View Full Version : Alzheimer the result of an infection? ApoE2 gene brains low risk

rock hunter
05-27-2016, 01:18 AM
Is Alzheimer, the result of an infection?
Florian Rötzer 05/27/2016
US scientists have found in tests that beta-amyloid, which leads to Alzheimer's plaques, antimicrobial effect

Until now it was only a daring hypothesis, Alzheimer's disease, the most common cause of dementia, due to infection. The disease is primarily associated with age, unclear but has so far, why make the specific protein deposits that amyloid plaques and tau protein fibers, leading to a progressive loss of nerve cells, shrink the brain and memory damage. Under 65 years Alzheimer's is extremely rare, only 2 percent of the patients are younger in Germany, while 80 percent aged 80 or older. In Germany fall ill each year about 300,000 new cases of Alzheimer's.
Beta-amyloid plaques in the brain.
Harvard scientists have now established that supported by experiments hypothesis that amyloid plaques might be toxic reactions of the immune system of the brain to infection by bacteria, viruses or fungi. On the track, the scientists brought the similarity of β-amyloid with the amyloid precursor protein (APP), which is part of a primitive immune system in the rest of the body and as antimicrobial peptides (AMP) antimicrobial acts to trap intruders. Later leukocytes destroy the prisoners.

In their article, which appeared in Science Translational Medicine, the scientists believe that infections that may lead to Alzheimer's, so happen at a later age, because the blood-brain barrier then is more porous and more viruses, bacteria and fungal spores can enter the brain. The brain builds a sense of the proteins amyloid plaques as antimicrobial peptides to capture the invaders and render them harmless. Unfortunately, the traps may remain, because they are no longer mined, which Alzheimer could begin.

Scientists have tested the hypothesis on mice with Salmonella Typhimurium, in the nematode C. elegans and in cell cultures with C. albicans and S. Typhimurium. In mice, it was transgenic mice that produce large quantities of the human β-amyloid (Aβ), but do not form plaques APP knockout mice do not possess the precursor to the formation of Aβ, and normal mice. The mice of the 3 groups of 65,000 cells of S. typhimurium were injected into the brain.

In the case of APP-knockout mice, the mortality was highest after the infection according to the hypothesis. They also made no plaques. The transgenic mice showed the highest survival rate and were due to increased resistance and better overall health. Also in C. elegans and cell cultures with human nerve cells and egg cells of hamsters showed the antimicrobial effect of Aβ. So far was Aβ as a byproduct or as a kind of waste. Unlike classical AMPs Aβ but a protective and damaging effects. Known but is that also AMPs as LL-37, when they occur in high concentrations, can be toxic to cells.

Should the hypothesis be true, then the question would arise as to why people with a brain infection do not develop Alzheimer's disease. Scientists say they can indeed show the normal antimicrobial effect of Aβ, resulting in but can be derived no explanation why the plaques are formed. You would not have found a direct indication of an infectious cause of Alzheimer's, but probably a "possible mechanism for a conditional pathogens β-amyloid amyloidosis". The experiments have shown the possibility that some microbial organisms can cause a deposit, but so far no specific organism was identified. therefore it would be important genetic identification of microbial pathogens in the brains of Alzheimer's sufferers. It is also not clear whether by

Rudolph Tanzi, one of the scientists suspected, so he told the NYTimes that Alkzheimer arises when the brain is unable to dissolve the β-amyloid-traps after the elimination of the invaders back. is known that people with the gene have ApoE2 brains that plaque can dissolve well and also have a low Alzheimer's risk.
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