin C
Dissolves Toxic Protein Aggregates in Alzheimer's Disease
ScienceDaily (Aug. 18, 2011)
— Researchers at Lund University have discovered a new
function for vitamin C. Treatment with vitamin C can dissolve
the toxic protein aggregates that build up in the brain in
Alzheimer's disease...
http://www.sciencedaily.com/releases/2011/08/110818101645.htm
What form of vitamin C? How much? Is it practical
for someone to take orally?
Fish Oil's Impact On Cognition
and Brain Structure Identified in New Study
ScienceDaily (Aug. 17, 2011)
— Researchers at Rhode Island Hospital's Alzheimer's
Disease and Memory Disorders Center have found positive
associations between fish oil supplements and cognitive
functioning as well as differences in brain structure between
users and non-users of fish oil supplements. The findings
suggest possible benefits of fish oil supplements on brain
health and aging...
http://www.sciencedaily.com/releases/2011/08/110817120220.htm
Exercise May Help Prevent
Brain Damage Caused by Alzheimer's Disease
ScienceDaily (Aug. 15, 2011)
— Regular exercise could help prevent brain damage
associated with neurodegenerative diseases like Alzheimer's,
according to research published this month in Elsevier's journal
Brain, Behavior, and Immunity...
http://www.sciencedaily.com/news/mind_brain/alzheimer%27s/
Moderate Drinking May Protect
Against Alzheimer's and Cognitive Impairment, Study Suggests
ScienceDaily (Aug. 15, 2011)
— Moderate social drinking may significantly reduce the
risk of dementia and cognitive impairment, suggests an analysis
of 143 studies by Loyola University Chicago Stritch School of
Medicine researchers...
http://www.sciencedaily.com/releases/2011/08/110816112134.htm
Red wine and resveratrol?
Alzheimer's disease - a
neurospirochetosis. Analysis of the evidence following Koch's
and Hill's criteria.
Judith Miklossy
Correspondence: Judith Miklossy judithmiklossy@bluewin.ch
Journal of Neuroinflammation 2011, 8:90
doi:10.1186/1742-2094-8-90
Published: 4 August 2011
Abstract (provisional)
It is established that chronic spirochetal infection can cause
slowly progressive dementia, brain atrophy and amyloid
deposition in late neurosyphilis.
Recently it has been suggested that various types of
spirochetes, in an analogous way to Treponema pallidum, could
cause dementia and may be involved in the pathogenesis of
Alzheimer's disease (AD).
Here, we review all data available in the literature on the
detection of spirochetes in AD and critically analyze the
association and causal relationship between spirochetes and AD
following established criteria of Koch and Hill.
The results show a statistically significant association between
spirochetes and AD (P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N =
247).
When neutral techniques recognizing all types of spirochetes
were used, or the highly prevalent periodontal pathogen
Treponemas were analyzed, spirochetes were observed in the brain
in more than 90% of AD cases.
Borrelia burgdorferi was detected in the brain in 25.3% of AD
cases analyzed and was 13 times more frequent in AD compared to
controls.
Periodontal pathogen Treponemas (T. pectinovorum, T. amylovorum,
T. lecithinolyticum, T. maltophilum, T. medium, T. socranskii)
and Borrelia burgdorferi were detected using species specific
PCR and antibodies.
Importantly, co-infection with several spirochetes occurs in AD.
The pathological and biological hallmarks of AD were reproduced
in vitro.
The analysis of reviewed data following Koch's and Hill's
postulates shows a probable causal relationship between
neurospirochetosis and AD.
Persisting inflammation and amyloid deposition initiated and
sustained by chronic spirochetal infection form together with
the various hypotheses suggested to play a role in the
pathogenesis of AD a comprehensive entity.
As suggested by Hill, once the probability of a causal
relationship is established prompt action is needed.
Support and attention should be given to this field of AD
research.
Spirochetal infection occurs years or decades before the
manifestation of dementia.
As adequate antibiotic and anti-inflammatory therapies are
available, as in syphilis, one might prevent and eradicate
dementia.
...
Conclusion
Various types of spirochetes, including B. burgdorferi, and six
periodontal pathogen spirochetes ((T. socranskii, T.
pectinovorum, T. denticola, T. medium, T. amylovorum and T.
maltophilum) were detected in the brains of AD patients.
