摘要：SummaryParvalbumin (PV)-expressing interneurons which are often associated with the specific extracellular matrix perineuronal net (PNN) play a critical role in the alteration of brain activity and memory performance in Alzheimer’s disease (AD). The integrity of these neurons is crucial for normal functioning of the hippocampal subfield CA2, and hence, social memory formation. Here, we find that social memory deficits of mouse models of AD are associated with decreased presence of PNN around PV cells and long-term synaptic plasticity in area CA2. Furthermore, single local injection of the growth factor neuregulin-1 (NRG1) is sufficient to restore both PV/PNN levels and social memory performance of these mice. Thus, the PV/PNN disruption in area CA2 could play a causal role in social memory deficits of AD mice, and activating PV cell pro-maturation pathways may be sufficient to restore social memory.Graphical abstractDisplay OmittedHighlights•Tg2576 mouse model of AD have normal sociability, but cannot form social memory•Tg2576 mice have less detectable PV interneurons and PNN in hippocampal area CA2•PV-dependent long-term plasticity is altered in CA2 of Tg2576 mice•NRG1 in CA2 increases PV/PNN and restores social memory of these AD miceBehavioral neuroscience; Molecular neuroscience; Cellular neuroscience
