Israel Sekler

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 Mfn2's role in promoting NCLX-mediated Ca2+ release from mitochondria, linking mitochondrial ROS to mitophagy via Ca2+ signaling.

This study identifies NCLX as the primary mitochondrial Ca2+ extruder in hepatocytes, linking hormone-mediated mitochondrial Ca2+ oscillations to gluconeogenesis.

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.

The paper shows that neuronal mitochondria respond to firing frequency and EPSP-spike timing by modulating Ca2+ and NAD(P)H levels, affecting metabolic rate and synaptic efficacy.