The problem with the amyloid-beta hypothesis was the assumption that these plaques were causing the Alzheimers and that removing them by itself could lead to a cure.
Cause -> cognitive disease Cause -> plaques
That is, that the same cause is behind both.
There may be some arrows from plaque to disease as well (i.e., that plaques also increase disease).
I dont know the truth, but just trying to understand/follow Alzheimers news and reading comments.
As I took it, understanding that there was a fraud doesn't mean that continually clearing the plaques wouldn't have a good chance of holding off cognitive disease indefinitely.
I also don't think "fraud" should be used in this discussion at all.
With all that said, if this One Weird Trick can clear/prevent the buildup of plaques (and thus the cognitive symptoms downstream of them), that's just a best possible outcome.
I still think it's more likely than not (70%) that it is a cause though farther upstream. There is a good amount of evidence tau is more likely the proximate cause due it more closely tracking disability in moderate to late stage Alzheimer's.
>Normally, the protein LRP1 acts as a molecular gatekeeper, binding to Aβ and transporting it across the BBB for elimination. In Alzheimer’s, this system becomes fragile, leading to Aβ accumulation. The supramolecular drugs mimic LRP1 ligands, binding to Aβ and initiating its clearance, effectively resetting the system and restoring vascular function.
My sense of the narrative is that "unclogging" the amyloid protein with this treatment allows innate repair functions to resume.
>"The long-term effect comes from restoring the brain’s vasculature. We think it works like a cascade: when toxic species such as amyloid-beta (Aβ) accumulate, disease progresses. But once the vasculature is able to function again, it starts clearing Aβ and other harmful molecules, allowing the whole system to recover its balance. What’s remarkable is that our nanoparticles act as a drug and seem to activate a feedback mechanism that brings this clearance pathway back to normal levels,”
>...
>Normally, the protein LRP1 acts as a molecular gatekeeper, binding to Aβ and transporting it across the BBB for elimination. In Alzheimer’s, this system becomes fragile, leading to Aβ accumulation. The supramolecular drugs mimic LRP1 ligands, binding to Aβ and initiating its clearance, effectively resetting the system and restoring vascular function.
So we may be lucky in that addressing the plaques as a symptom does indeed (allow for) repair of the underlying cause. I guess the question is how long the benefit lasts. What triggers the negative feedback loop in the first place? The article claims long term improvement for the mice, which were genetically programmed for amyloid production. (So maybe not an accurate simulation of the root cause, but perhaps actually more of a steel man test.)
Neither of those are particularly easy procedures, but certainly better than a biopsy (and autopsy!)
The most likely theory I've seen is amyloid causes tau buildup which leads to the majority of the damage. And by the time they give anti-amyloid drugs it's too late and the tau is doing the majority of the damage.
An analogy would be if you have a hole in your house which leads to getting a rat infestation. Once you notice the rat infestation patching the hole isn't going to solve your problem. The hole caused you to get rat shit on your counter, but by the time you fix the hole it's too late to stop the rats from shitting on your counter.
But treating symptoms, esp restoring cognitive function, is a good thing.