www.perpetualcommotion.com
"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
Newsletters
I have nothing to sell you but hope, and that I give you for free.
December 10, 2009Here is my Christmas gift
to you-- information. I hope you find something useful in all
this.
I
left out the section on the Grape Seed Extract in my first note to
you. I think it is an important development, so I corrected the
omission, and am re-sending you the whole thing.
You
will find that most of the research papers cited here talk about
Alzheimer's disease. Keep in mind two things: 1) The
diagnosis of CBD
based upon symptoms alone is notoriously wrong in about 50% of the
cases, so you have to consider other diseases as being the root cause
of the symptoms; 2) There is a LOT more money available for AD
research, so we are taking advantage of this in the cases where the AD
research applies to CBD.
Doctor
says
an oil lessened Alzheimer's effects on her husband
By Eve Hosley-Moore, Times Correspondent
In print: Wednesday, October 29, 2008
By Eve Hosley-Moore, Times Correspondent
In print: Wednesday, October 29, 2008
"
In Alzheimer's disease, certain brain cells may have difficulty
metabolizing glucose, the brain's principal source of energy. Without
fuel, these precious neurons may begin to die. But researchers have
identified an alternative energy source for brain cells — fats known as
ketone bodies, explained Dr. Theodore VanItallie, a medical doctor and
professor emeritus at the College of Physicians and Surgeons at
Columbia University in New York City. He has been researching ketones
for more than 35 years.
"Ketones are a high-energy fuel that nourish the brain," VanItallie said, explaining that when you are starving, the body produces ketones naturally. When digested, the liver converts MCT oil into ketones. In the first few weeks of life, ketones provide about 25 percent of the energy newborn babies need to survive.
"As Dr. Newport continued to read about MCT oil and the new medication, she discovered something surprising: Non-hydrogenated coconut oil is more than 60 percent MCT oil, and this medication derived its MCT oil from this readily available tropical tree."
http://www.tampabay.com/news/aging/article879333.ece
"Ketones are a high-energy fuel that nourish the brain," VanItallie said, explaining that when you are starving, the body produces ketones naturally. When digested, the liver converts MCT oil into ketones. In the first few weeks of life, ketones provide about 25 percent of the energy newborn babies need to survive.
"As Dr. Newport continued to read about MCT oil and the new medication, she discovered something surprising: Non-hydrogenated coconut oil is more than 60 percent MCT oil, and this medication derived its MCT oil from this readily available tropical tree."
http://www.tampabay.com/news/
Impaired
Energy
Metabolism Linked With Initiation Of Plaques In Alzheimer's Brain
ScienceDaily (Jan. 3, 2009)
"Here, for the first time we provide evidence linking impaired energy metabolism, an AD-relevant stress, with BACE1 translation mediated by eIF2α phosphorylation," says Dr. Vassar. "Our findings implicate phosphorylated eIF2α in both the initiation and progression of sporadic AD. Future experiments will determine whether inhibition of eIF2α phosphorylation could be an efficacious therapeutic approach for the prevention and treatment of AD..."
http://www.sciencedaily.com/releases/2008/12/081224215536.htm
ScienceDaily (Jan. 3, 2009)
"Here, for the first time we provide evidence linking impaired energy metabolism, an AD-relevant stress, with BACE1 translation mediated by eIF2α phosphorylation," says Dr. Vassar. "Our findings implicate phosphorylated eIF2α in both the initiation and progression of sporadic AD. Future experiments will determine whether inhibition of eIF2α phosphorylation could be an efficacious therapeutic approach for the prevention and treatment of AD..."
http://www.sciencedaily.com/
Brain
Starvation
As We Age Appears To Trigger Alzheimer's: Improving Blood
Flow
To Brain Is Preventive Strategy
ScienceDaily (Dec. 28, 2008)
"A slow, chronic starvation of the brain as we age appears to be one of the major triggers of a biochemical process that causes some forms of Alzheimer's disease..."
http://www.sciencedaily.com/releases/2008/12/081224215704.htm
To Brain Is Preventive Strategy
ScienceDaily (Dec. 28, 2008)
"A slow, chronic starvation of the brain as we age appears to be one of the major triggers of a biochemical process that causes some forms of Alzheimer's disease..."
http://www.sciencedaily.com/
Blood
Sugar
Linked To Normal Cognitive Aging
ScienceDaily (Dec. 31, 2008)
"Maintaining blood sugar levels, even in the absence of disease, may be an important strategy for preserving cognitive health, suggests a study published by researchers at Columbia University Medical Center (CUMC)..."
http://www.sciencedaily.com/releases/2008/12/081230072238.htm
ScienceDaily (Dec. 31, 2008)
"Maintaining blood sugar levels, even in the absence of disease, may be an important strategy for preserving cognitive health, suggests a study published by researchers at Columbia University Medical Center (CUMC)..."
http://www.sciencedaily.com/
Posts and articles from Dr. Mary Newport about MCT oil and coconut oil:
Doctor
says
an oil lessened Alzheimer's effects on her husband
Eve Hosley-Moore, Times Correspondent
St. Petersburg Times
In Print: Wednesday, October 29, 2008
"After two weeks of taking coconut oil, Steve Newport's results in an early onset Alzheimer's test gradually improved says his wife, Dr. Mary Newport. Before treatment, Steve could barely remember how to draw a clock. Two weeks after adding coconut oil to his diet, his drawing improved. After 37 days, Steve's drawing gained even more clarity. The oil seemed to "lift the fog," his wife says..."
http://www.tampabay.com/news/aging/article879333.ece
Eve Hosley-Moore, Times Correspondent
St. Petersburg Times
In Print: Wednesday, October 29, 2008
"After two weeks of taking coconut oil, Steve Newport's results in an early onset Alzheimer's test gradually improved says his wife, Dr. Mary Newport. Before treatment, Steve could barely remember how to draw a clock. Two weeks after adding coconut oil to his diet, his drawing improved. After 37 days, Steve's drawing gained even more clarity. The oil seemed to "lift the fog," his wife says..."
http://www.tampabay.com/news/
More posts by Dr. Newport
Dr. Newport's web site: http://www.coconutketones.com
Dr. Newport's blog: http://coconutketones.
Dr. Newport's April 2009 "update" (.pdf version)
Dr. Newport's September 2009 "Diet guidelines" (.pdf version)
I thought I should bring Dr. Newport's Thursday, October 29, 2009 blog entry to your attention. There are some very intriguing ideas here. And, they involve supplements that could easily be obtained by the average person who would like to pursue these ideas further.Here is an excerpt:
I
hear from some people who are very discouraged because they do not see
improvement in their loved one with Alzheimer's. About half of the
people in the MCT oil studies declined minimally rather than improving,
but declined less than the people who took the placebo. So this
strategy may be worthwhile continuing even if results are not obvious
in the beginning. Also, some people improve rather slowly but over two
to three months, the changes may become more apparent, or perhaps you
will see that things are not worse.
