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Effects of voluntary exercise on cognition, neurogenesis, and plaque load in a mouse model of Alzheimers disease.
Author(s) -
MaliszewskaCyna Ewelina,
McLaurin JoAnne,
Aubert Isabelle
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.712.33
Subject(s) - neurogenesis , genetically modified mouse , hippocampal formation , hippocampus , neun , cognition , neuroplasticity , neuroscience , transgene , alzheimer's disease , physical exercise , psychology , medicine , disease , biology , immunohistochemistry , gene , biochemistry
Alzheimer's disease (AD) is a neurodegenerative disorder leading to cognitive impairment and disruption of adult neurogenesis. It has been shown that exercise influences adult neurogenesis, synaptic plasticity, and cognitive functions in animal models. In healthy adults and AD patients, studies are suggesting that exercise has potential benefits on cognitive functions. However, we only begin to understand the global effects that exercise can have on amyloid pathology, neuronal plasticity, and cognition in AD mouse models. Here we evaluated the effects of moderate voluntary exercise on cognition, neurogenesis, and plaque burden by giving mice access to running wheels for 1 and 2 months and assessing their functional recovery. We used an AD mouse model of amyloid pathology and their non‐transgenic littermates as control. Our results show an improvement in hippocampal‐dependent spatial and non‐spatial memory in transgenic mice exercising for 2 months compared to non‐running transgenic mice. Transgenic exercising animals also showed significantly greater levels of hippocampal adult neurogenesis (increase in BrdU/NeuN positive cells), and increase in survival of newborn cells (increase in BrdU positive cells). Plaque burden, evaluated as the mean plaque size and plaque number, in the hippocampus was not statistically different in runners compared to non‐runners transgenic mice. In summary, exercise improved spatial working memory in an AD mouse model of amyloidoisis without reducing plaque burden. This improvement was accompanied by an increase in neurogenesis. We conclude that physical voluntary exercise has the potential to improve cognition even in presence of high levels of amyloid pathology.