title: Moderate exercise delays the motor performance decline in a transgenic model of ALS.
abstract: The relationship between exercise and amyotrophic lateral sclerosis (ALS), a neurodegenerative disorder characterized by motor neuron loss, rapidly progressive weakness and early death has been controversial. We studied the effect of a high (HEX) and moderate-level exercise (MEX) on body weight, motor performance and motor neuron counts in the ventral horn of spinal cords in a transgenic mouse model of ALS (G93A-SOD1) that overexpresses a mutated form of the human SOD1 gene that is a cause of familial ALS. These transgenic mice show several similarities to the human disease, including rapid progressive motor weakness from 100 days of age and premature death at around 135 days of age. Mice were exposed to high or mid-level exercise of left sedentary (SED). At 70, 95 and 120 days of age, spinal cords were processed following euthanasia. Motor neurons larger than 15 mum in diameter were counted with a design-based stereological protocol using an optical fractionator probe in the ventral horn of different regions of the cord and compared to wild-type littermates. Moderate exercise delayed the onset of motor deficit by over a week. High exercise slightly but significantly hastened the onset of motor performance deficits. Motor neuron density in the lumbar cord was significantly higher in MEX group compared to SED at 95 days of age. These results show the beneficial effects of moderate exercise on the preservation of motor performance that correlates with higher motor neuron density in the ventral horn of the lumbar spinal cord in G93A mice.
authors.affiliation: Department of Biochemistry, Boston University School of Medicine, Boston, MA, USA.
authors.forename: Isabel
authors.initials: I
authors.lastname: Carreras
authors.forename: Sinan
authors.initials: S
authors.lastname: Yuruker
authors.forename: Nurgul
authors.initials: N
authors.lastname: Aytan
authors.forename: Lokman
authors.initials: L
authors.lastname: Hossain
authors.forename: Ji-Kyung
authors.initials: JK
authors.lastname: Choi
authors.forename: Bruce G
authors.initials: BG
authors.lastname: Jenkins
authors.forename: Neil W
authors.initials: NW
authors.lastname: Kowall
authors.forename: Alpaslan
authors.initials: A
authors.lastname: Dedeoglu
mesh_terms: D017668:Age of Onset; D000690:Amyotrophic Lateral Sclerosis / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D001835:Body Weight / Q000502:physiology; D002452:Cell Count; D004195:Disease Models, Animal; D020820:Dyskinesias / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008159:Lumbar Vertebrae; D008297:Male; D051379:Mice; D008822:Mice, Transgenic; D009043:Motor Activity / Q000502:physiology; D009046:Motor Neurons / Q000473:pathology / Q000502:physiology; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011897:Random Allocation; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology; D013482:Superoxide Dismutase / Q000235:genetics; D000072105:Superoxide Dismutase-1; D013997:Time Factors
chemical_list: C000606290:SOD1 protein, human; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1