5 ms·
> The molecule, DDL-920, works differently from recent FDA-approved drugs for Alzheimer’s disease such as lecanemab and aducanumab, which remove harmful plaque
by noleary 2y ago
> The molecule, DDL-920, works differently from recent FDA-approved drugs for Alzheimer’s disease such as lecanemab and aducanumab, which remove harmful plaque that accumulates in the brains of Alzheimer’s disease patients. While removing this plaque has been shown to slow the rate of cognitive decline, it does not restore the memory or remedy cognitive impairments.
Thankful researchers are exploring some new approaches now. The amyloid hypothesis was fine, but its dominance seems to have set Alzheimer's research back by years.
- PaulKeeble 2y agoThere was always a lot of evidence to suggest that Amyloid plaque was not the cause of the problem but a sign of the activity causing the issue and the fact it was the only pursued strategy for years speaks to a problem in medicine and research funding getting very railroaded at times. Many diseases have many potential causes but once a favourite gets selected there is a real tendency for all efforts to go towards that theory and even when early signs are its wrong it continues for years. Alzheimer research went seriously wrong for multiple decades.
- feoren 2y agoIn the particular case of Alzheimer's, some of the foundational studies supporting the amyloid plaque hypothesis were literally fraudulent. Railroading is a problem in general, but won't combat just straight-up fraud. Better fraud detection is needed in cases like these, but of course it's an arms race.
- m3kw9 2y ago[flagged]