3 ms·

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 r

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 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=17446016 https://news.ycombinator.com/item?id=17540512 https://news.ycombinator.com/item?id=17540512 https://news.ycombinator.com/item?id=17540094 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 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 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 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 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.

stephengillie 8y ago
From a previous discussion, beta-ameloyd isn't well studied, but it appears to be a viral catch-all, attaching to many viruses. The reason herpes is so significant is because it uses time-release capsules to continually reinfect a host user, and continually caught in the beta-ameloid. So herpes sufferers have more beta-ameloid to clear away most nights.
- eganist 8y ago
  Yup. Working thread here: https://news.ycombinator.com/item?id=18306921 https://news.ycombinator.com/item?id=18306921 (between you and me, incidentally.)
delbel 8y ago
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.
- eganist 8y ago
  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 :/

stephengillie 8y ago

From a previous discussion, beta-ameloyd isn't well studied, but it appears to be a viral catch-all, attaching to many viruses. The reason herpes is so significant is because it uses time-release capsules to continually reinfect a host user, and continually caught in the beta-ameloid. So herpes sufferers have more beta-ameloid to clear away most nights.

eganist 8y ago
Yup. Working thread here: https://news.ycombinator.com/item?id=18306921 https://news.ycombinator.com/item?id=18306921 (between you and me, incidentally.)

delbel 8y ago

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.

eganist 8y ago
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 :/