Decline of astrocyte Ca2+ signalling in Alzheimer′s disease: STIM1 to the rescue!

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.

Automated summary

Lia et al. discovered the critical role of the STIM1 ER Ca2+ sensor in the functional decline of astrocytes in AD-like pathology in PS2APP mice. The downregulation of STIM1 expression in astrocytes resulted in decreased ER Ca2+ content and impaired astrocytic Ca2+ signaling, leading to synaptic and memory deficits. Overexpression of STIM1 in astrocytes restored Ca2+ excitability and improved synaptic and memory function.