if you have a blood parasite, the virus will hide inside the parasite and re-infect you, and it won't matter if you are on a drug that kills the virus (unless the drug can get into the parasite and kill it as well). Even worse the virus could theoretically hide in your DNA or immune system as instructions-to-run-later, and your system could screw up and accidentally re-create it -- I am not sure how exactly that would work but it is worth exploring the possibility. If it was easy to kill, it'd be dead by now.
I apologize -- I think I'm missing the question...
The working hypothesis now is that if the root cause is pathogenic, then suppressing the pathogen(s) should delay or even prevent onset of the disorder by warding off collateral damage from the innate immune response. Applied: An indefinite (Val)acyclovir supplement should suppress recurring outbreaks of latent Herpes-class viruses, thereby avoiding the immune response which is speculated to eventually lead to Alzheimer's and Dementia-class disorders. All the other ancillary links (e.g. cortisol -> increase in risk, sleep deprivation -> increase in risk) may be explained through the same vehicle (e.g. cortisol -> increase in Herpes-class virus reactivation, sleep deprivation -> impairment in processes used to flush the brain, hastening onset of collateral damage from immune byproducts e.g. beta-amyloid), and it's the many different connections which may have thrown researchers off the scent.
If it took this long to potentially understand the connection, it would explain why "If it was easy to kill, it'd be dead by now" doesn't apply here.
Hopefully I answered your question, but I should restate that I don't quite understand what you asked :/
