| This seems to be referencing the path to mainstream exposure for the infectious theory of Alzheimer's. Prior discussions (not the same link) on HN, posted for reference because they touch on the past research that was previously posted here: https://news.ycombinator.com/item?id=18306381 (this one's a comment I made associating the cortisol/Alz risk to the microbial Alz connection; it's nothing more than a hypothesis) https://news.ycombinator.com/item?id=17446016 https://news.ycombinator.com/item?id=17540512 https://news.ycombinator.com/item?id=17540094 (this is the parent link for the antiviral risk reduction study -- a good read, comments and source article) There's a decent amount of reading when scholar-googling: https://scholar.google.com/scholar?q=hsv1+alzheimers Moir's paper specifically: the relationship between β-Amyloid and viruses in the brain: https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9 (study link) There's also research pointing to sleep's function as helping clear out plaques such as beta-amyloid. https://news.ycombinator.com/item?id=16026655 Finally, there's at least a bit of research pointing to boosted susceptibility of herpes viral infections when carrying ApoE4: https://scholar.google.com/scholar?q=hsv1+apoe4 The novel conclusion from all of this, which I suspect is being actively investigated, is that there's a potentially complicated interplay of an enhanced viral infection (HSV/HHV enabled by ApoE4) + evolutionary defense going into overdrive (β-Amyloid) + (potentially) sleep deprivation keeping the body from clearing out the residue -> disease. --- I'm particularly motivated to track this research because of its prevalence in my family background and because, from what I can tell, I've thus far managed to avoid the environmental trigger-pull. I can already tell you I'll probably go on (val)acyclovir lifetime if I'm ever diagnosed with any particular strain, as it looks like active infection, with outbreaks, is what's likely to act as the first domino to tip. |