Right? And if you extrapolate research like the sleep deprivation research further out, it ties in pretty well with the thinking that sleep deprivation keeps the brain from clearing the byproducts of a fight against herpes reactivation.
Edit:
Less sleep -> more beta amyloid link: https://news.ycombinator.com/item?id=16026655
Beta amyloyd -> herpes entanglement: https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9
None of this is definitive, mind you, but as each new bit of research comes out, a new piece of the puzzle appears to be put in place. Ultimately the question ends up being answered by a more comprehensive wide-scale experimental study tracking herpes mitigations of any sort and any possible reduction in alzheimer's occurrences, basically a larger version of this: https://www.medicalnewstoday.com/articles/322463.php
Wikipedia might have good references as a starting point though. https://en.wikipedia.org/wiki/Amyloid_beta
Most of the page is dedicated to the Alzheimer's connection. Even that quote came from Alzheimer's research.
[7]Hiltunen M, van Groen T, Jolkkonen J (2009). "Functional roles of amyloid-beta protein precursor and amyloid-beta peptides: evidence from experimental studies". Journal of Alzheimer's Disease. 18 (2): 401–12. doi:10.3233/JAD-2009-1154. PMID 19584429.
Linked previously but I'll link again:
https://www.ncbi.nlm.nih.gov/pubmed/26836158 dated 22 Feb 2016
https://www.cell.com/neuron/fulltext/S0896-6273(18)30526-9 dated 11 Jul 2018
These seem to reference Alzheimer's only in passing or potentially in relation to the infectious theory, but they specifically speak to the action of Beta Amyloid.
In short, it's based on number of virus infections, which herpes greatly increases. So I agree that your hypothesis is sound.