It's correlated, much as body temperature is correlated with infection. But much like lowering body temperature won't cure the infection, directly addressing the amyloid-beta plaques doesn't seem likely to directly address Alzhimer's. Addressing the actual root cause may also make the plaques go away.
>"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.)
