Delfina Larrea

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.

The paper investigates how traumatic brain injury (TBI) increases mitochondria-associated ER membranes (MAMs) and C99 levels, linking these changes to Alzheimer's disease (AD) through lipid metabolism alterations.

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

The paper investigates how APOE4 affects bioenergetic pathways in specific brain regions of aged mice, finding region-specific differences that may contribute to Alzheimer's disease risk.

This study identifies Cyb5r3 as a mediator of FoxO1-dependent mitochondrial dysfunction in beta-cells, leading to impaired insulin secretion and glucose intolerance.

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