The pathological and biological hallmarks of AD, including
increased AβPP level, Aβ deposition and tau phosphorylation were
induced by spirochetes in vitro.
The statistical analysis showed a significant association
between spirochetes and AD. The strongly significant
association, the high risk factor and the analysis of data
following Koch’s and Hill’s criteria, are indicative of a causal
relationship between neurospirochetoses and AD.
Spirochetes are able to escape destruction by the host immune
reactions and establish chronic infection and sustained
inflammation.
In vivo studies with long exposure times will be necessary to
efficiently study the sequence of events and the cellular
mechanisms involved in spirochete induced AD-type host reactions
and Aβ-plaque, “tangle” and “granulovacuolar” formation.
The characterization of all types of spirochetes and
co-infecting bacteria and viruses is needed, in order to develop
serological tests for the early detection of infection.
The pathological process is thought to begin long before the
diagnosis of dementia is made therefore, an appropriate targeted
treatment should start early in order to prevent dementia.
Persisting spirochetal infection and their persisting toxic
components can initiate and sustain chronic inflammatory
processes through the activation of the innate and adaptive
immune system involving various signaling pathways.
In the affected brain the pathogens and their toxic components
can be observed, along with host immunological responses.
The response itself is characteristic of chronic inflammatory
processes associated with the site of tissue damage.
The outcome of infection is determined by the genetic
predisposition of the patient, by the virulence and biology of
the infecting agent
and by various environmental factors, such as exercise, stress
and nutrition.
The accumulated knowledge, the various views, and hypotheses
proposed to explain the pathogenesis of AD form together a
comprehensive entity when observed in the light of a persisting
chronic inflammation and amyloid deposition initiated and
sustained by chronic spirochetal infection.
As suggested by Hill, once the probability of a causal
relationship is established prompt action is needed. Similarly
to syphilis, one may prevent and eradicate dementia in AD.
The impact on healthcare costs and on the suffering of the
patients would be substantial.
http://www.jneuroinflammation.com/content/8/1/90/abstract
http://www.jneuroinflammation.com/content/pdf/1742-2094-8-90.pdf
J Neuroinflammation. 2011 Aug 4;8(1):90. [Epub ahead of print]
Alzheimer's disease - a neurospirochetosis. Analysis of the
evidence following Koch's and Hill's criteria.
Miklossy J.
Abstract
ABSTRACT: It is established that chronic spirochetal infection
can cause slowly progressive dementia, brain atrophy and amyloid
deposition in late neurosyphilis. Recently it has been suggested
that various types of spirochetes, in an analogous way to
Treponema pallidum, could cause dementia and may be involved in
the pathogenesis of Alzheimer's disease (AD). Here, we review
all data available in the literature on the detection of
spirochetes in AD and critically analyze the association and
causal relationship between spirochetes and AD following
established criteria of Koch and Hill. The results show a
statistically significant association between spirochetes and AD
(P = 1.5 x 10-17, OR = 20, 95% CI = 8-60, N = 247). When neutral
techniques recognizing all types of spirochetes were used, or
the highly prevalent periodontal pathogen Treponemas were
analyzed, spirochetes were observed in the brain in more than
90% of AD cases. Borrelia burgdorferi was detected in the brain
in 25.3% of AD cases analyzed and was 13 times more frequent in
AD compared to controls. Periodontal pathogen Treponemas (T.
pectinovorum, T. amylovorum, T. lecithinolyticum, T.
maltophilum, T. medium, T. socranskii) and Borrelia burgdorferi
were detected using species specific PCR and antibodies.
Importantly, co-infection with several spirochetes occurs in AD.
The pathological and biological hallmarks of AD were reproduced
in vitro. The analysis of reviewed data following Koch's and
Hill's postulates shows a probable causal relationship between
neurospirochetosis and AD. Persisting inflammation and amyloid
deposition initiated and sustained by chronic spirochetal
infection form together with the various hypotheses suggested to
play a role in the pathogenesis of AD a comprehensive entity. As
suggested by Hill, once the probability of a causal relationship
is established prompt action is needed. Support and attention
should be given to this field of AD research. Spirochetal
infection occurs years or decades before the manifestation of
dementia. As adequate antibiotic and anti-inflammatory therapies
are available, as in syphilis, one might prevent and eradicate
dementia.
