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"Give with a free hand, but give only your own."
-- J.R.R. Tolkien The Children of Hurin
- Alzheimer's Disease -
General Information:
Names:
Wikipedia entry:
Dr. Ray Shahelien entry:
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Observations:
General Information:
"People with Alzheimer's disease have abnormal clumps (amyloid
plaques) and tangled bundles of fibers (neurofibrillary
tangles) in their brains. Nerve cells are lost in areas of the
brain that are vital to memory and other mental abilities.
There also are lower levels of chemicals in the brain that
carry complex messages back and forth between nerve cells
(neurotransmitters). Alzheimers may disrupt normal thinking
and memory by blocking messages between nerve cells."
[Typical "official" introduction]
[Not necessarily so. See Dr. Mirkin & Dr. McDougall
and the "Kentucky Nuns Study"]
http://www.connecticutcenterforhealth.com/alzheimers.html
"There is a tragedy looming within Australia's ageing
population. As more and more Australians join the ranks of the
elderly, more and more will be affected by the burden of
dementia... personally and through connections with loved ones.
This is the story of a maverick Australian scientist whose
theory about Alzheimer's has led to a breakthrough in
understanding and a potential new treatment for the disease."
http://www.abc.net.au/catalyst/stories/s1134238.htm
[Interesting info from someone calling herself "Moondragon"
- AD intro [typical of intros]
"Other disorders can cause symptoms similar to those of
Alzheimer's disease. Dementia may result from arteriosclerosis
(hardening of the arteries) that slowly cuts off the supply of
blood to the brain. The death of brain tissue from a series of
minor strokes, or from pressure exerted by an accumulation of
fluid in the brain, may cause damage. The presence of small
blood clots in vessels that supply the brain, a brain tumor,
hypothyroidism, and advanced syphilis can all cause symptoms
similar to those of Alzheimer's."
-Some interesting speculation as to nutritional and toxic causes
-Aluminum
-Zinc deficinency
-Mercury
-Immune response
[With regard to AD being the result of an immune response, could
it be that the statin drugs, which are known to also reduce
inflamation are supressing some sort of response by the immune
system, and that is why they show positive effects on AD?]
http://www.moondragon.org/health/disorders/alzheimers.html
Are You at Risk of Alzheimer's?
"Alzheimer’s disease begins to damage the brain years before
symptoms appear. Why pathological changes occur in the brain
leading to such profound damage is not clear. Risk factors are
things that increase your chances of developing Alzheimer's
disease. Some are preventable, such as exercise, some not, for
example genetic factors and age."
"Lets look at some risk factors for Alzheimer's disease..."
[Typical AD info. Not sure if it represents the latest
ideas.]
http://alzheimers.about.com/od/diagnosisissues/a/alz_risk_factor.htm
Misdiagnosis of Alzheimer's Disease
"Because AD is so well-known, it is sometimes an over-diagnosed
condition. Other causes of dementia or memory loss symptoms may
be overlooked. Other possible diagnoses include normal aging (if
very mild symptoms), emotional
problems (such as grief), fatigue, depression, and certain
physical medical conditions such as thyroid disease, brain
tumors, multi-infarct disease, or Huntington's disease. In its
early stages, a correct diagnosis of AD can also be overlooked
itself and misdiagnosed as other conditions such as depression,
dementia, simple forgetfulness, or senility."
http://www.wrongdiagnosis.com/a/alzheimers_disease/misdiag.htm
What are the risk factors for dementia?
While there is still much to learn about the brain, researchers
have highlighted some important factors that affect our risk of
developing different types of dementia. Most researchers now
believe that our risk of developing dementia depends upon a
combination of genetic and environmental factors. We are all at
some risk of developing dementia, but
some of us more than others. A person who has some of the risk
factors for dementia will not necessarily go on to develop the
condition. And avoiding risk factors does not guarantee that you
will be healthy, although it makes this more likely.
http://www.alzheimers.org.uk/Facts_about_dementia/Risk_factors/info_amIatrisk.htm
Is it Alzheimer's disease or something else?
10 disorders that may feature impaired memory and cognition
Anna M. Barrett, MD
VOL 117 / NO 5 / MAY 2005 / POSTGRADUATE MEDICINE
http://www.postgradmed.com/issues/2005/05_05/barrett.htm
Alzheimer's Disease Treatment &
Prevention:
See also...
COGNIShunt
Desferrioxamine & Deferasirox
EDTA
Herbs
Iron
McDougall
Mirkin
Can Alzheimer's Disease and
Vascular Dementia be Prevented?
