KEVIN R. VELASCO

This study shows that cholesterol availability through HDLs and SR-B1 drives MAM formation, which regulates ER-mitochondria communication and cholesterol metabolism.

This study identifies how C99 disrupts ACSL4 activity and phospholipid homeostasis in Alzheimer's disease by remodeling MAMs and altering PC composition.

This study shows that SR-B1-mediated cholesterol uptake from HDL stimulates MAM formation, which suppresses de novo cholesterol biosynthesis.

This study shows that disrupted MAM function in ALS models leads to altered mitochondrial metabolism, specifically a shift from pyruvate to fatty acid utilization.

This study shows that the C99 fragment of APP regulates cholesterol trafficking between the plasma membrane and ER, contributing to AD pathogenesis.