The headline is broadly defensible, but the qualifications matter. Effect sizes vary by population, the strongest claims rest on shorter trials, and credible voices push back on how it's typically framed.
and there's no ambiguity that ID is responsible for the — the changes that we see in the brain but it's not crystal clear because there are lots of autopsies that are done on people that are completely healthy and have died with no cognitive impairment and they're chalk full of amalo
Every Sunday: the week’s new conflicts and verdict changes — and nothing else.
Native comments, Twitter mentions, and Reddit threads about this claim — surfaced together so the conversation isn't fragmented across platforms.
Bookmarking — the dossier-vs-overview split is the right call. Most of the time I want overview; sometimes I want receipts.
Would love a "what would change this verdict" RSS feed. Sign me up if it exists.
it could be that you need to have a Molloy betta deposition to cause dementia but that is not sufficient it is only a necessary condition and that you might need other factors to coalesce around that
the second is the autopsy studies of people who died without any clinical evidence of Alzheimer's disease who still have amyloid making me wonder if amyloid is necessary but not sufficient
there's some people who think that you can have as much amyloid as you want and it's not until you start to have tau we're understanding more that tau whereas amyloid is sort of widespread kind of from the beginning and builds up all these years beforehand
if that were true of amyloid it could explain part of the observation that lots of people have amyloid without symptoms because it's only necessary but by itself it's not sufficient
So the amaloid hypothesis has a lot of baggage with it right. So I think tal maybe I am amaloid and we have ptow that we can look at but there's other things in the pipeline.