Résumé :
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Communication n° 355 A closer insight into the cellular and molecular replies to physical exercise would ave important consequences both at a fundamental and clinical level, notably in the case of human pathologies of the locomotive system. The development of mutant mice designed as models of genetic pathologies of the motor neurons opens new perspectives to test the potential improvement of the motor behaviour induced by exercise. We have recently evaluated the efficiency of swimming-based training on SOD1 (G93A) transgenic mice, a model of Amyotrophic Lateral Sclerosis (ALS) and have shown that the swimming program sustained the motor function and the life span of the ALS mice. Exercised spinal cords displayed a significant delay in the onset of neurone death, as revealed by TUNEL analysis. Histological evaluation of neurone population showed a greater protection of the large motor neurones, considered as particularly liable to toxicity-induced degeneration in ALS. Interestingly, studies using running-based training reported a beneficial albeit modest effect in comparison to the swimming-based protocol in the same strain of ALS mice. To this day, the concept of a differential effect of the training protocol on the neuroprotection potential is not documented. Furthermore, data dealing with the molecular mechanism basis of the exercise-induced neuroprotection are still lacking. Further molecular analysis at the level of the spinal cord are likely to explain why differences between running- and swimming-based training exist in exercise-induced benefices of trained ALS mice.
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