Unveiling the biological mechanisms underlying misfolded Amyloid-β clearance at the Blood-Brain Barrier
Misfolded Amyloid-β (Aβ) accumulation in the brain is a key feature of Alzheimer’s disease, primarily linked to impaired clearance rather than overproduction. The blood-brain barrier (BBB) controls Aβ transport via lowdensity lipoprotein receptors (LDLR), which sort cargo based on avidity. High-avidity molecules are retained and degraded, while mid-avidity cargoes are transcytosed through tubular vesicles stabilized by PACSIN2. Our research focuses on unveiling the cellular mechanisms triggered by different Aβ assemblies at the BBB to identify potential therapeutic targets for Alzheimer’s disease.
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