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

Annamaria Lia, Gabriele Sansevero, Angela Chiavegato, Miriana Sbrissa, Diana Pendin, Letizia Mariotti, Tullio Pozzan, Nicoletta Berardi, Giorgio Carmignoto (), Cristina Fasolato () and Micaela Zonta ()
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Annamaria Lia: National Research Council (CNR)
Gabriele Sansevero: National Research Council (CNR)
Angela Chiavegato: University of Padua
Miriana Sbrissa: University of Padua
Diana Pendin: National Research Council (CNR)
Letizia Mariotti: National Research Council (CNR)
Tullio Pozzan: National Research Council (CNR)
Nicoletta Berardi: National Research Council (CNR)
Giorgio Carmignoto: National Research Council (CNR)
Cristina Fasolato: University of Padua
Micaela Zonta: National Research Council (CNR)

Nature Communications, 2023, vol. 14, issue 1, 1-15

Abstract: Abstract Calcium dynamics in astrocytes represent a fundamental signal that through gliotransmitter release regulates synaptic plasticity and behaviour. Here we present a longitudinal study in the PS2APP mouse model of Alzheimer’s disease (AD) linking astrocyte Ca2+ hypoactivity to memory loss. At the onset of plaque deposition, somatosensory cortical astrocytes of AD female mice exhibit a drastic reduction of Ca2+ signaling, closely associated with decreased endoplasmic reticulum Ca2+ concentration and reduced expression of the Ca2+ sensor STIM1. In parallel, astrocyte-dependent long-term synaptic plasticity declines in the somatosensory circuitry, anticipating specific tactile memory loss. Notably, we show that both astrocyte Ca2+ signaling and long-term synaptic plasticity are fully recovered by selective STIM1 overexpression in astrocytes. Our data unveil astrocyte Ca2+ hypoactivity in neocortical astrocytes as a functional hallmark of early AD stages and indicate astrocytic STIM1 as a target to rescue memory deficits.

Date: 2023
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DOI: 10.1038/s41467-023-37240-2

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