Since I am new to the discussion, I am not allowed to post links. You can contact me for the URLs/links **


In mid December 2010, I posted a file to the Internet detailing studies and articles by scientists who believe Alzheimer's is a misfolding prion/protein disease: On pages 33 and 34, I cited the Parkinson's/prion disease work by Dr. Olanow and Dr. Prusiner.

I have noticed an interesting commonality of prion/protein misfolding diseases: the neuropathology finds that most all of them have neurofibrillary tangles in the brain.

Explanation of neurofibrillary tangles:


Alzheimer’s destroys the nerve cells that process, store and retrieve information in the brain. This nerve cell destruction is thought to be the result of accumulation of amyloid plaques and neurofibrillary tangles. Amyloid is a general term for protein fragments that the body produces normally. In a healthy brain, these protein fragments would be broken down and eliminated. In AD patients, the fragments accumulate to form hard, insoluble plaques. Neurofibrillary tangles are insoluble twisted strands of a protein called tau protein that form inside brain cells. Scientists do not yet know whether the plaques or tangles cause AD or are a byproduct of some other process. "

To confirm, Google "neurofibrillary tangles" and the neurodegenerative disease of choice: Alzheimer's, Parkinson's, Creutzfeldt Jakob, DLB Dementia with Lewy bodies, FTLB (frontotemporal lobar degeneration), ALS - Amyotrophic Lateral Sclerosis, GSS - Gerstmann-Straussler syndrome, and now, very disturbing - autism.

If the scientists are correct, and Alzheimer's IS a misfolding prion/protein disease, then it is not confined to the elderly. Victims of early onset Alzheimer's (ages 50 to 64) are soaring.

And now the scientists suspect children and young adults with autism may also be prion disease victims . . .


A study released in December 2009 by the Centers for Disease Control (CDC) reported that autism prevalencehas increased from the 1994 rate of one in 150 to one in 110 for children born in 1998. This is a staggering 57 percent increase in just four years. More children are diagnosed with autism than cancer, diabetes, and AIDS combined.





Funding: $698,400
Research Lead: Dr. David Westaway, University of Alberta
Project: "Extending the spectrum of Prionopathies to Amyotrophic Lateral Sclerosis and Autism"
This project proposes to link the chemistry of the prion protein to the new territory of other nervous system diseases, such as ALS (Lou Gehrig's disease) and the socialization disorder autism-diseases which are at least one thousand times more common than prion diseases. It is believed that a different type or prion protein may operate in other types of brain diseases, which could lead to new ways of thinking about incurable disorders. The project will create changes in the amounts of the various forms of the new membrane protein, and then perform an array of analyses on the behavior and nervous system transmission of laboratory mice. Nervous transmission by electrical impulse can be measured in isolated brain cells, a system that is also convenient to study the effect of stress by adding small amounts of toxins to the fluids bathing the cultures. By these means, the project aims to extend the boundaries of what is considered "prion disease."

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By separate message, I will post a theory of what is causing all these prion diseases. Helane Shields, Alton, NH

we love theories here and are very open minded.

thank you

I am frustrated because I cannot share the prion/AD/PD information, including possible cause of the epidemic, without posting links . *edit*

http://www.huffingtonpost.com/dr-david-perlmutter-md/alzheimers-herpes-could-be-a-cause_b_814047.html

I thought this seemed to be an article related to the discussion.
All along, I've been thinking of getting rid of the alpha synuclein, here beta amyloid (also a mis-folded protein that aggregates in the brain) appears to be the hero on the white horse instead of the enemy

If beta amyloid were the cause of Alzheimer's disease, then why would ridding the brain of this protein actually cause patients to worsen? Harvard researcher Dr. Stephanie Soscia and her associates may have the answer. Their recently published research questioned why beta amyloid accumulates in the Alzheimer's brain in the first place, and concluded that in fact, the protein actually serves to rid the brain of a variety of bacteria and viruses. They described beta amyloid as an "antimicrobial peptide" which accumulated in response to an infectious agent. Their work looks upon beta amyloid in a new light as they stated, "If the normal function of beta amyloid is to function as an antimicrobial peptide, then an absence of the peptide may result in increased vulnerability to infection." Rather than causing the disease, beta amyloid may be our brain's natural response to an infectious agent, accumulating as a way of defending us against a pathogen. So perhaps we should reconsider beta amyloid since it has been said that "the enemy of my enemy is my friend."

