title: The combination of exercise training and alpha-lipoic acid treatment has therapeutic effects on the pathogenic phenotypes of Alzheimer's disease in NSE/APPsw-transgenic mice.
abstract: Exercise training was suggested as a practical therapeutic strategy for human subjects suffering from Alzheimer's disease (AD) in our previous study. Therefore, the purpose of this study was to investigate the effects of combining exercise training with the administration of antioxidants on the pathological phenotype of AD. To accomplish this, non-transgenic mice (Non-Tg) and NSE/APPsw Tg mice were treated with alpha-lipoic acid and treadmill exercised for 16 weeks, after which their brains were evaluated to determine whether any changes in the pathological phenotype-related factors occurred. The results indicated that (i) the combination-applied (COMA) Tg group with exercise training (ET) and alpha-lipoic acid administration (LA) showed ameliorated spatial learning and memory compared to the sedentary (SED)-Tg and single-treatment groups; (ii) there were no differences in the level of Abeta-42 peptides across groups; (iii) the level of glucose transporter-1 and brain-derived neurotrophic factor proteins were highly increased in the COMA group, (iv) ET and LA did not induce a synergistic effect on the expression of heat shock protein-70 and apoptotic proteins including Bax and caspase-3; (v) the levels of SOD-1 and CAT suppressing oxidative stress were extensively higher in the COMA than in the single-treated groups and (vi) there were no significant differences across groups regarding these serum characteristics, although these levels were lower than the SED-Tg group. Taken together, these results suggest that the combination with ET and LA may contribute to protect the neuron injury induced by Abeta peptides and may be considered an effective therapeutic strategy for human subjects suffering from AD.
authors.affiliation: Exercise Biochemistry Laboratory, Korea National Sport University, Seoul 138-763, Korea. chojy86@knsu.ac.kr
authors.forename: Joon Y
authors.initials: JY
authors.lastname: Cho
authors.forename: Hyun S
authors.initials: HS
authors.lastname: Um
authors.forename: Eun B
authors.initials: EB
authors.lastname: Kang
authors.forename: In H
authors.initials: IH
authors.lastname: Cho
authors.forename: Chul H
authors.initials: CH
authors.lastname: Kim
authors.forename: Jung S
authors.initials: JS
authors.lastname: Cho
authors.forename: Dae Y
authors.initials: DY
authors.lastname: Hwang
mesh_terms: D000544:Alzheimer Disease / Q000473:pathology / Q000503:physiopathology / Q000628:therapy; D016229:Amyloid beta-Peptides / Q000235:genetics / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D019208:Brain-Derived Neurotrophic Factor / Q000378:metabolism; D053148:Caspase 3 / Q000378:metabolism; D002374:Catalase / Q000378:metabolism; D002415:Cats; D005081:Exercise Therapy; D051272:Glucose Transporter Type 1 / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000378:metabolism; D006801:Humans; D008568:Memory / Q000187:drug effects / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D009483:Neuropsychological Tests; D010751:Phosphopyruvate Hydratase / Q000235:genetics*; D010805:Physical Conditioning, Animal; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000378:metabolism; D013482:Superoxide Dismutase / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D008063:Thioctic Acid / Q000627:therapeutic use*; D051028:bcl-2-Associated X Protein / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D000975:Antioxidants; D019208:Brain-Derived Neurotrophic Factor; D051272:Glucose Transporter Type 1; D018840:HSP70 Heat-Shock Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; C000606290:SOD1 protein, human; D051028:bcl-2-Associated X Protein; D008063:Thioctic Acid; D002374:Catalase; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D053148:Caspase 3; D010751:Phosphopyruvate Hydratase