There’s uncertainty as to what protein is responsible for the degenerative effects.[1]
My bias exists for the fact that I believe the cure to Alzheimer’s is removing or preventing the development of this plaque. At least I’ve been lead to believe this is among the most promising cures.[2] Amyloid protein is particularly tricky because it’s insoluble. I don’t think we could develop a purely chemical solution for the fact that it would likely be destructive to our own biology. And I think both gene expression and enzyme production are unlikely to be able to changed with just a drug.
[0] https://www.sciencedaily.com/releases/2018/03/180326161000.h...
[1] https://www.sciencemag.org/news/2016/05/tau-protein-not-amyl...
[2] https://rupress.org/jem/article/215/3/927/42616/BACE1-deleti...
https://www.sciencemag.org/news/2019/11/colombian-woman-s-ge...
Imo Alzheimer's is probably more related to the brain falling into dysdunctional, self reinforcing patterns of synaptic connectivity.
Neural plaques might exacerbate this problem by disrupting connectivity, but clearly the brains of many people with plaques learn to route around this damage to retain functionality.
Any sources for this? I’d be very interested to read the literature on this.
Just a jumping off point review on the weakness of the amyloid theory.
The connectome dysregulation theory is my own, it hasn't appeared in the scientific literature as of yet due to our inability to perform fine mapping of synaptic connections without microtoming a cadaver brain.
https://www.sciencedaily.com/releases/2019/10/191007113314.h...
The disruption of serotonergic pathways probably isn’t something that can be amended by a serotonergic therapy. I’d actually predict that individuals with Alzheimer’s would experience a diminished effect when taking LSD.
My bias here is more broad. I’m of the belief that the cure to Alzheimer’s is more likely biological than it is chemical. Not overlooking the interoperability of these two things, but rather suggesting that it’s probably a problem that requires a more sophisticated treatment than purely consuming a drug.
That said, I’m very excited to see microdosing being studied and interested in the outcomes of this trial, whatever they may be. Certainly, the results here could tell us something we haven’t yet discovered about LSD or Alzheimer’s, even if there is no therapeutic application in this case.