Resistance Exercise Slows the Onset of Pathology in a Mouse Model of Alzheimer's Disease

With the caveat that mouse models of Alzheimer's disease are quite artificial, as aged wild-type mice do not suffer from any condition resembling Alzheimer's, and the models are thus built upon assumptions about which processes are important to the progression of the condition, researchers here show that resistance exercise slows the pathology and loss of cognitive function in one such model. Resistance exercise is well demonstrated to improve metabolism, immune function, and reduce mortality in both older animals and humans. It would not be too surprising to find that sedentary individuals are performing more poorly in the onset of dementia in addition to other aspects of degenerative aging.

Physical exercise has beneficial effects by providing neuroprotective and anti-inflammatory responses to Alzheimer's disease (AD). Most studies, however, have been conducted with aerobic exercise, and few have investigated the effects of other modalities that also show positive effects on AD, such as resistance exercise (RE). In addition to its benefits in developing muscle strength, balance and muscular endurance favoring improvements in the quality of life of the elderly, RE reduces amyloid load and local inflammation, promotes memory and cognitive improvements, and protects the cortex and hippocampus from the degeneration that occurs in AD.

Therefore, the aim of this study was to investigate the effects of 4 weeks of RE intermittent training on the prevention and recovery from these AD-related neuropathological conditions in APP/PS1 mice. For this purpose, 6-7-month-old male APP/PS1 transgenic mice and their littermates, negative for the mutations (Control), were distributed into three groups: Control, APP/PS1, APP/PS1+RE. RE training lasted four weeks and, at the end of the program, the animals were tested in the open field test for locomotor activity and in the object recognition test for recognition memory evaluation. The brains were collected for immunohistochemical analysis of Aβ plaques and microglia, and blood was collected for plasma corticosterone by ELISA assay.

APP/PS1 transgenic sedentary mice showed increased hippocampal Aβ plaques and higher plasma corticosterone levels, as well as hyperlocomotion and reduced central crossings in the open field test, compared to APP/PS1 exercised and control animals. The intermittent program of RE was able to recover the behavioral, corticosterone and Aβ alterations to the Control levels. In addition, the RE protocol increased the number of microglial cells in the hippocampus of APP/PS1 mice. Altogether, the present results suggest that RE plays a role in alleviating AD symptoms, and highlight the beneficial effects of RE training as a complementary treatment for AD.


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