PMID: 21816039 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/21816039
Vitamin B12 status and rate of
brain volume loss in community-dwelling elderly
doi: 10.1212/01.wnl.0000325581.26991.f2 Neurology September 9,
2008 vol. 71 no. 11 826-832
Conclusion: Low vitamin B12 status should be further
investigated as a modifiable cause of brain atrophy and of
likely subsequent cognitive impairment in the elderly.
http://www.neurology.org/content/71/11/826.abstract
Vitamin B clue to dementia
Thursday September 9 2010
NHS News (UK)
“Vitamin B tablets could slow and even halt the devastating
march of Alzheimer's disease,” The Daily Telegraph reported.
According to the newspaper, large daily doses of vitamin B can
halve the rate of brain shrinkage, a process that can precede
Alzheimer’s disease and dementia.
http://www.nhs.uk/news/2010/09September/Pages/vitamin-B12-brain-shrink-dementia.aspx
AD and dental work
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/3194074997
Tau-mediated neurodegeneration
in Alzheimer’s disease and related disorders
Nature Reviews Neuroscience | AOP, published online 8 August
2007; doi:10.1038/nrn2194
http://neuro.pathology.pitt.edu/webstuff/Journal%20Club/tau%20review.pdf
SARASOTA - A blood-pressure drug found by the Roskamp
Institute to show promise for arresting Alzheimer's disease
has been approved for a five-year, $8.4 million Phase III
human trial in Europe.
A Phase III clinical trial, which comes after studies on
safety in human patients, is usually the last stop on a drug's
long journey to market. The few medicines available for
Alzheimer's merely address symptoms that result from this
progressive brain disease. Just a handful that target
suspected causes — like the Roskamp drug, Nilvadipine — have
made it as far as Phase III, required for approval by the U.S.
Food and Drug Administration.
http://www.heraldtribune.com/article/20110525/ARTICLE/110529725
http://www.rfdn.org/news_release_052511.html
April 23, 2010
Reduction of β-amyloid pathology by celastrol in a transgenic
mouse model of Alzheimer’s disease
Filed under: alzheimer — Tags: Alzheimers disease, amyloid,
Celastrol — admin @ 2:59 pm
Daniel Paris, Nowell J Ganey, Vincent Laporte, Nikunj S Patel,
David Beaulieu-Abdelahad, Corbin Bachmeier, Amelia March,
Ghania Ait-Ghezala and Michael J Mullan
The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL
34243, USA
Journal of Neuroinflammation 2010,
7:17doi:10.1186/1742-2094-7-17
Published: 8 March 2010
Abstract
Background
Aβ deposits represent a neuropathological hallmark of
Alzheimer’s disease (AD). Both soluble and insoluble Aβ
species are considered to be responsible for initiating the
pathological cascade that eventually leads to AD. Therefore,
the identification of therapeutic approaches that can lower Aβ
production or accumulation remains a priority. NFκB has been
shown to regulate BACE-1 expression level, the rate limiting
enzyme responsible for the production of Aβ. We therefore
explored whether the known NFκB inhibitor celastrol could
represent a suitable compound for decreasing Aβ production and
accumulation in vivo.
Methods
The effect of celastrol on amyloid precursor protein (APP)
processing, Aβ production and NFκB activation was investigated
by western blotting and ELISAs using a cell line
overexpressing APP. The impact of celastrol on brain Aβ
accumulation was tested in a transgenic mouse model of AD
overexpressing the human APP695sw mutation and the
presenilin-1 mutation M146L (Tg PS1/APPsw) by immunostaining
and ELISAs. An acute treatment with celastrol was investigated
by administering celastrol intraperitoneally at a dosage of 1
mg/Kg in 35 week-old Tg PS1/APPsw for 4 consecutive days. In
addition, a chronic treatment (32 days) with celastrol was
tested using a matrix-driven delivery pellet system implanted
subcutaneously in 5 month-old Tg PS1/APPsw to ensure a
continuous daily release of 2.5 mg/Kg of celastrol.
