3 ms·
With Lecanemab only a relatively small positive effect was able to be shown. With Aducanumab by the same companies, which works similar, even that wasn’t possib
by legulere 4y ago
With Lecanemab only a relatively small positive effect was able to be shown. With Aducanumab by the same companies, which works similar, even that wasn’t possible even though it’s effective against amyloid oligomers. And there are many more failed treatments targeting amyloid beta.
No matter how the causal relationships are, targeting amyloid beta for treatment does not seem to help enough for treatment.
I would be very interested how genetic evidence can rule out confounding effects.
- zosima 4y agoLecanemab had an extremely strong effect, from a statistical point of view. The average clinical efficacy could be stronger. But Lecanemab is definitely the largest step in Alzheimer's disease research in a very long time. Well, when you have a large number of different mutations in the amyloid beta gene, and in the genes for the machinery for cutting the precursor protein APP to amyolid beta, that all leads to early and fast progressing Alzheimer's disease, which from a pathological perspective is indistinguishable from normal Alzheimer's disease, then the evidence is quite clear. When you then see that people who have duplicates or triplicates of the amyloid beta gene, also have a much higher risk of Alzheimer's disease and the risk increases with more duplicates, the evidence is extremely strong.
- legulere 4y agoIsn’t the effect small but the significance good? If I understood it correctly there’s no amyloid beta gene, but genes for APP an genes for proteases cutting APP. As a layman that leaves a lot of other explanations open, for instance other byproducts of the proteolysis, other breakdown mechanisms for APP, …