If you are considering giving up on this, you might consider the possibility that this strategy could at least stabilize or slow down the process for your loved one. Hopefully we will be able to learn why some people improve and others don't. After attending the American College of Nutrition Conference at the beginning of October, I have some ideas about why this happens. It could be that the cells are so depleted of the various substances they need to make energy inside the cell that the cells don't recover simply by providing ketone. I learned more about other disease processes where there is also a problem with energy production in mitochondria, the organelles inside of the cells that manufacture ATP, the very basic energy that drives the whole function of the cell. Each cell has hundreds to thousands of mitochondria.
Dr. Stephen Sinatra discussed several dietary supplements that help people with severe congestive heart failure by providing certain subtances involved in manufacturing ATP in the mitochondria in the cells. In the case of congestive heart failure, the cardiac cells have become depleted of these substances and are not making enough ATP to keep the cell going. Three of the supplements we have been giving Steve for quite some time, CoQ10, L-carnitine and magnesium, but the fourth I did not know about, D-ribose. D-ribose is a simple sugar normally made inside the cell from glucose, and is one of the building blocks for ATP. It makes sense that if glucose cannot even get into the cell that the cell will not be able to make D-ribose, which is critical to making ATP. It is not stored elsewhere in the body and it is not present in any quantity in foods, but is used by body builders and available as a supplement. For people with cardiac diseases, Dr. Sinatra recommends taking about 5 - 7 grams of D-ribose per day. It comes in a powder (disappears without much taste in coffee or any drink) or chewable tablet (not so good to my tastebuds.) I have many questions about it, such as does it cross the blood brain barrrier and how does it enter the cell, and of course, it is safe? I have not been able to find out much about it. If there is a chemist or other scientist out there with more information about D-ribose, I would appreciate hearing from you. When I learn more I will post something about it.
Dr. Sinatra has a book called, "The Sinatra Solution: Metabolic Cardiology" that discusses these supplements in detail, but is very technical. I believe that this strategy could help people with AD since the mitochondria work the same as far as producing enery in all of the cells. After reading up about this, part of the problem in AD may be that the cells become depleted of these substances, such as CoQ10, from some of the medications our people with AD are often on (anti-depressants, statins.) Also the whole process of making energy in the mitochondria depends on being able to get glucose (or ketone bodies as an alternative) into the cells in the first place and this is not happening...
If you are considering giving up on this, you might consider the possibility that this strategy could at least stabilize or slow down the process for your loved one. Hopefully we will be able to learn why some people improve and others don't. After attending the American College of Nutrition Conference at the beginning of October, I have some ideas about why this happens. It could be that the cells are so depleted of the various substances they need to make energy inside the cell that the cells don't recover simply by providing ketone. I learned more about other disease processes where there is also a problem with energy production in mitochondria, the organelles inside of the cells that manufacture ATP, the very basic energy that drives the whole function of the cell. Each cell has hundreds to thousands of mitochondria.
Dr. Stephen Sinatra discussed several dietary supplements that help people with severe congestive heart failure by providing certain subtances involved in manufacturing ATP in the mitochondria in the cells. In the case of congestive heart failure, the cardiac cells have become depleted of these substances and are not making enough ATP to keep the cell going. Three of the supplements we have been giving Steve for quite some time, CoQ10, L-carnitine and magnesium, but the fourth I did not know about, D-ribose. D-ribose is a simple sugar normally made inside the cell from glucose, and is one of the building blocks for ATP. It makes sense that if glucose cannot even get into the cell that the cell will not be able to make D-ribose, which is critical to making ATP. It is not stored elsewhere in the body and it is not present in any quantity in foods, but is used by body builders and available as a supplement. For people with cardiac diseases, Dr. Sinatra recommends taking about 5 - 7 grams of D-ribose per day. It comes in a powder (disappears without much taste in coffee or any drink) or chewable tablet (not so good to my tastebuds.) I have many questions about it, such as does it cross the blood brain barrrier and how does it enter the cell, and of course, it is safe? I have not been able to find out much about it. If there is a chemist or other scientist out there with more information about D-ribose, I would appreciate hearing from you. When I learn more I will post something about it.
Dr. Sinatra has a book called, "The Sinatra Solution: Metabolic Cardiology" that discusses these supplements in detail, but is very technical. I believe that this strategy could help people with AD since the mitochondria work the same as far as producing enery in all of the cells. After reading up about this, part of the problem in AD may be that the cells become depleted of these substances, such as CoQ10, from some of the medications our people with AD are often on (anti-depressants, statins.) Also the whole process of making energy in the mitochondria depends on being able to get glucose (or ketone bodies as an alternative) into the cells in the first place and this is not happening...
Tau Busters
There are five "tau buster" candidates known to me at this time: Cinnamon proanthocyanidins, methylene blue (Rember), niacinamide (nicotinamide), grape seed extract, and the newest member of the club, davunetide.
This brings to five the number of substances we have heard about since late 2007 that might be tau-busters. The other four are cinnamon proanthocyanidins, methylene blue, niacinamide and grape seed extract. The wording describing the action of these four is almost identical: "capable of inhibiting tau peptide aggregations, as well as dissociating preformed tau peptide aggregates"
Niacinamide
Here is a thread about niacinamide on the Alz.org forum. It is from early November of 2008:
http://alzheimers.infopop.cc/
Apparently, nicotinamide combats the tau protein problem common to so many of these neurodegenerative diseases. Also known as "niacinamide", it appears to be readily available from health food stores. The dosing given to the mice was 200 mg/kg/day in their drinking water. I don't know if this number is for the mass of the water, or the body weight of the mice. "The mice received the equivalence of about 2 g of nicotinamide for humans." Several supplement suppliers make 500mg capsules or tablets. This would mean one would have to take 4 of these per day. Not so bad.
Here are the article cited in the thread:
First, a Google search:
http://news.google.com/news?
Vitamin
Holds
Promise for Alzheimer's Disease
Treatment cured memory problems in mice, researchers found
U.S. News and World Report
Posted November 5, 2008
http://health.usnews.com/articles/health/healthday/2008/11/05/vitamin-holds-promise-for-alzheimers-disease.html
Treatment cured memory problems in mice, researchers found
U.S. News and World Report
Posted November 5, 2008
http://health.usnews.com/
The abstract for the niacinamide study:
Nicotinamide
Restores
Cognition
in Alzheimer's Disease Transgenic Mice via a
Mechanism Involving Sirtuin Inhibition and Selective Reduction of
Thr231-Phosphotau
Kim N. Green,1 Joan S. Steffan,2 Hilda Martinez-Coria,1 Xuemin Sun,3 Steven S. Schreiber,3,5 Leslie Michels Thompson,1,2,4 and Frank M.
