21–30 of 37 posts
Earlier quoted context omitted.
Disagree vehemently. HHMI funds what’s fashionable. Find me a HHMI investigator without a recent CNS paper. As with Nobel prizes, the true innovators always seem to make their discoveries outside the power circle.
How do the many innovations of bell labs fit your hypothesis?
For more information:
https://www.telegraph.co.uk/news/science/science-news/854683...
If so, then the plaques it forms might be the brain’s last-ditch effort to protect itself from microbes, a sort of Spider-Man silk that binds up pathogens to keep them from damaging the brain. Maybe they save the brain from pathogens in the short term only to themselves prove toxic over the long term.
I really like the thinking here.
Similarly: In people with CF, calcium and glutathione build up in the cells. High levels of calcium are associated with cell death, so much of the CF community believes calcium is harmful.
I believe the calcium and glutathione are desperate efforts to buffer the cell in the face of deranged cell chemistry. I believe the high calcium is indicative of other things being really bad and the body trying desperately to compensate.
If this guy wants another outside-the-box research project, there you go. I would love to see that looked into.
Edit: Is it me, or does the article actually switch from saying amyloid-beta to saying beta-amyloid midway through?
This month, however, he got an unheard-of email from NIH: The agency had found some extra money lying around in its budget. Would he please respond to the reviewers and resubmit his proposal? An over-the-moon Moir did. He expects to hear back in a few weeks.
Yay! I hope he gets it.
This isn't a particularly surprising story considering the history of science. To give an example of how this sort of thing played out historically, Marshall Nirenberg was basically persona non grata (or at least dutifully ignored) at many scientific conferences prior to his postdoc's discovery of the codon for phenylalanine. At the time, he was working at the NIH, which was considered very low prestige by many conte…
Earlier quoted context omitted.
Reminds me of Lockheed's Skunkworks. I've heard lots of businessmen say they're going to recreate skunkworks, but with improvements. The improvements, of course, make it not a skunkworks and these efforts never deliver skunkworks performance. Could the government create a skunkworks? Not likely, because they fought against Kelly Johnson constantly over how he ran it. I bet Paul Allen could have done it, because he ha…
I’m in the midst of listening to the Skunk Works audiobook. And it’s fascinating. It had been on my list of things to read but I just couldn’t wait. I bit the bullet and bought the audiobook. It’s worth every penny.
https://www.amazon.com/Kelly-More-Than-Share-All/dp/08747449...
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)…
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 woul…
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 :/
Earlier quoted context omitted.
How do the many innovations of bell labs fit your hypothesis?
He (or she)'s not disagreeing with the notion that unfettered funding produces innovation, he (or she)'s disagreeing with the notion that HHMI provides unfettered funding. Part of the beauty of Bell Labs was that it wasn't necessarily all about fame and grandstanding- a lot of folks who were working there were just normal, unassuming New Jersey folk who put in a good days work messing around with whatever they were t…
Drop into a DoE research facility. (Most will give tours to U.S. citizens.) Same playful approach to tinkering with whatever.
Amyloid-beta is associated with sleep deprivation. This new research could suggest that sleep is an essential component of the immune system. If so, then the plaques it forms might be the brain’s last-ditch effort to protect itself from microbes, a sort of Spider-Man silk that binds up pathogens to keep them from damaging the brain. Maybe they save the brain from pathogens in the short term only to themselves prove t…
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)…
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.
https://news.ycombinator.com/item?id=18306921
(between you and me, incidentally.)
Earlier quoted context omitted.
Disagree vehemently. HHMI funds what’s fashionable. Find me a HHMI investigator without a recent CNS paper. As with Nobel prizes, the true innovators always seem to make their discoveries outside the power circle.
How do the many innovations of bell labs fit your hypothesis?