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by brnaftr361
951 days ago
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But he's correct, amyloid plaque theory was founded on bad data. Amyloid plaques as causal agents is unclear, but it was made to appear clear by poisoned data, and many studies conducted afterwards, in good faith, assumed that the information and conclusions were sound. However it doesn't appear to be the case, and instead something along the amyloid beta pathway is more likely to be the true causal factor, and plaques an association. It has spawned something of a wild goose chase in Alzheimer's research and treatment. |
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> 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.
And
> Did the 56 Work Lead to Clinical Trials? That’s a question that many have been asking since this scandal broke a few days ago. And the answer is that no, I have been unable to find a clinical trial that specifically targeted the AB56 oligomer itself (I’ll be glad to be corrected on this point, though).