The potential problem here is that the mouse model is based on the Amyloid theory of the disease, which this year was largely determined to be wrong after a series of major frauds were found in the research implicating Amyloid. This drug might still work since it seems to act on other aspects of the condition in the bloodwork but there is every chance this doesn't work in practice.

[–] canihasaccount@lemmy.world 8 points 6 hours ago (1 children)

That's just *56. Amyloid has been known for decades to play some role, even though *56's data was fraudulent (for a lay-friendly discussion, see https://www.alzheimers.org.uk/what-we-do/researchers/news/explaining-amyloid-research-study-controversy). Amyloid is certainly not the only thing at play, but it does play some role.

[–] monotremata@lemmy.ca 7 points 6 hours ago (1 children)

Do we know it plays a role? I thought we basically just knew it was an associated biomarker. I kinda thought the research was leaning towards the underlying problem being some kind of issue that kept glial cells from clearing debris effectively, and that the amyloid plaques were mostly another consequence of that same cause, rather than a key mechanism in the chain that led to the dementia.

[–] canihasaccount@lemmy.world 7 points 5 hours ago (1 children)

Yes, it plays a role. What exactly it's doing is unclear, and it's probably more that it's setting up tau to do the real nasty stuff, but it contributes. We know that from experimental work in nonhuman animal models and converging longitudinal work in humans. See, for example: https://www.cell.com/neuron/pdfExtended/S0896-6273(22)00305-1

[–] monotremata@lemmy.ca 4 points 4 hours ago

Huh, I was misinformed about that. Thanks!