Results
In vitro, celastrol dose dependently prevented NFκB activation
and inhibited BACE-1 expression. Celastrol potently inhibited
Aβ1-40 and Aβ1-42 production by reducing the β-cleavage of
APP, leading to decreased levels of APP-CTFβ and APPsβ. In
vivo, celastrol appeared to reduce the levels of both soluble
and insoluble Aβ1-38, Aβ1-40 and Aβ1-42. In addition, a
reduction in Aβ plaque burden and microglial activation was
observed in the brains of Tg PS1/APPsw following a chronic
administration of celastrol.
Conclusions
Overall our data suggest that celastrol is a potent Aβ
lowering compound that acts as an indirect BACE-1 inhibitor
possibly by regulating BACE-1 expression level via an NFκB
dependent mechanism. Additional work is required to determine
whether chronic administration of celastrol can be safely
achieved with cognitive benefits in a transgenic mouse model
of AD.
http://www.roskampinstitute.us/articles/archives/70
Has a Tobacco Company Stumbled on an Alzheimer’s Cure?
Nicotene-based compound at the heart of clinical studies
Mar 1, 2011, 10:33 am EDT | By Jeff
Reeves, Editor, InvestorPlace.com
Tobacco stock Star Scientific (NASDAQ: CIGX) is a company that
focuses on smokeless tobacco products. But if Star Scientific
has its way, the public could have a very different perception
of tobacco — namely, as the plant that cured Alzheimer’s. That
could mean big things for tobacco, and even bigger things for
Star Scientific stock.
http://www.investorplace.com/32191/star-scientific-tobacco-alzheimers-cure-treatment-anatabine-cigrx/
Roskamp Institute Obtains
IRB Approval for Multi-Site Human Clinical Trial with Rock
Creek Pharmaceutical RCP-006 Compound
on February 28, 2011
GLEN ALLEN, Va., Feb. 28, 2011 /PRNewswire via COMTEX/ –
http://www.starscientific.com/news/roskamp-institute-obtains-irb-approval-for-multi-site-human-clinical-trial-with-rock-creek-pharmaceutical-rcp-006-compound/
Role of Anatabine (RCP006
from Rock Creek Pharmaceuticals) as an anti-inflammatory
agent
http://www.rfdn.org/inflammaging.html
Orally administrated
cinnamon extract reduces β-amyloid oligomerization and
corrects cognitive impairment in Alzheimer's disease animal
models.
Frydman-Marom A, Levin A, Farfara D,
Benromano T, Scherzer-Attali R, Peled S, Vassar R, Segal D,
Gazit E, Frenkel D, Ovadia M.
Source
Department of Molecular Microbiology
and Biotechnology, Tel Aviv University, Tel Aviv, Israel.
PLoS One. 2011 Jan 28;6(1):e16564.
Abstract
An increasing body of evidence
indicates that accumulation of soluble oligomeric assemblies
of β-amyloid polypeptide (Aβ) play a key role in Alzheimer's
disease (AD) pathology. Specifically, 56 kDa oligomeric
species were shown to be correlated with impaired cognitive
function in AD model mice. Several reports have documented the
inhibition of Aβ plaque formation by compounds from natural
sources. Yet, evidence for the ability of common edible
elements to modulate Aβ oligomerization remains an unmet
challenge. Here we identify a natural substance, based on
cinnamon extract (CEppt), which markedly inhibits the
formation of toxic Aβ oligomers and prevents the toxicity of
Aβ on neuronal PC12 cells. When administered to an AD fly
model, CEppt rectified their reduced longevity, fully
recovered their locomotion defects and totally abolished
tetrameric species of Aβ in their brain. Furthermore, oral
administration of CEppt to an aggressive AD transgenic mice
model led to marked decrease in 56 kDa Aβ oligomers, reduction
of plaques and improvement in cognitive behavior. Our results
present a novel prophylactic approach for inhibition of toxic
oligomeric Aβ species formation in AD through the utilization
of a compound that is currently in use in human diet.
PMID: 21305046 [PubMed] PMCID:
PMC3030596
http://www.ncbi.nlm.nih.gov/pubmed/21305046
Full article: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0016564
Alzheimer's Risk Gene Disrupts
Brain's Wiring 50 Years Before Disease Hits
ScienceDaily (May 16, 2011) — What if you were told you
carried a gene that increases your risk for Alzheimer's
disease? And what if you were told this gene starts to do its
damage not when you're old but when you're young?...
http://www.sciencedaily.com/releases/2011/05/110513091638.htm
Naturally Occurring Plant
Alkaloids Could Slow Down Alzheimer's Disease, Study
Suggests
ScienceDaily (May 27, 2011) — A family of naturally occurring
plant compounds could help prevent or delay memory loss
associated with Alzheimer's disease, according to a new study
by the Translational Genomics Research Institute (TGen).