LaFerla1
Departments of 1Neurobiology and Behavior, 2Psychiatry and Human Behavior, 3Neurology, 4Biological Chemistry, and 5Anatomy and Neurobiology, University of California, Irvine, Irvine, California 92697-4545
"Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed. Effective preventive strategies likely offer the greatest and most widespread benefits. Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance memory and synaptic plasticity. We evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD+-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated {alpha}-tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. Reduced phosphoThr231-tau was related to a reduction of monoubiquitin-conjugated tau, suggesting that this posttranslationally modified form of tau may be rapidly degraded. Overexpression of a Thr231-phospho-mimic tau in vitro increased clearance and decreased accumulation of tau compared with wild-type tau. These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability.
http://www.jneurosci.org/cgi/content/abstract/28/45/11500
Kim N. Green,1 Joan S. Steffan,2 Hilda Martinez-Coria,1 Xuemin Sun,3 Steven S. Schreiber,3,5 Leslie Michels Thompson,1,2,4 and Frank M.
LaFerla1
Departments of 1Neurobiology and Behavior, 2Psychiatry and Human Behavior, 3Neurology, 4Biological Chemistry, and 5Anatomy and Neurobiology, University of California, Irvine, Irvine, California 92697-4545
"Memory loss is the signature feature of Alzheimer's disease, and therapies that prevent or delay its onset are urgently needed. Effective preventive strategies likely offer the greatest and most widespread benefits. Histone deacetylase (HDAC) inhibitors increase histone acetylation and enhance memory and synaptic plasticity. We evaluated the efficacy of nicotinamide, a competitive inhibitor of the sirtuins or class III NAD+-dependent HDACs in 3xTg-AD mice, and found that it restored cognitive deficits associated with pathology. Nicotinamide selectively reduces a specific phospho-species of tau (Thr231) that is associated with microtubule depolymerization, in a manner similar to inhibition of SirT1. Nicotinamide also dramatically increased acetylated {alpha}-tubulin, a primary substrate of SirT2, and MAP2c, both of which are linked to increased microtubule stability. Reduced phosphoThr231-tau was related to a reduction of monoubiquitin-conjugated tau, suggesting that this posttranslationally modified form of tau may be rapidly degraded. Overexpression of a Thr231-phospho-mimic tau in vitro increased clearance and decreased accumulation of tau compared with wild-type tau. These preclinical findings suggest that oral nicotinamide may represent a safe treatment for AD and other tauopathies, and that phosphorylation of tau at Thr231 may regulate tau stability.
http://www.jneurosci.org/cgi/
Nicotinamide
Restores
Cognition in Alzheimer's Disease Reduces Alzheimer's tau
lesions and memory loss in mice
By Will Block Life Enhancement
"At the end of the trial, the AD mice performed as well in memory testing as healthy mice, a remarkable result strongly suggesting that nicotinamide had protected their brains from memory loss, and restored memory that would have been lost. “Cognitively, they were cured,” first author of the study, Dr. Kim Green said. “They performed as if they’d never developed the disease.”3 “The vitamin completely prevented cognitive decline associated with the disease, bringing them back to the level they’d be at if they didn’t have the pathology,” said Dr. Green. “It actually improved behavior in non-demented animals too.”4 Meaning that healthy mice fed nicotinamide outperformed mice on a normal diet. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said Dr. Frank LaFerla, the lead author of the study..."
"Nicotinamide is a water soluble member of the B vitamin group. Also known as niacinamide, nicotinamide is the amide of nicotinic acid (vitamin B3), also known as niacin. In vivo, niacin is converted to nicotinamide and although the two are identical in their vitamin functions, nicotinamide does not have the same pharmacologic effects of niacin, which may affect the liver negatively in some individuals. Unlike niacin, nicotinamide does not reduce cholesterol or cause flushing. In cells, niacin forms the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Although the pathways for nicotinamide and nicotinic acid are very similar. NAD+ and NADP+ are coenzymes in a wide variety of enzymatic oxidation-reduction reactions..."
"In their search for just what was going on, nicotinamide did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion. Given this lack of effect on beta amyloid levels, the researchers figured the compound must be improving cognition through some other mechanism. Upon analyzing protein extracts from whole brain samples of treated and control AD mice, they found a 20 percent reduction in levels of tau in the nicotinamide-treated animals. They saw no differences at several tau sites typically phosphorylated in AD mice at the end of eight months, but a whopping 60 percent reduction in Thr231-phospho-tau—a particular species of tau that has been reported to interfere with microtubule polymerization and is a commonly used biomarker for AD—in the nicotinamide group compared with vehicle. “It’s incredibly dramatic,” Green told the Alzheimer’s Research Forum. “This thing [a biomarker for AD] is just wiped from the brain very specifically...”5
References
1. Wang SS. When Alzheimer’s hits at 40. New York Times, Nov. 14, 2008.
2. Green KN, Steffan JS, Martinez-Coria H, Sun X, Schreiber SS, Thompson LM,LaFerla FM. Nicotinamide restores cognition in Alzheimer’s disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. J Neurosci 2008 Nov 5;28(45):11500-10.
3. Dotinga R. Vitamin holds promise for Alzheimer’s disease. Healthday Nov. 5, 2008.
4. Sample I. Vitamin pill that may slow Alzheimer’s goes on trial. The Guardian, Nov. 05 2008.
5. Anon. Alzheimer’s Research Forum. Nov. 8, 2008.
http://www.life-enhancement.com/article_template.asp?ID=2049
By Will Block Life Enhancement
"At the end of the trial, the AD mice performed as well in memory testing as healthy mice, a remarkable result strongly suggesting that nicotinamide had protected their brains from memory loss, and restored memory that would have been lost. “Cognitively, they were cured,” first author of the study, Dr. Kim Green said. “They performed as if they’d never developed the disease.”3 “The vitamin completely prevented cognitive decline associated with the disease, bringing them back to the level they’d be at if they didn’t have the pathology,” said Dr. Green. “It actually improved behavior in non-demented animals too.”4 Meaning that healthy mice fed nicotinamide outperformed mice on a normal diet. “This suggests that not only is it good for Alzheimer’s disease, but if normal people take it, some aspects of their memory might improve,” said Dr. Frank LaFerla, the lead author of the study..."
