https://www.nia.nih.gov/health/what-happens-brain-alzheimers-disease
Amyloid plaques
The beta-amyloid protein involved in Alzheimer’s comes in several different molecular forms that collect between neurons. It is formed from the breakdown of a larger protein, called amyloid precursor protein. One form, beta-amyloid 42, is thought to be especially toxic. In the Alzheimer’s brain, abnormal levels of this naturally occurring protein clump together to form plaques that collect between neurons and disrupt cell function. Research is ongoing to better understand how, and at what stage of the disease, the various forms of beta-amyloid influence Alzheimer’s.
https://actaneurocomms.biomedcentral.com/articles/10.1186/s40478-014-0135-5
ReplyDeletenot so clear
https://www.scientificamerican.com/article/alzheimers-inc-when-a-hypothesis-becomes-too-big-to-fail/
ReplyDeleteAlzheimer’s, Inc.: When a Hypothesis Becomes Too Big to Fail
in other words - the FDA approval of this drug is like, lehavdil, a Sanhedrin that errs, and then needs to bring Korbanot.
Except that the FDA recently approved a drug that causes the plaques to recede even though clinical trials showed no change in the course of the disease.
ReplyDeleteAs a teacher of mine in medical school taught us, "Everyone dies in bed but beds don't kill people so eliminating beds won't change the mortality rate."
By removing this plaque, many biotech and pharma researchers believe they can slow down the progression of the disease—although the amyloid thesis has not produced a new drug for the memory-stealing condition, and is full of failed drugs in its wake.
ReplyDeletehttps://www.fiercebiotech.com/biotech/analysts-amyloid-thesis-reports-my-death-are-greatly-exaggerated.
And
See https://www.fiercebiotech.com/biotech/alzheimer-s-hopes-dashed-as-lilly-gives-up-amyloid-drug-solanezumab.