期刊
NEUROSCIENCE RESEARCH
卷 178, 期 -, 页码 60-68出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neures.2022.01.003
关键词
Alzheimer ?s disease; Triple transgenic mice; Sensorimotor; Psychomotor; Spatial learning; Forced exercise
资金
- Alzheimers North Carolina, Inc. (Bareiss, Tran, and Lu)
- Harriet and John Wooten Laboratory for Alzheimers and Neurodegenerative Disease Research (Bareiss, Tran, and Lu)
Alzheimer's disease is associated with a decline in cognitive function as well as non-cognitive sensorimotor and psychomotor symptoms. While exercise is believed to be beneficial for AD, its effect on sensorimotor functions is not well understood. In this study, researchers found that exercise can improve sensorimotor function and reduce abnormal behavior in a mouse model of AD.
Alzheimer's disease (AD) is characterized by a progressive decline in cognitive function; however, recent evidence suggests that non-cognitive sensorimotor and psychomotor symptoms accompany early stages of the disease in humans and AD models. Although exercise is emerging as an important therapeutic to combat AD progression, little is known about the effect of exercise on sensorimotor domain functions. The purpose of this study was to determine if early sensorimotor symptoms accompany deficits in Morris water maze (MWM) performance in the 3xTg-AD model, and investigate if exercise could protect against early behavioral decline. 3xTgAD and wild-type (WT) control mice were subjected to 12 weeks of moderate intensity wheel running or remained sedentary. At 6 months of age, animals underwent a series of sensorimotor and MWM testing. 3xTg-AD mice displayed deficits in sensorimotor function (beam traversal, spontaneous activity, and adhesive removal) and MWM performance. Interestingly, 3xTg-AD animals exhibited increased freezing and unusual shaking/ tremoring behaviors not displayed by WT controls. Exercise improved beam traversal, adhesive removal, and reduced the unusual motor-related behaviors in 3xTg-AD mice. Our study shows that sensorimotor symptoms coincide with deficits in MWM performance, and suggest that exercise may mitigate deficits associated with early disease in 3xTg-AD mice.
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