Low intensity exercise attenuates disease progression and stimulates cell proliferation in the spinal cord of a mouse model with progressive motor neuronopathy

• Published in: Neuroscience 2008-03, Vol.152 (2), p.291-5
• Main Authors: Ferrer-Alcon, Marcel, Winkler-Hirt, Carine, Madani, Rime, Perrin, Florence E., Kato, Ann
• Format: Article
• Language: English
• Subjects: Analysis of Variance; Animals; Antibodies; Bromodeoxyuridine; Cell Count; Cell Proliferation; Disease Models, Animal; Disease Progression; Insulin-Like Growth Factor I; Life Sciences; Mice; Mice, Neurologic Mutants; Motor Neuron Disease; Motor Neurons; Muscle Fibers, Skeletal; Neurons and Cognition; Physical Conditioning, Animal; Spinal Cord
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2007.11.058

Physical exercise has been shown to stimulate neurogenesis, increase resistance to brain trauma and disease, improve learning and increase levels of growth factors. We show that low intensity exercise has profound effects on the phenotype of a mouse mutant with progressive motor neuronopathy. These animals normally die at 47 days of age due to motoneuron loss and muscle atrophy. When mice undergo low intensity exercise, their lifespan increased by 74%, they exhibited a decreased loss of motoneurons, improved muscle integrity and a twofold increase in proliferating cells in the spinal cord. The molecular mechanism of neuroprotection may be related to insulin-like-growth factor 1 (IGF-1) since injections of antibodies to IGF-1 abrogated the effects of exercise on the increased life-span. Thus IGF-1 may act as a possible "exercise-induced" neuroprotective factor.