Social housing promotes cognitive function through enhancing synaptic plasticity in APP/PS1 mice

Abstract

Previous studies have shown that loneliness increases the risk of AD (Alzheimer’s disease) onset, while active and frequent social housing delays the onset of cognitive impairment. The mechanism of how this occurs remains unclear. In this study, we investigated how social interaction affected cognitive function and AD pathology in APP/PS1 (amyloid precursor protein/presenilin-1) mice. APP/PS1 mice were divided into either a social isolation (SI) group, a social contact with one mouse (SCO) group, or a social contact with five mice (SCF) group. Our results demonstrated that social housing improved the behavioral performance of APP/PS1 mice in Morris Water Maze testing, without significantly altering the rates of amyloid plaque deposition or amyloidogenic APP processes. Furthermore, the synaptic function, dendritic spine density, and complexity of neuronal network were notably increased in the SCF group, as compared to the SI and SCO groups. Additional protein and mRNA analyses of isolated astrocyte and microglia revealed that several glial genes related to regulation and anti-inflammatory progression were significantly upregulated, while pro-inflammatory markers were decreased. These findings highlight the important role of quality social communication (five mice not one mice) on maintaining neuronal function during AD pathogenesis and provide evidence to place great emphasis of family care of AD patients.