Phosphorylated Tau may also play into the herpes story quite well. It regulates microtubule stability, and herpes viruses traffic on those microtubules to hop from one nueron to the next :
https://medium.com/@InfinoMe/cholesterol-have-we-shot-the-me...
Re:The amyloid hypothesis on trial
by pingofdoom on Thursday July 26, 2018 @01:47PM
(#17619321)
Several rats have been developed which manifest Alzheimer's disease with all the right symptoms: age-dependent cerebral amyloidosis that precedes tauopathy, gliosis, apoptotic loss of neurons in the cerebral cortex and hippocampus, and cognitive disturbance.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496102/ [2] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3720142/
So all of our models are pretty artificial. And we build our rat models off of our disease assumptions, like injecting rats with beta amyloid because we assume that's the primay cause of brain dysfunction.
But it's looking more and more like that's wrong and beta amyloid is not the central player in Alzheimer's but just one of many. With Tau/insulin resistance/herpes/glial dysfunction/neuroinflammation playing important rules as well.