TREADMILL EXERCISE ENHANCES SYNAPTIC PLASTICITY, BUT DOES NOT ALTER β-AMYLOID DEPOSITION IN HIPPOCAMPI OF AGED APP/PS1 TRANSGENIC MICE

Several studies reveal that the beneficial effects of exercise interventions are dependent on the progression of Alzheimer's disease (AD). We have previously shown that long-term treadmill exercise begun before the onset of beta-amyloid (A beta) pathology prevents the deficits of cognition and long-term potentiation (LTP) in amyloid precursor protein (APP)/presenilin 1 (PS1) transgenic mice (8 months of age) paralleled by the reduction of soluble A beta levels and A beta deposition in the hippocampus. In the present study, treadmill exercise was initiated at a developed A beta deposition stage in order to further investigate whether or not treadmill exercise in this phase can delay the progression of AD in aged APP/PS1 mice (17 months of age). Our results show that 5-month treadmill exercise ameliorates the impairment of spatial learning and memory with age paralleled by synaptic plasticity enhancement in aged APP/PS1 mice. In addition, exercise-induced enhancement of synaptic plasticity was accompanied by a significant reduction of soluble A beta levels rather than A beta plaque deposition. Therefore, the investigation demonstrates that long-term treadmill exercise has beneficial effects on cognition and synaptic plasticity even when the brain has developed A beta deposition, and changes in soluble A beta levels rather than A beta plaque deposition may contribute to exercise-induced benefits. (C) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.