> Over 56 days, the treatment reduced toxic amyloid-beta by 42 per cent and improved spatial learning by nearly 44 per cent

So there's some benefit. Sounds like their next step is a much larger trial to answer the question you are posing.

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mimicmagnet 5 hours ago | parent | next [-]

https://pubs.acs.org/doi/10.1021/acschemneuro.6c00252

In mice. This is a repeating trend in Alzheimer's research, where the amyloid-beta treatment works in the mouse model but not on humans, because the mouse model induces the amyloid-beta issue (mice don't really get Alzheimer's) and then we treat it.

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bluGill 5 hours ago | parent [-]

It is a repeating trend in all medical research. However enough does turn out to work in humans that we eventually make useful progress.

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wk_end 4 hours ago | parent [-]

In general, sure, but in this specific instance (treating Alzheimer's by clearing amyloid-beta) it's been shown over and over again to not work in humans.

	▲	russfink 20 minutes ago \| parent [-]
		I’m kinda new to this - so what you’re saying is the mouse model induces beta-amyliods directly, rather than finding ways to give mice Alzheimer’s, whereas the human tests are for humans that have Alzheimer’s? Meaning we aren’t doing any tests of simply stimulating BA growth in humans?

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TaupeRanger 4 hours ago | parent | prev [-]

The word "benefit" does not apply here. The only "benefits" patients and families care about are: 1) does the patient live longer, and/or 2) does the quality of life improve in a meaningful way? Amyloid plaques are a surrogate marker, and (as already explained by many people in this thread) have not been established as a causal factor in disease. In fact, some work has even suggested a protective role for plaques. So we do not have enough evidence to say that a 42% reduction in amyloid-beta IN MICE relays any benefit at all to humans.

You are correct that a series of clinical trials, which would take 7-10 years, would clear things up. But for now, we simply don't know.