Abstract
Lia et al. [1] discovered the critical role of STIM1 ER Ca2+ sensor in the functional decline of astrocytes in the AD-like pathology in PS2APP mice. Profound downregulation of STIM1 expression in astrocytes in the disease results in the decreased ER Ca2+ content and severely impaired evoked as well as spontaneous astrocytic Ca2+ signalling. Aberrant astrocytic Ca2+ signalling translated into impaired synaptic plasticity and memory. Astrocyte-specific overexpression of STIM1 restored Ca2+ excitability and rectified synaptic and memory deficits.
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