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 β-amyloid (Aβ) 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 Aβ levels and Aβ deposition in the hippocampus. In the present study, treadmill exercise was initiated at a developed Aβ 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 Aβ levels rather than Aβ 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 Aβ deposition, and changes in soluble Aβ levels rather than Aβ plaque deposition may contribute to exercise-induced benefits.
Department of Sports Medicine, China Medical University, Shenyang 110122, PR China; Department of Human Anatomy, China Medical University, Shenyang 110122, PR China.
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G
Zhao
Department of Sports Medicine, China Medical University, Shenyang 110122, PR China.
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HL
Liu
Department of Sports Medicine, China Medical University, Shenyang 110122, PR China.
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H
Zhang
Department of Human Anatomy, China Medical University, Shenyang 110122, PR China. Electronic address: txjcmu@aliyun.com.
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XJ
Tong
D000375:Aging; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology / Q000534:rehabilitation*; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D004195:Disease Models, Animal; D004558:Electric Stimulation; D005080:Exercise Test; D006624:Hippocampus / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D009154:Mutation / Q000235:genetics; D009473:Neuronal Plasticity / Q000502:physiology*; D010805:Physical Conditioning, Animal / Q000379:methods*; D053764:Presenilin-1 / Q000235:genetics; D011930:Reaction Time / Q000235:genetics; D065852:Spatial Memory / Q000502:physiology; D055366:Synaptic Potentials / Q000235:genetics
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C508853:PSEN1 protein, human; D053764:Presenilin-1
APP/PS1 transgenic mice; Alzheimer’s disease; learning and memory; synaptic plasticity; treadmill exercise; β-amyloid