"Nicotinamide is a water soluble member of the B vitamin group. Also known as niacinamide, nicotinamide is the amide of nicotinic acid (vitamin B3), also known as niacin. In vivo, niacin is converted to nicotinamide and although the two are identical in their vitamin functions, nicotinamide does not have the same pharmacologic effects of niacin, which may affect the liver negatively in some individuals. Unlike niacin, nicotinamide does not reduce cholesterol or cause flushing. In cells, niacin forms the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). Although the pathways for nicotinamide and nicotinic acid are very similar. NAD+ and NADP+ are coenzymes in a wide variety of enzymatic oxidation-reduction reactions..."
"In their search for just what was going on, nicotinamide did not affect levels of the protein beta amyloid, which clumps in the brain to form plaques, the second type of Alzheimer’s lesion. Given this lack of effect on beta amyloid levels, the researchers figured the compound must be improving cognition through some other mechanism. Upon analyzing protein extracts from whole brain samples of treated and control AD mice, they found a 20 percent reduction in levels of tau in the nicotinamide-treated animals. They saw no differences at several tau sites typically phosphorylated in AD mice at the end of eight months, but a whopping 60 percent reduction in Thr231-phospho-tau—a particular species of tau that has been reported to interfere with microtubule polymerization and is a commonly used biomarker for AD—in the nicotinamide group compared with vehicle. “It’s incredibly dramatic,” Green told the Alzheimer’s Research Forum. “This thing [a biomarker for AD] is just wiped from the brain very specifically...”5
References
1. Wang SS. When Alzheimer’s hits at 40. New York Times, Nov. 14, 2008.
2. Green KN, Steffan JS, Martinez-Coria H, Sun X, Schreiber SS, Thompson LM,LaFerla FM. Nicotinamide restores cognition in Alzheimer’s disease transgenic mice via a mechanism involving sirtuin inhibition and selective reduction of Thr231-phosphotau. J Neurosci 2008 Nov 5;28(45):11500-10.
3. Dotinga R. Vitamin holds promise for Alzheimer’s disease. Healthday Nov. 5, 2008.
4. Sample I. Vitamin pill that may slow Alzheimer’s goes on trial. The Guardian, Nov. 05 2008.
5. Anon. Alzheimer’s Research Forum. Nov. 8, 2008.
http://www.life-enhancement.
Understanding neurofibrillary tangles (image)
http://www.life-enhancement.
Methylene Blue
Methylene Blue:
Potential Alzheimer's, Parkinson's Cure Found In Century-old Drug
ScienceDaily (Aug. 18, 2008)
"A new study conducted by researchers at Children's Hospital & Research Center Oakland shows that a century-old drug, methylene blue, may be able to slow or even cure Alzheimer's and Parkinson's disease. Used at a very low concentration – about the equivalent of a few raindrops in four Olympic-sized swimming pools of water – the drug slows cellular aging and enhances mitochondrial function, potentially allowing those with the diseases to live longer, healthier lives."
"Methylene blue, first discovered in 1891, is now used to treat methemoglobinemia, a blood disorder. But because high concentrations of methylene blue were known to damage the brain, no one thought to experiment with low concentrations. Also, drugs such as methylene blue do not easily reach the brain."
http://www.sciencedaily.com/
Rember:
Daily pill that halts Alzheimer's is hailed as 'biggest breakthrough against disease for 100 years'
Daily Mail (UK)
By Jenny Hope
Last updated at 11:57 PM on 29th July 2008
(excerpts:)
"A new drug halts the devastating progress of Alzheimer's disease, say British scientists.
"It is said to be more than twice as effective as current treatments.
"A daily capsule of rember [sic], as the drug is known, stops Alzheimer's disease progressing by as much as 81 per cent, according to trial results.
"Patients with the brain disorder had no significant decline in their mental function over a 19-month period.
"It is the first time medication has been developed to target the `tangles' in the brain that destroy nerve cells, leading to deteriorating memory.
"The drug helps to disrupt this process, preventing the formation of new tangles and loosening those already created."
http://www.dailymail.co.uk/
errrr... no it isn't the "first time". The "water soluble component of common cinnamon" identified by Prof. Graves at the University of California in Santa Barbara also "inhibits the aggregation of tau and disassembles fibers that have already formed".
If this drug from the UK works, and I certainly hope that it does, then the water-soluble cinnamon extract should too. And we have anecdotal evidence that it does.
What this means is, don't despair that you can't get this new wonder drug. You have alternatives! Check out cinnamon proanthocyanidins and niacinamide.
Rember for Alzheimer's: Methylene Blue's Comeback
corante.com July 31, 2008
"Methylene blue has been around forever, used for urinary tract infections, malaria, and all sorts of things, up to treating protozoal infections in fish tanks. (For that matter, it's turned up over the years as a surreptitious additive to blueberry pies and the like, turning the unsuspecting consumer's urine greenish/blue, generally to their great alarm: a storied med school prank from the old days)."
http://pipeline.corante.com/
Vienna (and Burkina Faso): What's New With Methylene Blue?
Alzheimer Research Forum
30 July 2009
At ICAD in Vienna, Wischik discussed further analysis of the same Phase 2 trial of RemberTM, his biotech company's patented formulation of methylene blue. Wischik noted in his talk that the company had patented a new form called leuco-methylthioninium or LMT, which is no longer blue and renders the drug more bioavailable and less toxic at higher doses. For their part, Schirmer's group had characterized a reduced white version of methylene blue (called leucoMB or methylene white) as a possibly superior form of this drug for use in a colorless drug syrup to treat malaria (see Buchholz et al., 2008 and Schirmer essay). TauRx's new formulation is presently undergoing preclinical studies. For a detailed first-person account of what happened with the high dose of RemberTM in the Phase 2 trial and related topics...
http://www.alzforum.org/new/
Curcumin
Curcumin
Definitions: Free Dictionary
Wikipedia
"Curcumin is the principal curcuminoid of the Indian curry spice turmeric. The curcuminoids are polyphenols and are responsible for the yellow color of turmeric. Curcumin can exist in at least two tautomeric forms, keto and enol. The enol form is more energetically stable in the solid phase and in solution"
"Curcumin is known for its antitumor, antioxidant, anti-amyloid and anti-inflammatory properties. Anti-inflammatory properties may be due to inhibition of eicosanoid biosynthesis."
