It's important to remember that there is growing doubt that amyloid plaques are that important to Alzheimer's disease, or at least that they are a direct cause.
Here is a Nature news story explaining some of the controversy:
In short, it seems Amyloid plaques can be found in the brains of many people who died of old age without developing any kind of dementia, and there are people with advanced Alzheimer's disease and almost no amyloid plaques at all; and there has been no success whatsoever in even slowing the disease with drugs that reduce the levels of amyloid plaques.
The debate seems to be pretty complex. From that article:
>Critics of the hypothesis note that the brains of many people who did not have Alzheimer’s disease have been shown to contain plaques on post-mortem. And they point to the failure of many clinical trials of treatments designed to dissolve amyloid plaques, none of which has slowed the disease. Researchers who support the amyloid theory counter that although the density of the plaques varies a lot between individuals, the density of tau tangles that they trigger correlates tightly with the severity of disease. And clinical trials probably failed, they say, because the treatments were given too late in the course of disease.
>They also have strong evidence on their side. There are certain rare and aggressive forms of Alzheimer’s disease that emerge early — between the ages of 30 and 60 — and run in families; these conditions are caused by mutations in genes that govern the amyloid-making process and inflammation in the brain. Scores of other genes have been associated with the risk of the more common late-onset form of the disease. Several code for proteins that comprise elements of the amyloid cascade, and some are involved in the innate immune system — a group of mechanisms that activate quickly to prevent the spread of pathogens in the body, and which drive inflammation.
Yeah, even with those limitations, it's still possible that the relationship between plaque buildup and Alzheimer could be similar to the one between smoking and lung cancer - you can get the latter without the former (randomly or triggered by other causes), you can have the former without getting the latter, but in most people, the former will massively increase the risk of getting the latter. Then again, the plaque could also be a co-symptom caused by some third factor. We'll see eventually
The debate is complex, but the amyloid plaque people have been steamrollering everybody else into submission--which is unfortunate as their hypothesis has failed every single time it has been put to the test.
However, Big Pharma is no longer backing amyloid plaque research because every single drug targeting them has failed for Alzheimer's.
At this point, it's very likely that amyloid isn't the problem. It's probably a response--and likely one that occurs long after the damage is done.
Here is a Nature news story explaining some of the controversy:
https://www.nature.com/articles/d41586-020-03084-9
In short, it seems Amyloid plaques can be found in the brains of many people who died of old age without developing any kind of dementia, and there are people with advanced Alzheimer's disease and almost no amyloid plaques at all; and there has been no success whatsoever in even slowing the disease with drugs that reduce the levels of amyloid plaques.