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So @Merck’s BACE-1 inhibitor Verubecestat resulted in “near-maximal reduction” of amyloid-beta in cerebrospinal fluid and “modest reduction” in brain amyloid. But it didn’t help even #Alzheimer’s disease, even "mild" Alzheimer's. A few thoughts:
1. Many companies are holding on to the hope that giving #tau- and #amyloid-busting drugs earlier, before Alzheimer's sets in, could prevent the disease. The FDA might even be open to using tau and amyloid as biomarkers to approve #Alzheimers drugs cen.acs.org/articles/96/i9…
2. But if we already know these drugs can lower amyloid-beta levels and *not* stop disease progression, is that really a good idea? I'd love to see the long term studies done, but the idea of drug approval based on biomarkers, and not cognitive markers, seems like a can of worms.
3. The world is waiting for an Alzheimer's drug, but the last thing the U.S. healthcare system needs is a new, expensive Alzheimer's "drug" that offers barely noticeable benefits, or worse yet, distracts us with biomarker tests and does nothing for cognition.
4. And then, of course, there’s this in the NEJM paper: “...the amyloid hypothesis of Alzheimer’s disease may not be correct.” Is there any other biological molecule that's caused such prolonged furor and disappointment for scientists?