Curcumin Inhibits Formation of Amyloid {beta} Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo
J. Biol. Chem., Vol. 280, Issue 7, 5892-5901, February 18, 2005
"Alzheimer's disease (AD) involves amyloid {beta} (A{beta}) accumulation, oxidative damage, and inflammation, and risk is reduced with increased antioxidant and anti-inflammatory consumption. The phenolic yellow curry pigment curcumin has potent anti-inflammatory and antioxidant activities and can suppress oxidative damage, inflammation, cognitive deficits, and amyloid accumulation. Since the molecular structure of curcumin suggested potential A{beta} binding, we investigated whether its efficacy in AD models could be explained by effects on A{beta} aggregation... When fed to aged Tg2576 mice with advanced amyloid accumulation, curcumin labeled plaques and reduced amyloid levels and plaque burden. Hence, curcumin directly binds small {beta}-amyloid species to block aggregation and fibril formation in vitro and in vivo. These data suggest that low dose curcumin effectively disaggregates A{beta} as well as prevents fibril and oligomer formation, supporting the rationale for curcumin use in clinical trials preventing or treating AD."
http://www.jbc.org/cgi/
A Potential Role of the Curry Spice Curcumin in Alzheimer’s Disease
UCLA Dept. of Neurology, Alzheimer’s Disease Research Center
"There is substantial in-vitro data indicating that curcumin has antioxidant, anti-inflammatory, and anti-amyloid activity. In addition, studies in animal models of Alzheimer’s disease (AD) indicate a direct effect of curcumin in decreasing the amyloid pathology of AD. As the widespread use of curcumin as a food additive and relatively small short-term studies in humans suggest safety, curcumin is a promising agent in the treatment and/or prevention of AD. Nonetheless, important information regarding curcumin bioavailability, safety and tolerability, particularly in an elderly population is lacking. We are therefore performing a study of curcumin in patients with AD to gather this information in addition to data on the effect of curcumin on biomarkers of AD pathology."
http://www.pubmedcentral.nih.
also http://www.ingentaconnect.com/
An Indian Spice for Alzheimer's?
"Researchers here in the United States have been pursuing clues to the effects of curcumin, a compound found in the spice turmeric that is responsible for the yellow color of Indian curry and American mustard. Studies show that elderly villagers in India appear to have the lowest rate of Alzheimer's disease in the world. Researchers speculate that curcumin, which has powerful antioxidant and anti-inflammatory properties might play a role, because Indians eat turmeric with almost every meal."
http://www.drweil.com/drw/u/
Curcumin, the Curry Spice
Part 2
"The levels of beta-amyloid in AD mice that were given low doses of curcumin were decreased by around 40% in comparison to those AD mice that were not treated with curcumin. In addition, low doses of curcumin also caused a 43% decrease in the so-called "plaque burden" that these beta-amyloids have on the brains of AD mice. Surprisingly, those AD mice that received high doses of curcumin did not show any decreases in beta-amyloid levels or plaque burden in comparison with untreated mice. While the exact reason for this finding is not yet clear, the results of it are intriguing: low doses of curcumin were actually more effective than high doses in combating the neurodegenerative process of AD."
http://www.stanford.edu/group/
Curcumin has potent anti-amyloidogenic effects for Alzheimer's beta-amyloid fibrils in vitro.
"Inhibition of the accumulation of amyloid beta-peptide (Abeta) and the formation of beta-amyloid fibrils (fAbeta) from Abeta, as well as the destabilization of preformed fAbeta in the central nervous system, would be attractive therapeutic targets for the treatment of Alzheimer's disease (AD). We reported previously that nordihydroguaiaretic acid (NDGA) and wine-related polyphenols inhibit fAbeta formation from Abeta(1-40) and Abeta(1-42) and destabilize preformed fAbeta(1-40) and fAbeta(1-42) dose-dependently in vitro..."
http://www.ncbi.nlm.nih.gov/
Spice Protects Brain Cells, Could Prevent Alzheimer's Disease
"In their study, researchers exposed rat brain cells to various concentrations of curcumin, then analyzed the cells 24 hours later. Indeed, they found HO-1 as well as two other protective enzymes. However, higher concentrations of curcumin caused substantial cell damage -- with no increase in the protective HO-1 protein, she reports."
http://www.webmd.com/
The Curry Spice Curcumin Reduces Oxidative Damage and Amyloid Pathology in an Alzheimer Transgenic Mouse The Journal of Neuroscience, November 1, 2001, 21(21):8370-8377
"To evaluate whether it could affect Alzheimer-like pathology in the APPSw mice, we tested a low (160 ppm) and a high dose of dietary curcumin (5000 ppm) on inflammation, oxidative damage, and plaque pathology. Low and high doses of curcumin significantly lowered oxidized proteins and interleukin-1beta , a proinflammatory cytokine elevated in the brains of these mice. With low-dose but not high-dose curcumin treatment, the astrocytic marker GFAP was reduced, and insoluble beta -amyloid (Abeta ), soluble Abeta , and plaque burden were significantly decreased by 43-50%. However, levels of amyloid precursor (APP) in the membrane fraction were not reduced. Microgliosis was also suppressed in neuronal layers but not adjacent to plaques. In view of its efficacy and apparent low toxicity, this Indian spice component shows promise for the prevention of Alzheimer's disease."
http://www.jneurosci.org/cgi/
Curcumin helps clear Alzheimer's plaques
Oct. 4 (UPI)
"Curcumin improved ingestion of amyloid beta by immune cells in 50 percent of patients with Alzheimer's disease," said Fiala.
http://www.upi.com/
UCLA/VA Study Finds Chemical Found in Curry May Help Immune System Clear Amyloid Plaques Found in Alzheimer’s Disease
Date: October 3, 2006
"UCLA/VA researchers found that curcumin — a chemical found in curry and turmeric — may help the immune system clear the brain of amyloid beta, which form the plaques found in Alzheimer's disease. Published in the Oct. 9 issue of the Journal of Alzheimer's Disease, the early laboratory findings may lead to a new approach in treating Alzheimer's disease by enhancing the natural function of the immune system using curcumin, known for its anti-inflammatory and anti-oxidant properties."
http://newsroom.ucla.edu/page.
also, http://www.hbri.org/
Molecular Orbital Basis for Yellow Curry Spice Curcumin's Prevention of Alzheimer's Disease
"It is demonstrated by using high-level ab initio computations that the yellow curcumin pigment, bis(4-hydroxy-3-methoxyphenyl)
http://pubs.acs.org/cgi-bin/
Preserve brain function with spicy foods.
By PsychologyToday.com
"About a tablespoon of curry a day, or 200 mg of curcumin, does the trick, says Dr. Sally Frautschy, associate professor of medicine at UCLA. “I eat curry at least 4 times a week,” she reports."
