Gary A. Silverman

This study investigates age-related changes in mitochondrial dynamics and autophagy in reprogrammed human neurons, finding that autophagy enhancement can reverse these age-dependent alterations.

This study identifies de novo ATP5F1A variants causing neurological disorders through dominant negative mechanisms, expanding the known phenotypic and genotypic spectrum of complex V deficiency.

This study shows that a mutation in the MAPT gene disrupts autophagy in neurons, leading to Tau accumulation, and that an autophagy enhancer drug reduces Tau levels.

The paper functionally validates a de novo PPP5C variant in a human proband using C. elegans, showing it causes loss-of-function and is likely responsible for the patient's phenotypes.

The paper performs a quantitative systems pharmacology analysis of 225 autophagy modulators to uncover their molecular mechanisms and regulatory pathways.

This paper builds a computational model to study how cells decide between autophagy and apoptosis under stress, revealing that cytoplasmic Ca2+ acts as a rheostat regulated by G-protein signaling and AMPK.