'Researchers expect that the extensive molecular and clinical data that they produce will help to uncover more about the mechanisms of Alzheimer’s. “Evidence so far points to tau as the initiator of Alzheimer’s symptoms, disabilities and eventually death,” says Boxer. “But this hypothesis needs to be tested in humans.”
@noyes @cyrilpedia
I'm a muggle, but interested due to family history and my own cognitive impairment. I'm betting on the inflammation theory - lots of tau and amyloid has been found in brains of people without Alzheimers.
Those amyloid plaques are crusted in and out with inflammatory compounds that have precipitated of of the extracellular fluid. The amyloid is soaking it up like a sponge. Without the sponge, that junk gets deposited directly on tissue in the brain. The notion that an AD brain without amyloid might be worse off than an AD brain with amyloid needs to be explored.
@noyes @cyrilpedia
Or maybe without those sponges those compounds can be eventually flushed out and eliminated
@cyrilpedia
The Tau Hypothesis strikes me as an attempt to salvage the Amyloid Hypothesis, which was very good at manipulating market valuations, but absolutely terrible at generating Txs. The picture attached—the lecanemab-savaged brain of a Phase 3 trial participant—shows that Lecanemab's approval is not indicative of lowered risk and increased efficacy compared to previous AH offerings, but rather of a lowering of standards in the approval process. Bad science makes bad medicine.