"Other spices are thought to possibly contain medicinal properties. Ginger and cinnamon are getting a close look. A powerful antioxidant in ginger called zingerone appears so far to have brain-protective properties like curcumin. Cinnamon may also have effects in the brain."
http://health.msn.com/centers/
Curcuminoids as potential new iron-chelating agents: spectroscopic, polarographic and potentiometric study on their Fe(III) complexing ability
Authors: Borsari M.; Ferrari E.; Grandi R.; Saladini M.1
Source: Inorganica Chimica Acta, Volume 328, Number 1, 30 January 2002 , pp. 61-68(8)
Marco Borsari, Erika Ferrari, Romano Grandi and Monica Saladini
Department of Chemistry, University of Modena and Reggio Emilia, Via Campi 183, 41100 Modena, Italy
Abstract
"The pKa values of curcumin and diacetylcurcumin are, here doubtless, determined by means of spectroscopic and potentiometric measurements, and the enolic proton is the more acidic one. The interaction of Fe3+ with curcumin and diacetylcurcumin, in water/methanol 1:1 solution, leads to the formation of the complex species [FeH2CU(OH)2] and [FeDCU(OH)2] (H2CU and DCU=curcumin or diacetylcurcumin monoanion, respectively) which prevails near pH 7. At more basic condition the prevailing species are [FeH2CU(OH)3]− and [FeDCU(OH)3]−, which prevent metal hydroxide precipitation. 1H NMR data state that the dissociated β-diketo moiety of the ligands is involved in metal chelation. The pKa value of the deprotonation reaction is strongly anticipated by the metal ion, as shown by UV spectral data. The stability constants, evaluated from potentiometric data, are near to that of desferrioxamine, which is, by now, the only iron-chelating agent for clinical use...Curcumin and diacetylcurcumin coordinate Fe(III) through β-diketone moiety, form stable complexes. The prevailing species at physiological pH is [FeH2CU(OH)2] whose stability constant is near to those of iron-sequestering agents for clinical use."
http://www.sciencedirect.com/
Curcumin interaction with copper and iron suggests one possible mechanism of action in Alzheimer's disease animal models.
J Alzheimers Dis. 2004 Aug;6(4):367-77; discussion 443-9.
Baum L, Ng A.
Department of Medicine and Therapeutics, Chinese University of Hong Kong, Shatin. lwbaum@cuhk.edu.hk
"Curcumin is a polyphenolic diketone from turmeric. Because of its anti-oxidant and anti-inflammatory effects, it was tested in animal models of Alzheimer's disease, reducing levels of amyloid and oxidized proteins and preventing cognitive deficits. An alternative mechanism of these effects is metal chelation, which may reduce amyloid aggregation or oxidative neurotoxicity. Metals can induce Abeta aggregation and toxicity, and are concentrated in AD brain. Chelators desferrioxamine and clioquinol have exhibited anti-AD effects. Using spectrophotometry, we quantified curcumin affinity for copper, zinc, and iron ions. Zn2+ showed little binding, but each Cu2+ or Fe2+ ion appeared to bind at least two curcumin molecules. The interaction of curcumin with copper reached half-maximum at approximately 3-12 microM copper and exhibited positive cooperativity, with Kd1 approximately 10-60 microM and Kd2 approximately 1.3 microM (for binding of the first and second curcumin molecules, respectively). Curcumin-iron interaction reached half-maximum at approximately 2.5-5 microM iron and exhibited negative cooperativity, with Kd1 approximately 0.5-1.6 microM and Kd2 approximately 50-100 microM. Curcumin and its metabolites can attain these levels in vivo, suggesting physiological relevance. Since curcumin more readily binds the redox-active metals iron and copper than redox-inactive zinc, curcumin might exert a net protective effect against Abeta toxicity or might suppress inflammatory damage by preventing metal induction of NF-kappaB."
PMID: 15345806 [PubMed]
http://iospress.metapress.com/
Curcumin stimulates proliferation of embryonic neural progenitor cells and neurogenesis in the adult hippocampus.
Kim SJ, Son TG, Park HR, Park M, Kim MS, Kim HS, Chung HY, Mattson MP, Lee J.
Pharmacy, Pusan National University, Busan 609-735.
"Curcumin is a natural phenolic component of yellow curry spice, which is used in some cultures for the treatment of diseases associated with oxidative stress and inflammation. Curcumin has been reported capable of preventing the death of neurons in animal models of neurodegenerative disorders, but its possible effects on developmental and adult neuroplasticity are unknown. In the present study, we investigated the effects of curcumin on mouse multi-potent neural progenitor cells (NPC) and adult hippocampal neurogenesis. Curcumin exerted biphasic effects on cultured NPC - low concentrations stimulated cell proliferation, whereas high concentrations were cytotoxic. Curcumin activated extracellular signal regulated kinases (ERKs) and p38 kinases, cellular signal transduction pathways known to be involved in the regulation of neuronal plasticity and stress responses. Inhibitors of ERKs and p38 kinases effectively blocked the mitogenic effect of curcumin in NPC. Administration of curcumin to adult mice resulted in a significant increase in the number of newly-generated cells in the dentate gyrus of hippocampus, indicating that curcumin enhances adult hippocampal neurogenesis. Our findings suggest that curcumin can stimulate developmental and adult hippocampal neurogenesis, a biological activity that may enhance neural plasticity and repair."
PMID: 18362141 [PubMed - as supplied by publisher]
http://www.ncbi.nlm.nih.gov/
Vitamin D, Curcumin May Help Clear Amyloid Plaques Found In Alzheimer's Disease
ScienceDaily (July 15, 2009)
"UCLA scientists and colleagues from UC Riverside and the Human BioMolecular Research Institute have found that a form of vitamin D, together with a chemical found in turmeric spice called curcumin, may help stimulate the immune system to clear the brain of amyloid beta, which forms the plaques considered the hallmark of Alzheimer's disease. The early research findings, which appear in the July issue of the Journal of Alzheimer's Disease, may lead to new approaches in preventing and treating Alzheimer's by utilizing the property of vitamin D3 — a form of vitamin D — both alone and together with natural or synthetic curcumin to boost the immune system in protecting the brain against amyloid beta..."
http://www.sciencedaily.com/
Apple Juice
Apple Juice Can Delay Onset Of Alzheimer's Disease, Study Suggests
ScienceDaily (Jan. 24, 2009)
In the most recent study Shea and his team demonstrated that mice receiving the human equivalent of 2 glasses of apple juice per day for 1 month produced less of a small protein fragment, called "beta-amyloid" that is responsible for forming the "senile plaques" that are commonly found in brains of individuals suffering from Alzheimer's disease.
http://www.sciencedaily.com/
Cinnamon
CINNAMON EXTRACT USEFUL FOR INHIBITING THE AGGREGATION OF TAU AND TREATING ALZHEIMER'S DISEASE
by Donald Graves, University of California, Santa Barbara
Published on 2/22/2008???
