"Give with a free hand, but give only your own."
 -- J.R.R. Tolkien The Children of Hurin
- Amyloid Beta -

General Information:

Wikipedia entry: 


See also Curcumin
         Apple Juice
         EGCG (Green Tea Extract)

There has been some discussion that perhaps amyloid beta proteins are not a step in the process of Alzheimer's disease, but rather a symptom.  This would explain the rather disappointing results from drug trials for medications that target amyloid beta plaques.

Alzheimer's Memory Problems Originate With Protein Clumps Floating in the Brain, Not Amyloid Plaques

ScienceDaily (Apr. 28, 2010) — Using a new mouse model of Alzheimer's disease, researchers at Mount Sinai School of Medicine have found that Alzheimer's pathology originates in amyloid-beta (Abeta) oligomers in the brain, rather than the amyloid plaques previously thought by many researchers to cause the disease...

Cold Sore Virus Linked To Alzheimer's Disease: New Treatment, Or Even Vaccine Possible
ScienceDaily (Dec. 7, 2008)

"Professor Itzhaki explains: "We suggest that HSV1 enters the brain in the elderly as their immune systems decline and then establishes a dormant infection from which it is repeatedly activated by events such as stress, immunosuppression, and various infections."

"The ensuing active HSV1 infection causes severe damage in brain cells, most of which die and then disintegrate, thereby releasing amyloid aggregates which develop into amyloid plaques after other components of dying cells are deposited on them."

"Her colleague Dr Matthew Wozniak adds: "Antiviral agents would inhibit the harmful consequences of HSV1 action; in other words, inhibit a likely major cause of the disease irrespective of the actual damaging processes involved, whereas current treatments at best merely inhibit some of the symptoms of the disease..."

"They believe the herpes simplex virus is a significant factor in developing the debilitating disease and could be treated by antiviral agents such as acyclovir, which is already used to treat cold sores and other diseases caused by the herpes virus."

New Evidence Found Linking Herpes And Alzheimer’s
ScienceDaily (May 12, 2000)
"Could Lead to New Treatments Targeting the Herpes Virus"

"Researchers have long suspected a connection between the herpes virus and Alzheimer’s disease. A new study provides a potential explanation that could lead to development of a vaccine to prevent the disease or new drugs to treat it, according to the researchers. The study appears in the May 16 issue of Biochemistry, a peer-reviewed publication of the American Chemical Society, the world’s largest scientific society."

"Researchers at the University of California, Irvine, demonstrated that a synthetic protein that resembles the herpes simplex 1 virus (HSV-1) mimics the structure and function of a protein called beta-amyloid, a toxic agent that accumulates in the brains of Alzheimer’s patients."

"Genetic sequencing revealed that two-thirds of a portion of the viral protein is identical to the beta-amyloid protein. The researchers showed that, like beta-amyloid, it could kill brain neurons, a key feature in the development of Alzheimer’s. Moreover, in laboratory experiments, the viral protein formed abnormal twisted fibers like those found in the brains of Alzheimer’s patients — the definitive hallmark of the disease..."

The Alzheimer's Disease-Associated Amyloid β-Protein Is an Antimicrobial Peptide
Soscia, Kirby, Washicosky, Tucker, Ingelsson, Hyman, Burton, Goldstein, Duong, Tanzi, Moir
March 3, 2010



The amyloid β-protein (Aβ) is believed to be the key mediator of Alzheimer's disease (AD) pathology. Aβ is most often characterized as an incidental catabolic byproduct that lacks a normal physiological role. However, Aβ has been shown to be a specific ligand for a number of different receptors and other molecules, transported by complex trafficking pathways, modulated in response to a variety of environmental stressors, and able to induce pro-inflammatory activities.

Methodology/Principal Findings

Here, we provide data supporting an in vivo function for Aβ as an antimicrobial peptide (AMP). Experiments used established in vitro assays to compare antimicrobial activities of Aβ and LL-37, an archetypical human AMP. Findings reveal that Aβ exerts antimicrobial activity against eight common and clinically relevant microorganisms with a potency equivalent to, and in some cases greater than, LL-37. Furthermore, we show that AD whole brain homogenates have significantly higher antimicrobial activity than aged matched non-AD samples and that AMP action correlates with tissue Aβ levels. Consistent with Aβ-mediated activity, the increased antimicrobial action was ablated by immunodepletion of AD brain homogenates with anti-Aβ antibodies.


Our findings suggest Aβ is a hitherto unrecognized AMP that may normally function in the innate immune system. This finding stands in stark contrast to current models of Aβ-mediated pathology and has important implications for ongoing and future AD treatment strategies.

