02-17-2023, 09:56 AM
Since that article, this I no longer correct:
https://www.nejm.org/doi/full/10.1056/NEJMoa2212948
The amyloid hypothesis is controversial, but the success of lecanemab does suggest amyloid likely is at least a partial contributor to the pathophysiology of Alzheimer's disease.
BC
Quote:7. Those trials have failed. But every single Alzheimer’s trial has failed. I think that any ultimate explanation of Alzheimer’s disease is going to have to include beta-amyloid as a big part of the story - but if attacking the disease from that standpoint is going to lead to viable treatments, we sure as hell haven’t been seeing it. We have to put money and effort down on other hypotheses and stop hammering, hammering, hammering on beta-amyloid so much. It isn’t working.
https://www.nejm.org/doi/full/10.1056/NEJMoa2212948
Quote:CONCLUSIONS
Lecanemab reduced markers of amyloid in early Alzheimer’s disease and resulted in moderately less decline on measures of cognition and function than placebo at 18 months but was associated with adverse events. Longer trials are warranted to determine the efficacy and safety of lecanemab in early Alzheimer’s disease. (Funded by Eisai and Biogen; Clarity AD ClinicalTrials.gov number, NCT03887455. opens in new tab.)
The amyloid hypothesis is controversial, but the success of lecanemab does suggest amyloid likely is at least a partial contributor to the pathophysiology of Alzheimer's disease.
BC
