Kirstin A. Tamucci

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

This study shows how non-coding variants in CD33 affect Alzheimer's risk by altering CD33M dimerization and interactions with clusterin and Aβ, impacting microglial function.

This study identifies CD45 as a sialic acid-dependent binding partner of CD33, showing that their interaction contributes to Alzheimer's disease susceptibility through impaired microglial function.

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.