The "standard" theory is that amyloid leads to tau protein accumulation which leads to neurodegeneration: https://www.astralcodexten.com/p/in-defense-of-the-amyloid-h.... Which would explain why current treatments don't really work: by the time Alzheimer's has progressed to noticeable impairment there's already too much tau, so reducing amyloid will at best slow the rate of decline by reducing the formation of new tau.

ever since the discovery of amyloid plaques, it's been an open question. Are they causative or a symptom? Would reducing or eliminating them help treat the disease? There is lots of data that supports amyloid as a disease treatment target, particularly in animal models. Of course the abject failure to actually develop a good anti-amyloid treatment that actually provable and significantly mitigates the disease weighs against the idea that amyloid is a good target. And the high profile frauds that have been discovered haven't helped. But, the biomedical community are not a bunch of morons. All these drug companies wouldn't have spent these billions of dollars on anti-amyloid and anti-tau if they were such obviously terrible ideas.

That's the viewpoint of everyone sensible outside of Alzheimer's research.

Those in it are still throwing billions per year at the idea.

Meanwhile, back in reality, no amyloid-beta drug has had any clinical effect in humans, other than reducing the plaques. But both the shingles and RSV vaccines are proven to reduce Alzheimer's risk.