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Exercise improves cognition and hippocampal plasticity in APOE ɛ4 mice
Author(s) -
Nichol Kathryn,
Deeny Sean P.,
Seif Joseph,
Camaclang Kevin,
Cotman Carl W.
Publication year - 2009
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2009.02.006
Subject(s) - synaptophysin , hippocampal formation , apolipoprotein e , hippocampus , neurotrophic factors , brain derived neurotrophic factor , endocrinology , genetically modified mouse , medicine , psychology , synaptic plasticity , synapsin i , cognition , neuroplasticity , neuroscience , cognitive decline , transgene , receptor , dementia , biology , immunohistochemistry , biochemistry , vesicle , disease , membrane , gene , synaptic vesicle
Background Human studies on exercise, cognition, and apolipoprotein E ( APOE ) genotype show that ɛ4 carriers may benefit from regular physical activity. Methods We examined voluntary wheel‐running, memory, and hippocampal plasticity in APOE ɛ3 and APOE ɛ4 transgenic mice at 10–12 months of age. Results Sedentary ɛ4 mice exhibited deficits in cognition on the radial‐arm water maze (RAWM), a task dependent on the hippocampus. Six weeks of wheel‐running in ɛ4 mice resulted in improvements on the RAWM to the level of ɛ3 mice. Hippocampal brain‐derived neurotrophic factor (BDNF) levels were similar in ɛ3 and ɛ4 mice, and after exercise BDNF was similarly increased in both ɛ3 and ɛ4 mice. In sedentary ɛ4 mice, tyrosine kinase B (Trk B) receptors were reduced by 50%. Exercise restored Trk B in ɛ4 mice to the level of ɛ3 mice, and in ɛ4 mice, exercise dramatically increased synaptophysin, a marker of synaptic function. Conclusions Our results support the hypothesis that exercise can improve cognitive function, particularly in ɛ4 carriers.