Early influence of voluntary exercise against impairment of learning and memory function in mice induced byβ-amyloid peptide 25-35

Objective To investigate the early influence and the relevant pathway of voluntary exercise against impairment of learning and memory in mice with sporadic Alzheimer’s disease. Methods Twenty-four male C57bl/6 mice (weight (22.5±2.5) g) were randomly divided into 4 groups: control group，exercise control group，model group and treatment group，6 in each group.Intracerebroventricular injection of β-amyloid peptide-25-35 (Aβ25-35) was used to make mock Alzheimer’s disease，and then mice in exercise control group and treatment group were allowed to exercise training for 12 days，non-exercise to control group and model group.Y-maze and open field test were arranged to measure the short-term change of learning，memory and emotions，respectively.Neuronal damage in the hippocampal CA1region was observed by HE staining.The expression level of glial inflammatory response was quantitatively determined with method of immunohistochemistry. Results Aβ25-35 could cause impairment of learning and memory (accuracy in Y maze:52.60±1.46，65.50±2.78，t=4.111，P=0.003;% of dark neruons in CA1in HE staining: 5.11±0.57，2.52±0.52，t=-4.894，P=0.003)，and it could be significantly improved after exercise (accuracy in Y maze:58.57±2.17，52.60±1.46，t=-2.385，P=0.044).Additionally，the level of activated astrocytes and microglia expression in hippocampus decreased by 17.86% (ratio to control: 0.99±0.13，1.17±0.10，t=2.455，P=0.036) and 26.23% (ratio to control:0.93±0.04，1.19±0.11，t=2.412，P=0.043)，respectively. Conclusion Exercise plays an anti-inflammatory role in the progression of Alzheimer’s disease，reducing the nerve cell damage and improving learning and memory function. Key words: Alzheimer disease; Amyloid beta-protein; Exercise; Neuroglia