title: Treadmill exercise slows cognitive deficits in aging rats by antioxidation and inhibition of amyloid production.
abstract: Chronic administration of D-galactose simulates the changes in natural senescence and accelerates aging in animal models and has been used in aging research. The present study was undertaken to investigate the molecular mechanisms underlying the effects of exercise on learning and memory in rats with D-galactose-induced aging. The learning and memory performance in aging rats, either after exercise or without exercise, was assessed with the Morris water maze test. The effect of treadmill exercise on the expression of amyloid-β 42 and two key enzymes involved in processing of the β-amyloid precursor protein, a disintegrase and metalloprotease domain 17 and β-site amyloid precursor protein-cleaving enzyme 1, in the hippocampi of rats were monitored using real-time quantitative PCR. Moreover, oxidative stress-associated changes, including changes in superoxide dismutase activity and malondialdehyde content, in the hippocampi were assessed after exercise. Our results showed that treadmill exercise significantly improved learning and memory performance in aging rats. The behavioral changes were likely induced by repression of amyloid-β 42 protein levels, through the upregulation of a disintegrase and metalloprotease domain 17 mRNA and downregulation of β-site amyloid precursor protein-cleaving enzyme 1 mRNA, and a concomitant increase in superoxide dismutase activity and decrease in malondialdehyde content, in rat hippocampi. Our data suggest that exercise may be an effective therapy for alleviating learning and memory decline due to aging or the onset of neurodegenerative diseases.
authors.affiliation: Key Laboratory of Adolescent Health Assessment and Exercise Intervention, Ministry of Education, East China Normal University, Shanghai, China.
authors.forename: Feng
authors.initials: F
authors.lastname: Yu
authors.forename: Bo
authors.initials: B
authors.lastname: Xu
authors.forename: Chenghui
authors.initials: C
authors.lastname: Song
authors.forename: Liu
authors.initials: L
authors.lastname: Ji
authors.forename: Xianliang
authors.initials: X
authors.lastname: Zhang
mesh_terms: D051722:ADAM Proteins / Q000378:metabolism; D000072198:ADAM17 Protein; D000375:Aging / Q000187:drug effects / Q000523:psychology*; D000682:Amyloid / Q000096:biosynthesis*; D053829:Amyloid Precursor Protein Secretases / Q000378:metabolism; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D016282:Aspartic Acid Endopeptidases / Q000378:metabolism; D015153:Blotting, Western; D003071:Cognition / Q000502:physiology*; D005690:Galactose; D006624:Hippocampus / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000502:physiology; D008569:Memory Disorders / Q000139:chemically induced / Q000517:prevention & control / Q000523:psychology; D010446:Peptide Fragments / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000523:psychology*; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D051381:Rats; D017207:Rats, Sprague-Dawley; D060888:Real-Time Polymerase Chain Reaction; D012420:Running / Q000502:physiology; D013482:Superoxide Dismutase / Q000378:metabolism
chemical_list: D000682:Amyloid; D016229:Amyloid beta-Peptides; D000975:Antioxidants; D010446:Peptide Fragments; D012333:RNA, Messenger; C075222:amyloid beta-protein (1-42); D008315:Malondialdehyde; D013482:Superoxide Dismutase; D053829:Amyloid Precursor Protein Secretases; D016282:Aspartic Acid Endopeptidases; C509281:Bace1 protein, rat; D051722:ADAM Proteins; D000072198:ADAM17 Protein; D005690:Galactose