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
I can't find it now, but there's also a past HN discussion about a week prior to the HSV/HHV causative study that points to the function of beta-amyloid as potentially to tangle and disable Herpes in the brain, leading one to believe that β-Amyloid overproduction and its associated side-effects may potentially be a trade for substantially longer life and a slower passing versus a more immediate exit through e.g. encephalitis from an active infection.
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) + sleep deprivation keeping the body from clearing out the residue -> disease.
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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.