Estela Área-Gómez

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.

The paper identifies a serum lipidomic signature in asymptomatic Alzheimer's disease mutation carriers that differentiates them from non-carriers and correlates with dementia risk factors.

This study shows that loss of nuclear TDP-43 in microglia-like cells disrupts lipid metabolism, leading to increased lipid droplets, phagocytosis, and inflammation, which can be mitigated by DGAT inhibitors.

This paper investigates the role of alpha-synuclein in lipid regulation at MAM domains in synucleinopathies, showing disease-specific lipid alterations and Syn's impact on phosphatidylserine metabolism.

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

The paper uses single-nucleus RNA- and ATAC-sequencing to identify a CD83+ microglial subpopulation depleted in Parkinson's disease, with implications for neuronal vulnerability.

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