> Hasn’t the entire amyloid theory been coming under a huge amount of scrutiny Yes. > recently I'm using Derek Lowe as my litmus test for how the field react

> Hasn’t the entire amyloid theory been coming under a huge amount of scrutiny Yes. > recently I'm using Derek Lowe as my litmus test for how the field reacts, and he's been leaning against it since around 2015-ish. So "recently" might not be all that recent. > for being almost a mafia-like cabal of somewhat questionable science? Uh, what? It recently came out that one of the papers in Alzheimer's research was faked. However, the importance of that faking on the field is actually relatively little: what it purported to establish was a direct causative link between a single amyloid precursor and memory decline--which was already the prevailing theory. As Derek Lowe describes it (https://www.science.org/content/blog-post/faked-beta-amyloid-data-what-does-it-mean https://www.science.org/content/blog-post/faked-beta-amyloid...): > I could be wrong about this, but from this vantage point the original Lesné paper and its numerous follow-ups have largely just given people in the field something to point at when asked about the evidence for amyloid oligomers directly affecting memory. I’m not sure how many groups tried to replicate the findings, although (as just mentioned) when people did it looks like they indeed couldn’t find the 56 oligomer. And judging from the number of faked Westerns, that’s probably because it doesn’t exist in the first place. But my impression is that a lot of labs that were interested in the general idea of beta-amyloid oligomers just took the earlier papers as validation for that interest, and kept on doing their own research into the area without really jumping directly onto the 56 story itself. The bewildering nature of the amyloid-oligomer situation in live cells has given everyone plenty of opportunities for that! The expressions in the literature about the failure to find 56 (as in the Selkoe lab’s papers) did not de-validate the general idea for anyone - indeed, Selkoe’s lab has been working on amyloid oligomers the whole time and continues to do so. Just not Lesné’s oligomer. In other words, amyloid hypothesis was prevailing before the paper anyways, it would have remained prevailing without the paper, and the paper itself never appears to have directly inspired actual clinical work on any of the failing drugs. It's hard to believe that the field would have abandoned amyloid hypothesis without the failure: there are many other reasons to believe the amyloid hypothesis, and the main reason to not believe it is only because clearing amyloid hasn't improved Alzheimer's in actual drug candidates*.