"There are various levels of evidence which might show that
dementia can be postponed."
NOTE: This is an Adobe Acrobat "PDF" file
http://www.alzheimers.org.au/upload/Update%20Sheet%20-%20Prevention%20Sept%202004.pdf
Live Discussion: Does Blocking Metal-Aβ Interactions Work?
http://www.alzforum.org/res/for/journal/bush/bush_transcript.asp
[Interesting results from an Altavista search on "alzheimer's
disease" "halt progression".]
http://www.altavista.com/web/results?itag=ody&q=%22alzheimer%27s+disease%22+%22halt+the+progression%22&kgs=1&kls=0
Red Wine May Help Prevent Alzheimer's
By LiveScience Staff
"A new study finds that moderate red wine consumption,
specifically Cabernet Sauvignon, might help reduce the incidence
of Alzheimer's disease.
"Previous Alzheimer's research has indicated similar potential
benefits of red wine.
"The new research, done only on mice, will be detailed in the
November 2006 issue of the FASEB Journal and will be presented
at the Society for Neuroscience Meeting next month in Atlanta.
""This study supports epidemiological evidence indicating that
moderate wine consumption, within the range recommended by the
FDA dietary guidelines of one drink per day for women and two
for men, may help reduce the relative risk for AD [Alzheimer's
disease] clinical dementia," write Giulio Maria Pasinetti and
Jun Wang of the Mount Sinai School of Medicine."
http://www.livescience.com/humanbiology/060928_red_wine.html
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Known sources:
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Natural sources:
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References:
G101 ALZHEIMER'S DISEASE
Gabe Mirkin, M.D.
"The most common cause of senility in North America is
Alzheimer's disease, a horrible condition in which a person
loses his capacity to reason, think, recognize and function. A
study in the New England Journal of Medicine shows that people
who have high blood levels of a protein called homocysteine are
the ones most likely to suffer Alzheimer's disease(1)."
http://www.drmirkin.com/morehealth/G101.htm
AD Cause Speculation:
[Beta]-Amyloid protein
oligomers induced by metal ions and acid pH are distinct from
those generated by slow spontaneous ageing at neutral pH
"Amyloid protein (A1–40) aggregation and conformation was
examined using native and sodium dodecyl sulfate/polyacrylamide
gel electrophoresis, and the results compared with those
obtained by atomic force microscopy, and with Congo red binding,
sedimentation and turbidity assays. The amount of A aggregation
measured was different, depending upon the method used.
Incubation for 15 min at pH 5.0 or in the presence of Fe2+, Cu2+
or Zn2+ did not alter the level of A oligomers observed on SDS
and native gels. However, the slow aggregation of A to form high
molecular mass species over 5 days was inhibited. In contrast,
when A aggregation was monitored using a Congo red binding assay
or sedimentation assay, a rapid increase in A aggregation was
observed after incubation for 15 min at pH 5.0, or in the
presence of Fe2+, Cu2+ or Zn2+. The low pH-, Zn2+- or
Cu2+-induced A aggregation measured in a turbidity assay was
reversible. In contrast, a considerable proportion of the A
aggregation measured by native and SDS/PAGE was stable. Atomic
force microscopy studies showed that A aged at pH 5.0 or in the
presence of Zn2+ produced larger looser rod-shaped aggregates
than at pH 7.4. A that had been aged at pH 7.4 was more
cytotoxic than A aged at pH 5.0. Taken together, the results
suggest that A oligomerizes via two mutually exclusive
mechanisms to form two different types of aggregates, which
differ in their cytotoxic properties."
http://content.febsjournal.org/cgi/content/full/270/21/4282
CURRENT HYPOTHESES
"We list here a collection of special seminars, on-line journal
club discussions, recorded talks and other presentations on the
Forum web site that describe a variety of scientific hypotheses
about the pathogenesis of Alzheimer's disease."
http://www.alzforum.org/res/adh/cur/default.asp
See also Globulomer
AD Research:
See
also Globulomer
Researchers Identify Brain Protein That Halts Progression Of
Alzheimer's
"Researchers have identified a protein in the brain that halts
the progression of Alzheimer's disease in human brain tissue.
