https://www.science.org/content/blog-post/reaction-alzheimer...
I guess my own question is whether Alzheimer's/amyloid thinking was atypically stuck on one hypothesis, vs. is this just the slow pace of progress as usual for a given field? I mean...it's not like the amyloid deposition isn't there...
I only play a AD expert on TV (haha I jest...I like to say this because I had no intention of specializing in this when I was training but, hey, in the real world, you have to treat the "market" that rolls in the door....). I work more in the Parkinson's world, and while I would say there are cliques, which do affect who gets NIH (or used to get...I have no idea what's going on there now...), I can't say there's one prevailing "cabal" that's obsessed with any one direction. the bigger issue is that current Parkinson's research is a bit scattershot in too many directions.
My other pet peeve is somewhat unrelated, where the article mentions other directions like neuroinflammation and oxidative stress; the problem is these are also vague/broad topics, that have been thrown around like panaceas for every disease from head to toe; my own superstition is that when a new drug candidate comes out for "neuroinflammation" or "oxidative stress", I'd bet a healthy bunch of nickels it won't amount to much.
GLP-1 (exenatide trial) failed to show benefit Phase 3
prasinezumab (synuclein targeted monoclonal ab) also have not been impressive although I think Novartis is chasing after some statistical signals that popped up in secondary endpoints
there is some academic chatter I heard about elucidating more the process of how normal synuclein turns into the abnormal insoluble form, so that might be the most promising direction.
A couple new stem cell implant trials but not sure if they solved the big problems w/ the last trials - the stem cells eventually develop parkinsonian features, and also it doesn't replace the connectivity/networks that is lost.
Other big question is really what starts the process in the first place since symptomatic patients at initial diagnosis now thought to have been "preclinical" w/ prodromal form for several years...we still don't know.
> This is looking like one of the crazy ideas that just might work - stipulating, for the moment, that amyloid really is the cause of Alzheimer's. . .
Research fraud in medicine is alarmingly common.
The other thing is that GLP-1As actually do appear to help with autoimmune conditions and has been, in my case and in the case of many others, one of the most effective medications for treating ME/CFS.
I wish it was a lack of a profit motive that caused medical researchers to be so off base but it appears what is more likely that they’re not very good with stats, as being good at stats would get in the way of all the ‘accidental’ p-hacking they’re so addicted to.
Edit: Added an email to my hacker news user details
ME/CFS: Myalgic Encephalomyelitis / Chronic Fatigue Syndrome
hEDS: Hypermobile Ehlers Danlos syndrome
TNXB: A gene for making the tenascin-X protein, it's one of the RCCX (Receptor of Complement component 4) gene cluster genes.
SNPs: Single nucleotide polymorphisms
WGS: Whole Genome SequencingMyalgic encephalomyelitis/chronic fatigue syndrome https://en.wikipedia.org/wiki/Myalgic_encephalomyelitis/chro...
For a disease as serious as ME/CFS, a treatment with a 22% recovery rate is far from good enough. Even if PACE stood up to scrutiny it wouldn’t have made sense to give up on finding better treatments.
Like, sure, shoot for 200% cure rate, but even a success rate of 1% cured of a previously unrecoverable situation is insanely informative.
- The great brain clearance and dementia debate - https://www.nature.com/articles/d41586-025-00962-y (2025)
- The Devastating Legacy of Lies in Alzheimer’s Science - https://www.nytimes.com/2025/01/24/opinion/alzheimers-fraud-... (2025), referencing the book Doctored https://en.m.wikipedia.org/wiki/Doctored_(book)
- The maddening saga of how an Alzheimer’s ‘cabal’ thwarted progress toward a cure for decades - https://www.statnews.com/2019/06/25/alzheimers-cabal-thwarte... (2019, by the late Sharon Begley)
https://direct.mit.edu/books/book/5216/How-Not-to-Study-a-Di...
The core problem is much older than stated in this focused review.
Trust the Scientist! For they are pure of heart and unswayed by pride, greed, lust, avarice, or envy
The alternative is what? A wrong understanding of Miasma theory?
I suppose if you only value this entire end to end process then the experiment is not being repeated at all, but yeah, most things just get discarded when they don't work.
Specifically, results are replicated wherever you want to build on something someone has done. For example I'm making specific glass off of a Nature paper for a totally unrelated use.
If the glass doesn't work out will I publish my results? No, too much work to get rejected.
yes, you want to test your Alzheimer treatment, and you measure the amyloid in the patients before the treatment, and you don't find it in some patients... Are you not going to publish that?
The Amyloid hypothesis is not disproven, it is still ONE of the primary candidates for AD.
The problem with any Alzheimer's research is that the disease is still not well understood. It is likely that multiple diseases are being bundled in as a single disease. The tests for AD, are somewhat rudimentary. Beginning with psychological and neurological tests, the blood work to rule out other conditions, followed by a PET scan to look for brain atrophy, and CSF measures for amyloid and tau levels.
It seems almost like they're basically ruling out any disease we can actually measure for and then if it isn't one of those, it's AD.
Does this mean the Amyloid hypothesis is wrong? Unlikely. Is it incomplete? Absolutely!
But articles shouting that all the research should be thrown out are not helpful .
The AD community know that they don't understand the disease, and though therapeutics have been mostly focused on amyloid and tau, research into how the disease works continues.
Good thing OP isn't one, then. In fact it makes a pretty similar point: all the non-amyloid research also should not have been thrown out. Or rather, killed before it got that far; you can decide whether that's equivalent or worse.
Despite even intentional fabrication, the truth of it was found in a few years and the field marches on.
I agree but 16 years is still significant. It represents 5% of the modern medicine era.
The amyloid hypothesis seems too simple and superficial to account for a decades long process (it is speculated that Alzheimer's starts up to 20 years before symptom onset). The ultimate problem is to find the underlining cause(s) and not correlations.
abetancort•18h ago
esafak•17h ago