Maria Ankarcrona

This study shows that modulating mitochondria-ER contacts reduces inflammasome activation and restores Aβ phagocytosis in AD microglia.

This study identifies mitoEV-mediated mitochondrial transfer from astrocytes to neurons as a compromised pathway in early Alzheimer's disease, revealing its role in supporting neuronal energy metabolism.

The paper develops a computational model of mitochondrial bioenergetics and integrates it with experimental data from Parkinson's Disease models to predict molecular defects and provide a resource for interpreting bioenergetic experiments.

This study identifies mitochondrial localization as a barrier to ubiquitin-dependent degradation of aggregation-prone proteins, showing that inhibiting eIF5A reduces mitochondrial retention and enhances degradation.

The paper introduces PRINCESS, a novel biosensor that simultaneously detects membrane contact sites and measures associated Ca2+ dynamics using splitFAST technology.

This study identifies early mitochondrial dysfunction, neuroinflammation, and autophagy impairment in App knock-in Alzheimer's mouse models through time-course transcriptome analysis.