Unveiling the biological mechanisms underlying misfolded amyloid-β clearance at the blood–brain barrier

Abstract

Amyloid-β build-up in the brain is a defining feature of Alzheimer's disease, and the evidence points to failed clearance rather than overproduction as the cause.

The blood–brain barrier handles that clearance through low-density lipoprotein receptors, which sort their cargo by avidity: high-avidity molecules are retained and degraded, mid-avidity ones are transcytosed in tubular vesicles stabilised by PACSIN2.

This work asks which cellular machinery different amyloid-β assemblies engage at the barrier, and whether any of it is a viable therapeutic target.

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