This newest research about asyn does not answer the question of whether those asyn clumps are good or bad, or whether they are cause or effect.

Since "normal" people have been found to have these clumps at autopsy, and some PWP have been found NOT to have them (latest read was about 30-35%, no small number even if you throw in some possible misdiagnosis)....what does this tell us? I don't know either.

To me, this "prion-like" theory seems to be the newest thing in PD research, and I think it's great we are looking at things other than just same-old, same-old dopamine... but I dont' know that it really answers all that many fundamental questions....such as:

why do these proteins misfold in the first place?
is the misfolding an attempt by the body to heal something, and if so, what?

I too read about the Alz. research where they got rid of the offensive protein placques and people got WORSE. Certainly not what the researchers expected.

Some or many of you might have already stumbled across this (see link, below). Apologies if this is redundant:

http://www.youtube.com/watch?v=LdAmm...eature=related

From my post above regarding the effect of curcumin:

"Greater than 32% decrease in mutant
alpha-synuclein aggregation was observed within 48 h subsequent to curcumin
addition. Our data suggest that curcumin inhibits AS oligomerization into higher
molecular weight aggregates and therefore should be further explored as a
potential therapeutic compound for PD and related disorders.
"

In light of 1) Ron Hutton's ten year trial of curcumin and 2) that India simultaneously has low prevalence of PD and high dietary consumption of curcumin, I think a preliminary conclusion that the elimination of these tangles is a step in the right direction is reasonable.

I wonder if a-synuclein, now known to misfold into pore like structures is deposited within the membrane by cleavage of a larger transmembrane protein, and in this position, in this form acts as an " synthetic ion channel" which "bleeds" or "chokes" the normal ion transfer of Ca, Na, or K, in and out of the cell. This would foul up the normal ionic intra-cellular cytosol ion balance, and possibly trigger apoptosis.
any ideas about this? cs

That seems like a possibility to me. This article
http://www.neurogenesis.com/Neurotra...w-it-works.php
on neuro transmitters that someone else posted on another thread, seems related. It talks about the increase of (or increased ratio to other neurotransmitters) norepinephrine or epinephrine from stress which in turn signals the body to produce more neurotransmitters (such as GABA).
And here's the related part, if something else (such as misfolded proteins) are in the neurotransmitters receptor sites.... they would fool the body into reducing or eventually stopping the production of those neurotransmitters as well as opening channels.
"As the GABA Sensitive Ring and either the Second or Third Neurotransmitter rings begin to fill with their respective molecules, they tighten the whole GABA complex, thereby widening the chloride channel to allow more chloride to enter. Since chloride neutralizes norepinephrine, this process can calm excessive nervousness, tension, and stress.

Since the Second and Third Neurotransmitter Rings are sensitive to external source substances such as benzodiazepines, barbiturates and alcohol, these external substances can cause the Chloride Channel to open, thereby assisting in the neutralizing of additional adrenaline.

However, prolonged use of any external substances that cause the GABA complex to widen without the natural production of GABA, can eventually send the message to the brain that GABA is no longer needed. The brain doesn't produce neurotransmitters to store, rather it produces them for immediate use. Therefore, if the brain continues to receive the message that GABA is not needed to widen the chloride channel, the brain may finally slow down the GABA production, thereby creating a deficiency."

I am sorry this is not presented more clearly- I can barely understand it myself. Do you think his relates to what you presented CS?

I do understand you and as you know I'm sure, neurologix is working on gaba and the insupportable Dr. Levesque thought that's what he had "fixed" in his one patient attempt to use autologous cells.

I like how you tied it together - don't know how accurate you are and not qualified to say anything but it sure fits many things together that i have read.

this may be a stupid question, but what transmits alpha -synuclein so that it travels? that is what makes it a prion disease is that correct?

my mantra - our brains are also lacking epinephrine in autopsy.

read this:http://www.ninds.nih.gov/news_and_ev...son_090400.htm