The Resurrection of Aducanumab Doesn ' t Change the Picture for Amyloid- β Clearance in Alzheimer ' s Disease

It took a long time and many failed attempts for the research community to get to the point at which amyloid-β could be successfully cleared from the brains of Alzheimer's patients. Unfortunately, the data to date strongly suggests that this isn't an effective approach to therapy, at least not on its own, even though it is clearly the case that the increased levels of amyloid-β in the aging brain should be removed. It is a characteristic difference between old brain tissue and young brain tissue, and there is plenty of evidence for it to be harmful.

This failure to achieve clinical success may be because amyloid-β aggregation ceases to be an important factor in later stage disease, once tau aggregation and neuroinflammation are firmly established. It may be because patients frequently have other neurodegenerative conditions, such as vascular dementia, that mask any benefits obtained by removing amyloid-β. It may be that amyloid-β accumulation is a side-effect of glial cell dysfunction, and it is glial cell dysfunction rather than amyloid-β accumulation that drives the condition from its early to later stages.

There has been a fair amount of discussion over the recent move of aducanumab back across the line of FDA approval, following an earlier declaration of failure. There is the usual skepticism regarding motivation on the part of the biotech companies involved. Yet this doesn't make much difference to the present situation with regard to amyloid-β clear...

Source: Fight Aging! - October 25, 2019 Category: Research Authors: Reason Tags: Medicine, Biotech, Research Source Type: blogs