You are wrong. This paper very clearly does not show that it "works". The debate exists for a good reason - the very thing this paper claims to show is the exact thing the person you replied to was questioning. And that is a central question in all of Alzheimer's research.

There are dozens of studies that show mice improving their memory/spatial reasoning as Alzheimer's models. None of them have led to a proven improvement in longevity or quality of life for human Alzheimer's patients. Some of them slightly slow the progression, but even then you're getting into a gray area - is it really "better" to be stuck in the Alzheimer's fog for longer? Are we actually improving quality of life? It's unclear.

So no, in order for us to say that this approach "works", we would need randomized controlled clinical trials in humans showing a strict improvement in quality of life and/or longevity. This is not even close to that level of evidence.

▲

dgoldstein0 5 hours ago | parent | next [-]

> 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.

▲

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.

▲

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.

▲

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 22 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?

▲

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.

▲

JackFr 5 hours ago | parent | prev [-]

In fairness to parent, while the article doesn't say the title claims 'restores memories'.