Interesting Alzheimer's paper provides alternative explanation regarding the mode of action of monoclonal antibodies such as lecanemab.

[jeffreyn]

"For decades, the prevailing theory in the field has stated that a protein made up of 42 amino acids called amyloid-beta 42 (Aβ42) hardens into clumps called amyloid plaques, and those plaques damage the brain, causing Alzheimer's disease."

"Led by UC's Alberto Espay, MD, the team have hypothesized that normal, soluble Aβ42 in the brain is crucial for neuron health and that the loss of Aβ42, rather than the buildup of plaques, drives Alzheimer's."

"According to Espay's research, the transformation of Aβ42 into plaques appears to be the brain's normal response to biological, metabolic or infectious stress."

"Espay and his colleagues noticed that these [monoclonal antibody] drugs unintentionally increased levels of Aβ42."

MedicalXpress article: Boosting brain protein levels may slow decline from Alzheimer's.

medicalxpress.com/news/2024...

Research paper: Increases in Aß42 Slow Cognitive and Clinical Decline in Alzheimer's Disease Trials.

academic.oup.com/brain/adva...

[jimcaster]

This seems very similar to the debate about whether the build up of alpha synuclein is the cause or a symptom of Parkinson's. So much money and effort has been spent to eliminate alpha synuclein in Parkinson's and beta amyloid in Alzheimer's. I'm glad someone is asking whether we're barking up the wrong tree.

[jeffreyn]

Some recent information regarding the status of monoclonal antibodies lecanemab and donanemab.

MedicalXpress article: Revolution or mirage? Controversy surrounds new Alzheimer's drugs.

medicalxpress.com/news/2024...

[jeffreyn]

On a related topic, a recent post by Benjamin Stecher, on his blog Tomorrow Edition.

tmrwedition.com/2024/09/24/...