Soscia "The Alzheimer’s Disease-Associated Amyloid b-Protein Is an Antimicrobial Peptide" PLOS March 2010,Volume 5, Issue 3, e9505: www.plosone.org

The Amyloid Question
Chemical & Engineering News Volume 88, Number 14 pp. 12 - 17
April 5, 2010
Lisa M. Jarvis

...The worry among some experts is that the development of amyloid-β-targeting compounds by Pfizer, Elan Pharmaceuticals, Eli Lilly & Co., Bristol-Myers Squibb, and others began long before the underlying biology of the peptide was well understood. New research suggests that amyloid-β may also play a beneficial role in the brain, whereas other studies claim the peptide is overproduced only after another neurotoxin does its dirty work. With nearly every drug in the pipeline targeting some aspect of the amyloid-β pathway, some Alzheimer’s researchers are concerned that industry has placed all its eggs in one fragile basket... Currently, patients’ only treatment options are drugs that dampen the symptoms of the disease. Pfizer’s Aricept keeps acetylcholinesterase from breaking down the neurotransmitter acetylcholine, maximizing the amount available to carry messages, and Forest Laboratories’ Namenda blocks a glutamate receptor thought to play a role in learning and memory...

Researchers Discover Weak Link in Alzheimer’s Drug Candidates
April 2nd, 2010

...Some current therapies being investigated for Alzheimer's disease may cause further neural degeneration and cell death, according to a breakthrough discovery by UC San Diego researchers. By combining three dimensional computer simulations with high resolution atomic force microscopy membrane protein and cell imaging, electrical recording and various cellular assays, UCSD nano-biophysicist Ratnesh Lal and his colleagues investigated the structure and function of truncated peptides, known as nonamyloidgenic peptides, formed by some Alzheimer's drug candidates...

The research paper:

Truncated β-amyloid peptide channels provide an alternative mechanism for Alzheimer’s Disease and Down syndrome
February 16, 2010

...The toxicity of nonamyloidogenic peptides via an ion channel mechanism necessitates a reevaluation of the current therapeutic approaches targeting the nonamyloidogenic pathway as avenue for AD treatment...

Alzheimer's drugs cause brain damage and actually worsen memory loss
April 21, 2010

...Big Pharma drugs that are being used on humans right now and promoted as potential treatments for Alzheimer's disease (AD) could cause the very brain damage and memory loss they are supposed to treat. That's the conclusion of University of California at San Diego (UCSD) scientists who just published their groundbreaking findings in the Proceedings of the National Academy of Sciences...

Insights Give Hope for New Attack on Alzheimer’s
December 13, 2010
...It turns out that most people with Alzheimer’s seem to make perfectly normal amounts of amyloid. They just can’t get rid of it. It’s like an overflowing sink caused by a clogged drain instead of a faucet that does not turn off...

The medical device CogniShunt was conceived as a way to drain CFS (cerebral-spinal fluid) in the hopes that this would lower the amyloid beta protein levels in the brain.

Alzheimer's Plaques Lead to Loss of Nitric Oxide in Brain

ScienceDaily (Jan. 17, 2011)... Levels of nitric oxide (NO) -- a signaling molecule that helps regulate blood flow, immune and neurological processes -- are known to be low in the brains of people who have Alzheimer's disease, but the reason for that hasn't been clear, said study co-author Jeffrey S. Isenberg, M.D., M.P.H., associate professor, Division of Pulmonary, Allergy, and Critical Care Medicine, Pitt School of Medicine.

"Our research sheds light on how that loss of NO might happen, and reveals biochemical pathways that drug discoverers might be able to exploit to find new medicines for Alzheimer's. There is evidence that suggests enhancing NO levels can protect neurons from degenerating and dying."...

An Alzheimer's Vaccine in a Nasal Spray?

ScienceDaily (Feb. 28, 2011)
...researchers led by Dr. Dan Frenkel of Tel Aviv University's Department of Neurobiology at the George S. Wise Faculty of Life Sciences are working on a nasally-delivered 2-in-1 vaccine that promises to protect against both Alzheimer's and stroke. The new vaccine repairs vascular damage in the brain by rounding up "troops" from the body's own immune system...

Alzheimer's-Like Brain Changes Found in Cognitively Normal Elders With Amyloid Plaques

ScienceDaily (Mar. 30, 2011) — Researchers using two brain-imaging technologies have found that apparently normal older individuals with brain deposits of amyloid beta -- the primary constituent of the plaques found in the brains of Alzheimer's disease patients -- also had changes in brain structure similar to those seen in Alzheimer's patients...

Reference: J. Alex Becker, Trey Hedden, Jeremy Carmasin, Jacqueline Maye, Dorene M. Rentz, Deepti Putcha, Bruce Fischl, Douglas N. Greve, Gad A. Marshall, Stephen Salloway, Donald Marks, Randy L. Buckner, Reisa A. Sperling, Keith A. Johnson. Amyloid-β associated cortical thinning in clinically normal elderly. Annals of Neurology, 2011

New findings contradict dominant theory in Alzheimer’s disease
28 October 2011
For decades the amyloid hypothesis has dominated the research field in Alzheimer’s disease. The theory describes how an increase in secreted beta-amyloid peptides leads to the formation of plaques, toxic clusters of damaged proteins between cells, which eventually result in neurodegeneration. Scientists at Lund University, Sweden, have now presented a study that turns this premise on its head. The research group’s data offers an opposite hypothesis, suggesting that it is in fact the neurons’ inability to secrete beta-amyloid that is at the heart of pathogenesis in Alzheimer’s disease...

