Many people criticize the amyloid hypothese of Alzheimer’s disease, so here’s a good article written in mostly non-technical terms that defends the hypothesis: In Defense Of The Amyloid Hypothesis
There’s a prediction market about the author’s forecast (a successful amyloid-based treatment in the next 12 years), people are rougly equally divided: Will David Schneider-Joseph's bet about Beta Amyloids and Alzheimer's end up true within 12 years? | Manifold
In the comments, someone mentioned the lithium orotate article we discussed here as well (see: Lithium Supplementation - #333 by adssx ). According to the blogpost’s author, a plausible mechanism of lithium orotate aligned with the amyloid hypothesis might be:
In the section of the paper titled Lithium and Microglial Function, they describe transcriptional changes to lithium-deficient microglia, which are immune cells that usually help clear amyloid beta from the brain - the last line of that section summarizes their findings as “Li deficiency leads to a reactive pro-inflammatory state and impaired Aβ clearance”.
So I think at least part of the causal pathway here is something like: 1) amyloid starts to build up and form plaques, which start to entangle lithium and reduce cortical lithium levels, which 2) impairs microglial function, reducing their ability to clear amyloid (and increases inflammation), leading to more plaques, and so on in a vicious feedback loop.