Maybe... I think we are getting closer....
..."If he and other scientists are right that beta-amyloid is an antimicrobial, that the brain goes on an amyloid-making immune rampage in response to pathogens, and that the rampage ignites neuron-killing inflammation, it suggests very different therapeutic approaches than the 30-year pursuit of amyloid destroyers.
One hint of what those approaches should be comes from a 2018 study in Taiwan. It found that people with a herpes virus infection are at 2.5-fold higher risk for dementia than similar people without that infection — and that those treated with anti-herpes drugs were 92 percent less likely to develop dementia than those whose infections were left untreated.
“It used to be thought that stopping the plaques early was ‘primary prevention,’” Tanzi said. “I think primary prevention is stopping the microbes.” Treatment would mean leaving amyloid mostly alone (since it protects the brain from herpes and other viruses) but targeting inflammation, a biological fire that “kills 10 neurons for every one killed by amyloid and tau directly,” he said. “Neuroinflammation is where we’re going to find [Alzheimer’s] drugs.”"...
It seems that beta-amyloid is an antimicrobial agent in the brain that protects the brain from microbial attack, such as the herpes virus HPV-1 and others. As we get older the brain/blood barrier begins to break down putting the brain at risk of infection, this in turn triggers an immune response from the amyloid cells that in their attack form net like structures that trap and kill the offending pathogens...this in turn causes inflammation which is of course the enemy of the neurons, this then cutting communication between neurons ie the thinking process....
Good read....
https://www.statnews.com/2018/10/29/alzheimers-research-outsider-bucked-prevailing-theory/
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