The protein, known as "transthyretin," protects brain cells from
gradual deterioration by blocking another toxic protein that
contributes to the disease process."
http://www.sciencedaily.com/releases/2004/10/041025131754.htm
Phenserine Shows Potential To Slow Or Stop Progression Of
Alzheimer's Disease
"April 4, 2002 - Results reported in an abstract on the
transgenic mouse confirmed that Phenserine, a third generation
acetylcholinesterase inhibitor (AChE-inhibitor), has the ability
to reduce both amyloid precursor protein (APP) and amyloid
peptide (amyloid-beta) formation in the brain which could have
important potential implications for the treatment of
Alzheimer's Disease (AD)."
http://www.seniorjournal.com/NEWS/Alzheimers/04-08-02Phenserine.htm
Protein 'Pump' May Aid in Alzheimer's Prevention
By Steven Reinberg
HealthDay Reporter
THURSDAY, Oct. 20 (HealthDay News) -- A protein well known to
scientists appears to clear the brain of amyloid beta, the main
component of the plaques that are found in Alzheimer's patients,
according to a new study with mice.
The protein, P-glycoprotein (Pgp), has long been known to
obstruct chemotherapy drugs and other drugs used in treating
brain disorders. But, by creating drugs that alter the natural
levels of Pgp, it may be possible to prevent and treat
Alzheimer's disease, the researchers suggest.
http://news.healingwell.com/index.php?p=news1&id=528648
Protein 'Pump' May Aid in Alzheimer's Prevention
In study with mice, it removed dangerous plaques from the
brain.
By Steven Reinberg
THURSDAY, Oct. 20 (HealthDay News) -- A protein well known to
scientists appears to clear the brain of amyloid beta, the main
component of the plaques that are found in Alzheimer's patients,
according to a new study with mice.
The protein, P-glycoprotein (Pgp), has long been known to
obstruct chemotherapy drugs and other drugs used in treating
brain disorders. But, by creating drugs that alter the natural
levels of Pgp, it may be possible to prevent and treat
Alzheimer's disease, the researchers suggest.
"We found a new way of getting amyloid out of the brain," said
lead author John Cirrito, a postdoctorate research fellow at
Washington University School of Medicine in St. Louis. "Now
there are avenues we can explore to try to find a treatment.
Anything you can do to prevent amyloid beta from being produced
or helping get it cleared is good."
http://www.healthfinder.gov/news/newsstory.asp?docID=528648
Alzheimer's
Plaques in PET Brain Scans Identify Future Cognitive Decline
ScienceDaily (July 11, 2012)
http://www.sciencedaily.com/releases/2012/07/120711210100.htm
http://www.dukehealth.org/health_library/news/alzheimers-plaques-in-pet-brain-scans-identify-future-cognitive-decline
[Could be used to test the effectiveness of drugs in clearing or
preventing AB.]
Amyloid-β assessed by
florbetapir F 18 PET and 18-month cognitive decline: A
multicenter study.
Doraiswamy PM, Sperling RA, Coleman RE, Johnson KA, Reiman EM,
Davis MD, Grundman M, Sabbagh MN, Sadowsky CH, Fleisher AS,
Carpenter A, Clark CM, Joshi AD, Mintun MA, Skovronsky DM,
Pontecorvo MJ; For the AV45-A11 Study Group.
Neurology. 2012 Jul 11. [Epub ahead of print]
Source: From the Duke University Medical Center (P.M.D.,
R.E.C.), Durham, NC; Massachusetts General Hospital (R.A.S.,
K.A.J.), Harvard Medical School, Boston; Banner Alzheimer's
Institute (E.M.R., A.S.F.), Phoenix, AZ; University of
Pennsylvania (M.D.D.), Philadelphia; Theorem Clinical Research
(M.D.D.), King of Prussia, PA; Global R&D Partners (M.G.),
San Diego, CA; University of California (M.G., A.S.F.), San
Diego; Banner-Sun Health Research Institute (M.N.S.), Sun City,
AZ; Nova SE University (C.H.S.), Ft. Lauderdale, FL; and Avid
Radiopharmaceuticals (A.C., C.M.C., A.D.J., M.A.M., D.M.S.,
M.J.P.), Philadelphia, PA.
Abstract
OBJECTIVES:
Florbetapir F 18 PET can image amyloid-β (Aβ) aggregates in the
brains of living subjects. We prospectively evaluated the
prognostic utility of detecting Aβ pathology using florbetapir
PET in subjects at risk for progressive cognitive decline.
METHODS:
A total of 151 subjects who previously participated in a
multicenter florbetapir PET imaging study were recruited for
longitudinal assessment. Subjects included 51 with recently
diagnosed mild cognitive impairment (MCI), 69 cognitively normal
controls (CN), and 31 with clinically diagnosed Alzheimer
disease dementia (AD). PET images were visually scored as
positive (Aβ+) or negative (Aβ-) for pathologic levels of
β-amyloid aggregation, blind to diagnostic classification.
