Please help

mindmystery · 08-22-2007, 05:51 AM

I would like to know why amyloid plaques (deposits in the brain of a sticky protein called amyloid beta peptide) "causes" neurodegeneration? I am aware that it doesn't directly CAUSE neurodegenerenation, but I want to know why that protein is so special in Alzheimer's Disease. Do neurons die because of it?
If I were to say that Alzheimer's Disease is a Tauopathy, I would be saying that it is "caused" by neurofibrilary tangles (overexpression of tau protein), right? So this amyloid plaque would not be that relevant?
Research done in this area, in tauopathies, has the aim of trying to find out a drug, compound, that will have a positive effect on reducing the amount of tau protein produced in the brain. Would this be a possible cure for Alzheimer's Disease and other tauopathies? Why do we want to reduce the amount of tau protein produced in the brain? To see if it is the cause of neurodegenerative diseases?
Please help. Do answer. Even if you do not have any good knowledge on this matter, I would like to know what you think and what makes sense to you. It can get me started. Thanks for at least reading

Lara · 08-22-2007, 03:50 PM

Hi there,
I have no idea how to answer your questions. I had 2 close family members who had Alzheimer's Disease but my knowledge is very basic in this area except for my fear of actually getting it. :/
I just wanted to alert you to a couple of areas of information. One I just read in the Health News Forum here this morning and there are some more links on the Psych Central site as well. The news item I just read today was specificially related to Tau. Down on the bottom of the PsychCentral url, the 2nd one, you'll find more Related Clinical Articles.

Quote:

Alzheimer?s Vaccine Effective
(Psych Central News) Researchers have proved for the first time that the immune system can combat the pathological form of tau protein, a key protein implicated in Alzheimer’s disease. The protein accumulates into harmful tangles in the memory center of the brains of Alzheimer’s patients.Einar Sigurdsson Ph.D., Assistant Professor of Psychiatry and Pathology at New York University School [...]

Read the full article...

http://neurotalk.psychcentral.com/sh...ad.php?t=26477

http://psychcentral.com/news/2007/08...ine-effective/

Quote:

The disease is associated with neurons in the memory center of the brain becoming choked by the buildup of two types of proteins: tau, which turns destructive when it is prone to forming fibrous tangles, and amyloid beta. Compared to extracellular amyloid plaques, tau aggregates are confined inside of brain cells, making them more difficult to reach.

“It’s likely that there’s a synergism in the pathology,” said Dr. Sigurdsson. “Amyloid pathology may cause tau pathology and tau pathology might cause more amyloid pathology. What you have is a vicious cycle. If you can target both of these proteins you’ll likely have more efficacious treatment.”

Quote:

“In this animal model—and also in Alzheimer’s disease—there’s a breakdown of the blood brain barrier. In addition, it is well established that neurons have receptors that can bind to and promote uptake of antibodies and our studies seem to indicate that sick neurons that are accumulating tau aggregates take up more antibodies than healthy neurons. The antibodies then end up at the site where they can interact with pathological tau protein in the neuron, and promote its clearance.”

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