Clearance of beta amyloid accumulation within neurons stops memory decline
the UCI research team is the first to identify that early beta amyloid accumulation within neurons is the trigger for the onset of memory decline in Alzheimer's.
"This finding has important and useful implications for the pharmaceutical industry in terms of developing drugs that can target beta amyloid as soon as it accumulates within the neurons," said Frank LaFerla, principal investigator of the research project, associate professor of neurobiology and behavior, and co-director of the UCI Institute for Brain Aging and Dementia. "Once the plaques and tangles form, it is too late."

Impaired β-Amyloid Secretion in Alzheimer's Disease Pathogenesis
Davide Tampellini, Nawreen Rahman, Michael T. Lin, Estibaliz Capetillo-Zarate1, and Gunnar K. Gouras
A central question in Alzheimer's disease (AD) research is what role β-amyloid peptide (Aβ) plays in synaptic dysfunction. Synaptic activity increases Aβ secretion, potentially inhibiting synapses, but also decreases intraneuronal Aβ, protecting synapses. We now show that levels of secreted Aβ fall with time in culture in neurons of AD-transgenic mice, but not wild-type mice. Moreover, the ability of synaptic activity to elevate secreted Aβ and reduce intraneuronal Aβ becomes impaired in AD-transgenic but not wild-type neurons with time in culture. We demonstrate that synaptic activity promotes an increase in the Aβ-degrading protease neprilysin at the cell surface and a concomitant increase in colocalization with Aβ42. Remarkably, AD-transgenic but not wild-type neurons show reduced levels of neprilysin with time in culture. This impaired ability to secrete Aβ and reduce intraneuronal Aβ has important implications for the pathogenesis and treatment of AD.

Vitamin C dissolves amyloid beta plaques?

Known sources:

Natural sources:


Aqueous Dissolution of Alzheimer's Disease Abeta  Amyloid Deposits by Biometal Depletion
J Biol Chem, Vol. 274, Issue 33, 23223-23228, August 13, 1999

"Zn(II) and Cu(II) precipitate Abeta  in vitro into insoluble aggregates that are dissolved by metal chelators. We now report evidence that these biometals also mediate the deposition of Abeta  amyloid in Alzheimer's disease, since the solubilization of Abeta  from post-mortem brain tissue was significantly increased by the presence of chelators, EGTA, N,N,N',N'-tetrakis(2-pyridyl-methyl) ethylene diamine, and bathocuproine. Efficient extraction of Abeta  also required Mg(II) and Ca(II). The chelators were more effective in extracting Abeta  from Alzheimer's disease brain tissue than age-matched controls, suggesting that metal ions differentiate the chemical architecture of amyloid in Alzheimer's disease. Agents that specifically chelate copper and zinc ions but preserve Mg(II) and Ca(II) may be of therapeutic value in Alzheimer's disease."

Strategies to Diminish the Ab Load in Alzheimer’s Disease
Curr. Med. Chem. – Central Nervous System Agents, 2005, 5, 15-28

"Abstract: Striking advances have been made in recent years toward potential therapies for Alzheimer’s disease. Alzheimer’s disease, which is the leading cause of dementia in the elderly, is pathologically defined by the presence of amyloid plaques, composed of the amyloid-beta protein, and neurofibrillary tangles. The amyloid pathology has been associated with decreased synaptic plasticity and neurodegeneration, thereby explaining the visibly decreased cognitive function and evident dementia. Subsequently, a large number of studies have been launched, which attempt to disrupt the progression
from Ab aggregation to plaque formation. These studies have involved the use of beta-sheet breakers, secretase inhibition, immunotherapy and anti-inflammatories, the most notable findings of which are discussed in this review."

Reviled Substance Involved in Alzheimer's Can Reverse Paralysis in Mice With Multiple Sclerosis
ScienceDaily (Aug. 1, 2012)
...In mice whose immune systems had been "trained" to attack myelin, which typically results in paralysis, A-beta injections delivered before the onset of symptoms prevented or delayed the onset of paralysis. Even when the injections were given after the onset of symptoms, they significantly lessened the severity of, and in some cases reversed, the mice's paralysis...

Reversal of Paralysis and Reduced Inflammation from Peripheral Administration of  -Amyloid in TH1 and TH17 Versions of Experimental Autoimmune Encephalomyelitis.
J. L. Grant, E. E. B. Ghosn, R. C. Axtell, K. Herges, H. F. Kuipers, N. S. Woodling, K. Andreasson, L. A. Herzenberg, L. A. Herzenberg, L. Steinman.
Science Translational Medicine, 2012; 4 (145): 145ra105 DOI: 10.1126/scitranslmed.3004145
[NO PubMed citation yet]




Home  Preface  Brain Failure  Notes  References pg. 1  References pg. 2
Nutritional Alternatives  Patricia's Protocol
  Tauopathy Discussion Forum
Correspondence  Newsletters  Poems  Memory Enhancement

Click to join tauopathies


Questions or comments, contact "perpetualcommotion.com" at gmail.com

Updated: July 2, 2012
Inception: July 2, 2012