http://www.ibridgenetwork.org/
"Researchers at the University of California, Santa Barbara have discovered an extract of common cinnamon that contains a class of small organic molecules that inhibit several key processes in Alzheimer's disease. The cinnamon extract inhibits the aggregation of tau and disassembles fibers that have already formed, suggesting that neurofibrillary tangles can possibly be reversed by these compounds. The extract exhibits potent inhibitory activity, is orally available, water-soluble, non-toxic, and the bioactive molecules are likely brain permeable. The extract is readily produced in large quantities and can be encapsulated in powder form for oral administration. These properties make the cinnamon extract a highly favorable substance for development into an effective therapeutic to slow or prevent Alzheimer's disease."
http://www.ibridgenetwork.org/
PROANTHOCYANIDINS FROM CINNAMON AND ITS WATER SOLUBLE EXTRACT INHIBIT TAU AGGREGATION
Abstract: Compositions comprising proanthocyanidin compositions (e.g. those extracted from cinnamomum species) that are observed to bind tau and inhibit its aggregation as well as methods for making and
using such compositions are disclosed. In certain embodiments of the invention, the proanthocyanidins can be used as a probe to identify and/or characterize tau isoforms in a variety of contexts. In other embodiments of the invention, these compositions are used in methods designed to treat neurological disorders associated with tau aggregation (e.g. Alzheimer's disease).
Pub. No.: WO/2008/121412 International Application No.: PCT/US2008/004236
Publication Date: 09.10.2008 International Filing Date: 31.03.2008
IPC: A61K 36/54 (2006.01)
Applicants: THE REGENTS OF THE UNIVERSITY OF CALIFORNIA [US/US]; 1111
Franklin Street, 12th Floor, Oakland, CA 94607 (US) (All Except US).
LEW, John [CA/US]; (US) (US Only).
GRAVES, Donald, J. [US/US]; (US) (US Only).
Inventors: LEW, John; (US).
GRAVES, Donald, J.; (US).
http://www.wipo.int/pctdb/en/
http://www.wipo.int/pctdb/en/
Cinnamon Extract Inhibits Tau Aggregation Associated with Alzheimer's Disease In Vitro
Journal Journal of Alzheimer's Disease
Publisher IOS Press
ISSN 1387-2877 (Print) 1875-8908 (Online)
Issue Volume 17, Number 3 / 2009
DOI 10.3233/JAD-2009-1083
Pages 585-597
Subject Group Neurosciences
Authors
Dylan W. Peterson1, Roshni C. George1, Francesca Scaramozzino1, Nichole E. LaPointe1, Richard A. Anderson2, Donald J. Graves1, John Lew1
1Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, CA, USA
2Beltsville Human Nutrition Center, Beltsville, MD, USA
Abstract
An aqueous extract of Ceylon cinnamon (C. zeylanicum) is found to inhibit tau aggregation and filament formation, hallmarks of Alzheimer's disease (AD). The extract can also promote complete disassembly of recombinant tau filaments and cause substantial alteration of the morphology of paired-helical filaments isolated from AD brain. Cinnamon extract (CE) was not deleterious to the normal cellular function of tau, namely the assembly of free tubulin into microtubules. An A-linked proanthocyanidin trimer molecule was purified from the extract and shown to contain a significant proportion of the inhibitory activity. Treatment with polyvinylpyrolidone effectively depleted all proanthocyanidins from the extract solution and removed the majority, but not all, of the inhibitory activity. The remainder inhibitory activity could be attributed to cinnamaldehyde. This work shows that compounds endogenous to cinnamon may be beneficial to AD themselves or may guide the discovery of other potential therapeutics if their mechanisms of action can be discerned.
http://iospress.metapress.com/
http://www.ncbi.nlm.nih.gov/
Research Project: CHROMIUM AND POLYPHENOLS FROM CINNAMON IN THE PREVENTION AND ALLEVIATION OF GLUCOSE INTOLERANCE
Location: Diet, Genomics and Immunology Lab
Title: Polyphenols, Insulin Sensitivity, and the Brain
Authors
item Anderson, Richard
item Panickar, Kiran
Submitted to: Meeting Abstract
Publication Type: Abstract
Publication Acceptance Date: June 1, 2009
Publication Date: N/A
Technical Abstract: We have isolated water-soluble polyphenols found in cinnamon that are multifunctional and improve insulin sensitivity, glucose uptake, and have antioxidant and anti-inflammatory properties in experimental animals and humans. These compounds may also be potentially neuroprotective as oxidative stress, abnormalities in glucose utilization, and inflammation, are also all implicated in neurological disorders. Abnormalities in insulin signaling in the brain can contribute to Alzheimer¿s disease (AD) and AD has recently been called ¿type 3 diabetes¿ due to the observation that abnormalities in insulin signaling in the brain associated with AD are similar to those observed in insulin sensitive tissues of people with type 2 diabetes. Neuropathologically, AD is characterized by the deposition of extracellular plaques, composed principally of amyloid ß protein, and intracellularly of neurofibrillary tangles, generally associated with hyperphosphorylated tau. Polyphenols from cinnamon inhibit both tau aggregation and amyloid ß filament formation. Oxidative stress and mitochondrial dysfunction are key events implicated in both neuronal and astrocytic dysfunction/death and cinnamon and tea polyphenols, as well as insulin, protect neuronal death in cultures from Aß toxicity. Mitochondrial dysfunction in neurons from Aß toxicity is also protected by these polyphenols. Ischemic stroke is caused by an interruption of cerebral blood flow, which can lead to vascular leakage, inflammation, tissue injury, and necrosis. Polyphenols from cinnamon and tea have neuroprotective effects in PC12 neuronal cells subjected to oxygen-glucose deprivation. One neuroprotective mechanism of such polyphenols may be due to their effects on improving mitochondrial membrane potential/mitochondrial function. Glial swelling, a key feature of cytotoxic edema, due to oxygen-glucose deprivation, is also prevented by cinnamon and tea polyphenols in C6 glial cells. In addition, green tea epigallocatechin-3-gallate improves insulin sensitivity, reduces beta-amyloid levels and plaques and delays memory regression in mice. In summary, in vitro studies demonstrate that cinnamon and tea polyphenols not only improve insulin sensitivity but also protect neuronal and glial cells from ischemic injury and amyloid ß toxicity. Animal studies demonstrate that tea polyphenols reverse or alleviate signs and symptoms of Alzheimer¿s disease and premature losses in memory regression. Human studies demonstrate that increased intake of cinnamon and tea polyphenols leads to improved insulin sensitivity and related pathologies associated with aging.
