Interval and continuous exercise overcome memory deficits related to β-Amyloid accumulation through modulating mitochondrial dynamics.

Exercise is a non-pharmacological strategy that may help to protect against cognitive decline and reduce the risk of Alzheimer's disease. However, the optimal exercise modes for cognitive benefits are controversial. Mitochondrial function has been related to both exercise and cognition. The present study aimed to investigate the effects of two exercise modes on cognitive function and mitochondrial dynamics in APP/PS1 transgenic mice. The results showed that 12-week high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) could improve exploratory behavior, spatial learning and memory ability of APP/PS1 transgenic mice. Both HIIT and MICT interventions significantly alleviated the hippocampal β-Amyloid (Aβ) burden and mitochondrial fragmentation and improved mitochondrial morphology in hippocampus. Furthermore, both HIIT and MICT interventions down-regulated dynamin-related protein 1 (DRP1) and fission 1 (FIS1), whereas mitofusin 1 (MFN1), mitofusin 2 (MFN2) and optic atrophy 1 (OPA1) were up-regulated. Hippocampal levels of total reactive oxygen species (ROS), malondialdehyde (MDA) and hydrogen peroxide (H2O2) were decreased, whereas activities of superoxide dismutase (SOD) and catalase (CAT) were elevated by HIIT and MICT. The study suggests that both HIIT and MICT alleviate cognitive decline and down-regulat Aβ level in the hippocampus in APP/PS1 transgenic mice, which may be mediated by improvements in mitochondrial morphology and dynamics.