A Larger Social Network Enhances Novel Object Location Memory and Reduces Hippocampal Microgliosis in Aged Mice

Abstract

The mammalian hippocampus shows marked decline in function with aging across many species, including humans and laboratory rodent models. This decline frequently manifests in memory impairments that occur even in the absence of dementia pathology. In humans, a number of factors correlate with preserved hippocampal memory in aging, such as exercise, cognitive stimulation and number of social ties. While interventional studies and animal models clearly indicate that exercise and cognitive stimulation lead to hippocampal preservation, there is relatively little research on whether a decline in social ties leads to cognitive decline or vice versa. Even in animal studies of environmental enrichment in aging, the focus typically falls on physical enrichment such as a rotating cast of toys, rather than the role of social interactions. The present studies investigated the hypothesis that a greater number of social ties in aging mice would lead to improved hippocampal function. Aged, female C57/Bl6 mice were housed for 3 months in pairs or large groups (7 mice per cage). Group-housed mice showed greater novel object location memory and stronger preference for a spatial navigation strategy in the Barnes maze, though no difference in escape latency, compared to pair-housed mice. Group-housed mice did not differ from pair-housed mice in basal corticosterone levels or adult hippocampal neurogenesis. Group-housed mice did, however, show reduced numbers of Iba1/CD68+ microglia in the hippocampus. These findings suggest that group housing led to better memory function and reduced markers of neuroinflammation in aged mice. More broadly, they support a causative link between social ties and hippocampal function, suggesting that merely having a larger social network can positively influence the aging brain. Future research should address the molecular mechanisms by which a greater number of social ties alters hippocampal function.

Tau Deletion Prevents Cognitive Impairment and Mitochondrial Dysfunction Age Associated by a Mechanism Dependent on Cyclophilin-D

“…Sociability and social memory are processed by the prefrontal cortex, hippocampus, hypothalamus, and amygdala ( Bicks et al, 2015 ). In aging, a reduced preference for novel conspecific individuals occurs ( Charles and Carstensen, 2010 ; Smith et al, 2018 ). To evaluate whether tau deletion modified social abilities during aging, we performed a social interaction test ( Figure 2 ; Jara et al, 2018 ).…”

Enriched Physical Environment Attenuates Spatial and Social Memory Impairments of Aged Socially Isolated Mice

“…It is well known that EE can enhance brain plasticity and cognitive reserves in the elderly ( Kempermann et al, 2002 ; Leal-Galicia et al, 2008 ). However, social interaction alone has been shown to improve novel object location memory and reduces hippocampal inflammation ( Smith et al, 2018 ). On the other hand, long-term exercise plays a positive effect on hippocampal neurogenesis throughout life ( Hamilton et al, 2015 ), but exercise-induced neurogenesis can be significantly averted by SI ( Stranahan et al, 2006 ; Leasure and Decker, 2009 ).…”

Methanolic extract of Tamarix Gallica attenuates hyperhomocysteinemia induced AD-like pathology and cognitive impairments in rats

“…Patients suffering from severe HHcy manifest typical clinical cardiovascular symptoms as well as neurological disorders, such as cerebral atrophy, dementia and seizures [38] while STAT3 overactivation in microglial cells plays an important role in Hcy-induced microglia activation and inflammatory response, both in the brain cortex and the dentate gyrus (DG) region of the hippocampus, following ischemic injury [38]. This inflammation manifests as increased pro-inflammatory cytokine expression by resident microglia, as well as microglia proliferation, and is markedly found in the hippocampus [39]. To determine whether the improvements in cognition found in behavioral tasks following TG treatment were associated with underlying changes in hippocampal neuro-inflammation, we assess inflammatory process in the hippocampus by western blot.…”