Project Team
Anderson, Richard
Urban, Joseph
Schoene, Norberta
http://www.ars.usda.gov/
Grape Seed Extract
A post appeared about this on the Yahoo "PSPinformatin" discussion group in late June of 2009:
I did a quick search with Google. This is all I came up with, but I probably
missed something:
Grape Seed Polyphenolic Extract as a Potential Novel Therapeutic Agent in Tauopathies
Journal Journal of Alzheimer's Disease
Publisher IOS Press
ISSN 1387-2877 (Print) 1875-8908 (Online)
Issue Volume 16, Number 2 / 2009
Pages 433-439
Abstract: "Abnormal misfoldings of the microtubule-associated protein tau, leading to the aggregation of tau into paired helical filaments that are ultimately deposited as neurofibrillary tangles, is a key neuropathologic feature of a number of neurodegenerative disorders collectively referred to as tauopathies. We recently observed that a particular grape seed polyphenolic extract (GSPE), namely, Meganatural-Az® may attenuate the generation and stability of misfolded proteins. We hypothesized that Meganatural-Az® GSPE might also attenuate tau protein misfolding that leads to the generation of tau filamentary aggregates that are critical for the initiation and progression of neurodegeneration and/or cognitive dysfunctions in tauopathies. In this study, we used in vitro aggregations of synthetic Ac-^{306}VQIVYK^{311} tau peptide as a model system to explore whether Meganatural-Az® GSPE might modulate aggregations of tau protein. We demonstrate that this GSPE is capable of inhibiting tau peptide aggregations, as well as dissociating preformed tau peptide aggregates. Results from this study suggest that this GSPE might provide beneficial disease-modifying bioactivities in tau-associated neurodegenerative disorders by modulating tau-mediated neuropathologic mechanisms. Our observation, in conjunction with the emonstrated bioavailability, as well as safety and tolerability, of this GSPE, supports the development of Meganatural-Az® GSPE for the prevention and/or treatment of tau-associated
neurodegenerative disorders."
http://iospress.metapress.com/
--- In pspinformation@yahoogroups.com
>
> Aletta, My nephew, a research doctor attended a seminar about psp. He had heard of the disease, but took more interest in it when my husband was diagnosed with it. He said that grape seed extract given to mice and rats in the laboratory reversed the symtoms in psp. It did not cure it, but the lab animals were able to function again with less help. However, the extract has not been tested in humans. He suggested to me that my husband take six pills a day, 2 each morning, noon and night. He said the pills would not hurt him as they are just grape seed extract, and it would take months to see a difference, if any. Since we are both home bound I put him on the extract so now, its a wait and see situation. The extract can be purchased at Sam's club, costco, bj's etc. very cheaply. Time will tell.
Epigallocatechin gallate (EGCG, Green Tea Extract)
Epigallocatechin gallate (EGCG) is a type of catechin and is the most abundant catechin in tea.
http://en.wikipedia.org/wiki/
Antioxidant in Green Tea May Fight Alzheimer's
Ingredient May Prevent Buildup of Plaque in Brain Linked to Alzheimer's Disease
http://www.webmd.com/
Reduction of iron-regulated amyloid precursor protein and beta-amyloid peptide by (-)-epigallocatechin-3-gallate in cell cultures: implications for iron chelation in Alzheimer's disease
J Neurochem. 2006 Apr;97(2):527-36. Epub 2006 Mar 15.
"Thus, the natural non-toxic brain-permeable EGCG may provide a potential therapeutic approach for AD and other iron-associated disorders."
http://www.ncbi.nlm.nih.gov/
A Fortune in Tea Leaves—Extract Blocks Amyloid Formation
"31 May 2008. Fortune telling aside, green tea has been touted as a potential cure for a myriad of conditions, including cancer and neurodegenerative diseases such as Alzheimer and Parkinson diseases. Scientific evidence that the brew might work has just become stronger. In yesterday’s Nature Structural & Molecular Biology, researchers in Germany report that (-)-epigallocatechin gallate (EGCG), a polyphenol found in green tea, prevents both amyloid-β (Aβ) and α-synuclein from forming toxic oligomers. The work suggests that EGCG works as a generic inhibitor of amyloids, making it a potential lead for treatments of not only AD and PD but perhaps any amyloidosis."
http://www.alzforum.org/new/
Green Tea Chemical Combined With Another May Hold Promise for Treatment of Brain Disorders
ScienceDaily (Dec. 6, 2009)
Scientists at Boston Biomedical Research Institute (BBRI) and the University of Pennsylvania have found that combining two chemicals, one of which is the green tea component EGCG, can prevent and destroy a variety of protein structures known as amyloids. Amyloids are the primary culprits in fatal brain disorders such as Alzheimer's, Huntington's, and Parkinson's diseases. Their study, published in the current issue of Nature Chemical Biology (December 2009), may ultimately contribute to future therapies for these diseases... The team then exposed the yeast amyloid structures to a combination of the EGCG and the DAPH-12 and found that all of the amyloid structures broke apart and dissolved...
http://www.sciencedaily.com/
This article isn't about any neurodegenerative disease, but I thought it would be of interest to the women out there, and to the rest of us who want to keep our women around a bit longer...
Spices Halt Growth of Breast Stem Cells, Study Finds
ScienceDaily (Dec. 8, 2009) — A new study finds that compounds derived from the spices turmeric and pepper could help prevent breast cancer by limiting the growth of stem cells, the small number of cells that fuel a tumor's growth... Researchers at the University of Michigan Comprehensive Cancer Center have found that when the dietary compounds curcumin, which is derived from the Indian spice turmeric, and piperine, derived from black peppers, were applied to breast cells in culture, they decreased the number of stem cells while having no effect on normal differentiated cells... Cancer stem cells are the small number of cells within a tumor that fuel the tumor's growth. Current chemotherapies do not work against these cells, which is why cancer recurs and spreads. Researchers believe that eliminating the cancer stem cells is key to controlling cancer. In addition, decreasing the number of normal stem cells -- unspecialized cells that can give rise to any type of cell in that organ -- can decrease the risk of cancer... In this study, a solution of curcumin and piperine was applied to the cell cultures at the equivalent of about 20 times the potency of what could be consumed through diet. The compounds are available at this potency in a capsule form that could be taken by mouth...
http://www.sciencedaily.com/
I know, I know... this is only preliminary data about a test done in a test tube, but we can dream, can't we?
This is but a small part of what there is to discover. Keep searching. Perhaps together we can find the answer.
Merry Christmas!
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Updated: December 22,
2009
Inception: November 27, 2009