Introduction: The beneficial effects of physical exercise, in both the treatment and the prevention of several diseases, have been extensively demonstrated. The most common dementia, Alzheimer's disease (AD), is a disorder in which exercise induces significant improvement at pathophysiopathological and cognitive levels. In the present work, we studied the relationship between physical exercise, oxidative stress, and cognition in the double transgenic mice model (2×Tg) for AD, APP/PSN1. This model is mainly based on the cerebral deposition of amyloid β plaques.
Material and methods: Eighteen ten-month-old mice were divided into four experimental groups: exercised 2×Tg (2×Tg-E) (n=5), rested 2×Tg (2×Tg-R) (n=5), exercised controls (control-E) (n=4) and rested controls (control-R) (n=4). We trained the animals for twelve weeks with a combination of forced exercise (treadmill running three days/week) and spontaneous wheel running. The animals were evaluated with physical and cognitive tests before and after the training period. We analyzed systemic and cortical oxidative damage and the induction of antioxidant enzymes.
Results: The 2×Tg-R mice showed a decrease in their grip strength and VO(2max) as they grew older which was prevented by training. The 2×Tg-E group showed better memory than the 2×Tg-R animals. All the trained groups demonstrated greater exploratory capacity and less anxiety than the sedentary animals. Systemic oxidative damage was slightly decreased in the 2×Tg, although we found no difference in the lipoperoxidation and in the induction of the antioxidant defense in cortex between groups.
Conclusions: Physical exercise leads to improvements in the grip strength, VO(2max), cognition, and memory in 2×Tg mice. These improvements are not significantly related to changes in the antioxidant defenses or a reduction in the oxidative damage brought about by exercise.
Copyright © 2012 SEGG. Published by Elsevier Espana. All rights reserved.