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Alzheimer’s is driven by the buildup of toxic proteins called amyloid-beta.

In the words of Derek Lowe:

Amyloid-directed therapies truly, truly do not appear to be the answer for Alzheimer’s treatment. When I started work in the field back in the early 1990s, I was convinced of the opposite - the evidence looked very strong that defects in amyloid processing were indeed the cause of the disease. But that was thirty-five years ago, thirty-five years in which therapy after therapy after therapy aimed at amyloid mechanisms has failed.

[…] We’re way past persistence, way past focus, way past optimism and multiple shots on goal and old-college-tries. Do something else! For God's sake, do something else.

— https://www.science.org/content/blog-post/anti-amyloid-antib...

I think people are reacting to the press-release more than the work.

I don't see why this is definitely doomed just because they discuss beta-amyloid plaques. Those exist and are real. They probably don't cause it any more than tombstones cause graveyards; very related, but not in the directly mechanistic way we wish.

> Alzheimer’s disease (AD) is a prevalent neurodegenerative disorder characterized by the accumulation of amyloid-beta (Aβ) peptides in the brain.

This can be true and still not be the specific mechanism.

You can treat a specific waste product or you can repair the waste stream. The issue may be waste, but not a specific product, or the issue may not be the waste stream at all.

This work appears to demonstrate evidence of waste stream repair via a well-known waste-product. That doesn't mean that any specific waste product is or is not the problem or that this particular stream is definitely going to remove enough of the waste (if that was the problem).

Maybe there have been a lot of drugs which have similarly attempted waste-stream repair so there's good reason to doubt it on that alone. But I don't think that mentioning beta-amyloid plaque is enough to discard this out-of-hand.

Great news! If you are a mouse.

For humans, not yet progressed to trials though safety has been evaluated for other diseases, so possible for trials to happen quickly?

" the compound has strong potential to quickly transition into human clinics because it has already undergone safety evaluations for other diseases."

Lithium, too! In mice. https://otd.harvard.edu/news/could-lithium-explain-and-treat...

In some parts of the world, it is recommended that drinking water be stored in copper containers. I'm wondering if these communities had figured something out about the health benefits of ingesting trace amounts of copper?

This pertinent paper appeared more than a decade ago about the flaws in the amyloid plaque hypothesis: https://pmc.ncbi.nlm.nih.gov/articles/PMC4207354/

Many people without dementia show amyloid plaques in their brains in autopsies. It's becoming more accepted now that there are multiple interrelated causes after decades pursuing the simplistic amyloid plaque theory.

The article is bordering on irresponsible.

My mother has early onset alzheimer's disease. We currently know very little about the disease and the current treatment options are controversial. The efficacy of the medications removing the amyloid plaque from the brain is questionable, as people still decline.

What makes alzheimer's difficult is that it is not really a single uniform disease. There are subtypes.

Since my mother has it, I was presented with an option of a genetic test. There are several genes which increase your risk. However, if one has PSEN1 that will 100% guarantee early onset alzheimer's at some point.

I'm still on the fence if I want to know.

I really hope we get some viable treatments for this terrible disease. Early onset azlheimer's is awful. I cannot imagine having malfunctioning brain.

"Alzheimer’s is driven by the buildup of toxic proteins called amyloid-beta."

That's the predominant theory, but nothing affecting them has yet proven to be efficacious so far (AFAIK).

Likewise, at one time everyone "knew" aluminum was a culprit, because it showed up in autopsy analyses of affected people. However, it turned out that correlation wasn't from aluminum causing it, so avoiding aluminum didn't affect the disease.

Flagged. Nonsense puff piece by the university. The headline itself is beyond terrible - this is a mouse model and would need years of further successful research to be able to say that it "restores memory" in any meaningful way, let alone in actual humans.

btw definitely related and seems significant:

they found people who use glucosamine (joint pain, knees etc)

have a 25% higher chance of Alzheimer's progression

https://thesciverse.org/scientists-found-that-a-supplement-t...

(still can't figure out if that website is "AI" but they have great articles)

..in Mice