While the article emphasizes the BBB repair aspect, it seems the treatment does ultimately target plaques directly at a mechanical level:
>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.
>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.