Rescue of astrocyte activity by the calcium sensor STIM1 restores long-term synaptic plasticity in female mice modelling Alzheimer’s disease

Abstract

Altered Ca2+ signaling is involved in the pathogenesis of Alzheimer’s disease. Here, the authors show Ca2+ hypoactivity in astrocytes at plaque deposition onset related to reduced expression of the Ca2+ sensor STIM1 and impaired synaptic plasticity that was rescued by STIM1 overexpression in astrocytes.