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Relevant_synapse OP t1_iycuijf wrote

It’s important to understand what the extent of the forgery was before making sweeping pronouncements. It’s a common misconception that the forgery invalidates the field. Holding such a frequently-parroted opinion has unfortunately become a litmus test for being uninformed in this space. You can read about the scandal yourself here: https://www.science.org/content/article/potential-fabrication-research-images-threatens-key-theory-alzheimers-disease

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Sarcastinator t1_iycwwgt wrote

It's not just about the forgery but don't take it from me:

https://www.science.org/content/blog-post/positive-amyloid-trial-finally

> At the same time, though, news like this needs to be examined carefully. As the world knows, the anti-amyloid clinical landscape for Alzheimer's is absolutely littered with failures in every direction: anti-amyloid antibodies of various types, attempts to inhibit beta-secretase and gamma-secretase enzymes, attempts to prevent aggregation, you name it. Nothing has worked. The presumption at this point is that such therapies will not succeed, so if lecanemab has indeed worked, the question is what makes it different. There's a ready answer (up to a point) because antibodies can indeed be quite different (that's their point!) and if you do manage to hit exactly what needs to be hit, you could expect efficacy when apparently similar attempts have led to nothing.

So being skeptical towards amyloid therapies isn't unwarranted, or casual dismissal.

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Relevant_synapse OP t1_iycyb3d wrote

Being skeptical is not the same as dismissing the entire connection as “bunk”. Derek is a much respected voice in the field. I actually agree with his take, and he is spot on with the quote you provided.

What makes lecanemab different? Compared to other drugs in its class that we’ve seen thus far, it has much higher affinity for amyloid fibrils and soluble oligomers than plaques.

https://www.frontiersin.org/articles/10.3389/fnins.2022.848215/full

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