Cerebral to cerebellar standardized uptake value ratios (SUVr)
were determined from the baseline PET images. Subjects were
followed for 18 months to evaluate changes in cognition and
diagnostic status. Analysis of covariance and correlation
analyses were conducted to evaluate the association between
baseline PET amyloid status and subsequent cognitive decline.
RESULTS:
In both MCI and CN, baseline Aβ+ scans were associated with
greater clinical worsening on the Alzheimer's Disease Assessment
Scale-Cognitive subscale (ADAS-Cog (p < 0.01) and Clinical
Dementia Rating-sum of boxes (CDR-SB) (p < 0.02). In MCI Aβ+
scans were also associated with greater decline in memory, Digit
Symbol Substitution (DSS), and Mini-Mental State Examination
(MMSE) (p < 0.05). In MCI, higher baseline SUVr similarly
correlated with greater subsequent decline on the ADAS-Cog (p
< 0.01), CDR-SB (p < 0.03), a memory measure, DSS, and
MMSE (p < 0.05). Aβ+ MCI tended to convert to AD dementia at
a higher rate than Aβ- subjects (p < 0.10).
CONCLUSIONS:
Florbetapir PET may help identify individuals at increased risk
for progressive cognitive decline.
PMID: 22786606 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/22786606
Timeline Maps Brain's Descent
Into Alzheimer's
ScienceDaily (July 11, 2012)
http://www.sciencedaily.com/releases/2012/07/120711205859.htm
http://news.wustl.edu/news/Pages/24026.aspx
Clinical and Biomarker Changes
in Dominantly Inherited Alzheimer's Disease.
Bateman RJ, Xiong C, Benzinger TL, Fagan AM, Goate A, Fox NC,
Marcus DS, Cairns NJ, Xie X, Blazey TM, Holtzman DM, Santacruz
A, Buckles V, Oliver A, Moulder K, Aisen PS, Ghetti B, Klunk WE,
McDade E, Martins RN, Masters CL, Mayeux R, Ringman JM, Rossor
MN, Schofield PR, Sperling RA, Salloway S, Morris JC; the
Dominantly Inherited Alzheimer Network.
N Engl J Med. 2012 Jul 11. [Epub ahead of print]
Source: The authors' affiliations are listed in the Appendix.
Abstract
Background The order and magnitude of pathologic processes in
Alzheimer's disease are not well understood, partly because the
disease develops over many years. Autosomal dominant Alzheimer's
disease has a predictable age at onset and provides an
opportunity to determine the sequence and magnitude of
pathologic changes that culminate in symptomatic disease.
Methods In this prospective, longitudinal study, we analyzed
data from 128 participants who underwent baseline clinical and
cognitive assessments, brain imaging, and cerebrospinal fluid
(CSF) and blood tests. We used the participant's age at baseline
assessment and the parent's age at the onset of symptoms of
Alzheimer's disease to calculate the estimated years from
expected symptom onset (age of the participant minus parent's
age at symptom onset). We conducted cross-sectional analyses of
baseline data in relation to estimated years from expected
symptom onset in order to determine the relative order and
magnitude of pathophysiological changes. Results Concentrations
of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years
before expected symptom onset. Aβ deposition, as measured by
positron-emission tomography with the use of Pittsburgh compound
B, was detected 15 years before expected symptom onset.
Increased concentrations of tau protein in the CSF and an
increase in brain atrophy were detected 15 years before expected
symptom onset. Cerebral hypometabolism and impaired episodic
memory were observed 10 years before expected symptom onset.
Global cognitive impairment, as measured by the Mini-Mental
State Examination and the Clinical Dementia Rating scale, was
detected 5 years before expected symptom onset, and patients met
diagnostic criteria for dementia at an average of 3 years after
expected symptom onset. Conclusions We found that autosomal
dominant Alzheimer's disease was associated with a series of
pathophysiological changes over decades in CSF biochemical
markers of Alzheimer's disease, brain amyloid deposition, and
brain metabolism as well as progressive cognitive impairment.
Our results require confirmation with the use of longitudinal
data and may not apply to patients with sporadic Alzheimer's
disease. (Funded by the National Institute on Aging and others;
DIAN ClinicalTrials.gov number, NCT00869817 .).
PMID: 22784036 [PubMed]
http://www.ncbi.nlm.nih.gov/pubmed/22784036
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Preface Brain Failure Notes Notes II
References pg. 1 References pg. 2
Nutritional Alternatives
Patricia's Protocol
Tauopathy
Discussion
Forum
Correspondence Newsletters Poems Memory Enhancement
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Updated: July 2, 2012
Inception: July 2, 2012