Beta-carboline alkaloids could potentially be used in
therapeutic drugs to stop, or at least slow down, the
progressively debilitating effects of Alzheimer's, according
to the study published recently in the scientific journal
Public Library of Science (PLoS) One....
http://www.sciencedaily.com/releases/2011/05/110526131244.htm
Tobacco-Derived Compound
Prevents Memory Loss in Alzheimer's Disease Mice
ScienceDaily (Apr. 28, 2011) — Cotinine, a compound derived
from tobacco, reduced plaques associated with dementia and
prevented memory loss in a mouse model of Alzheimer's disease,
a study led by researchers at Bay Pines VA Healthcare System
and the University of South Florida found... Some
epidemiological studies showed that people who smoke tend to
have lower incidences of Parkinson's disease and Alzheimer's
disease. Studies have widely attributed this apparently
beneficial effect to nicotine, which has been reported to
improve memory and reduce Alzheimer's-like plaques in mice.
However, nicotine's harmful cardiovascular effects and
addictive properties make the compound a less than ideal drug
candidate for neurodegenerative diseases.
The Bay Pines VA/USF team decided to look at the effects of
cotinine, the major byproduct of nicotine metabolism, in
Alzheimer's disease mice. Cotinine is nontoxic and longer
lasting than nicotine. Furthermore, its safety has already
been demonstrated in human trials evaluating cotinine's
potential to relieve tobacco withdrawal symptoms...
http://www.sciencedaily.com/releases/2011/04/110427131824.htm
Here's
the press release dated today 4-27-2011:
Tobacco-derived compound prevents memory loss in Alzheimer's
disease mice
Tampa, FL (For immediate release) -- Cotinine, a compound
derived from tobacco, reduced plaques associated with dementia
and prevented memory loss in a mouse model of Alzheimer's
disease, a study led by researchers at Bay Pines VA Healthcare
System and the University of South Florida found.
The findings are reported online in the Journal of Alzheimer's
Disease in advance of print publication...
More here: http://www.eurekalert.org/pub_releases/2011-04/uosf-tcp042711.php
Roskamp
Institute to Begin Human Alzheimer's Clinical Trials With a
Natural Compound in Tobacco
Oct 7, 2010
http://www.rfdn.org/news_release_100710.html
Also
look into "Anatabloc" from Star Scientific.
DHA
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/6894066487?r=8564020497#8564020497
Celiac
disease
http://alzheimers.infopop.cc/eve/forums/a/tpc/f/762104261/m/9514085397
MRI May Predict Which Adults
Will Develop Alzheimer's
ScienceDaily (Apr. 6, 2011) — Using MRI, researchers may be
able to predict which adults with mild cognitive impairment
are more likely to progress to Alzheimer's disease, according
to the results of a study published online and in the June
issue of Radiology...
http://www.sciencedaily.com/releases/2011/04/110406085054.htm
Compound Effectively Halts
Progression of Multiple Sclerosis in Animal Model
ScienceDaily (Apr. 17, 2011) — Scientists from the Florida
campus of The Scripps Research Institute have developed the
first of a new class of highly selective compounds that
effectively suppresses the severity of multiple sclerosis in
animal models. The new compound could provide new and
potentially more effective therapeutic approaches to multiple
sclerosis and other autoimmune diseases that affect patients
worldwide...
http://www.sciencedaily.com/releases/2011/04/110418093846.htm
Progression of Smell Loss Offers
Clues to the Treatment of Alzheimer's Disease
ScienceDaily (Apr. 6, 2011) — Loss of smell is a
characteristic early symptom among people with Alzheimer's
disease, but the relationship between olfactory dysfunction
and the progression of the disease is still relatively
unknown... Removing one olfactory bulb lowered the amount of
Aβ found 6 months later on that side of the brain by more than
50 percent, even in regions that receive no direct olfactory
bulb input. This supports a role for early-life olfactory bulb
output in the spread of Aβ throughout the brain...
http://www.sciencedaily.com/releases/2011/04/110406192513.htm
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