Robert A. Marr

This study shows that excess ER-Ca2+ release via RyR contributes to mitochondrial dysfunction in AD neurons, leading to cellular pathology and that pharmacological inhibition of RyR-Ca2+ release can reverse these effects.

This study identifies calcium dysregulation via RyR as a driver of lysosomal dysfunction and protein aggregation in Alzheimer's disease, showing that dantrolene can restore proteolytic activity in AD models.