title: Environmental enrichment compensates for the effects of stress on disease progression in Tg2576 mice, an Alzheimer's disease model.
abstract: Various environmental factors are known to influence the onset and progression of Alzheimer's disease (AD). Environmental enrichment was reported to improve cognitive performance in various Alzheimer's transgenic mice via an amyloid-related or unrelated mechanism. However, stress has been found to accelerate amyloid deposition and cognitive deficits in many AD models. The aim of this study was to determine whether environmental enrichment compensates for the effects of stress on disease progression in the Tg2576 mice, an established AD model. We housed Tg2576 mice under environmental enrichment, enrichment plus stress, stress, or control conditions at 3 months of age. In this study, we first report that environmental enrichment counteracts the effects of stress in terms of cognitive deficits, tau phosphorylation, neurogenesis, and neuronal proliferation during AD-like disease progression. These results strongly implicate the importance of environmental factors as a major modulator for the disease progression of AD.
authors.affiliation: Department of Pharmacology, College of Medicine, National Creative Research Initiative Centre for Alzheimer's Dementia and Neuroscience Research Institute, MRC, Seoul National University, Seoul, Korea.
authors.forename: Yun Ha
authors.initials: YH
authors.lastname: Jeong
authors.forename: Joon Min
authors.initials: JM
authors.lastname: Kim
authors.forename: Jongman
authors.initials: J
authors.lastname: Yoo
authors.forename: Sang Hyung
authors.initials: SH
authors.lastname: Lee
authors.forename: Hye-Sun
authors.initials: HS
authors.lastname: Kim
authors.forename: Yoo-Hun
authors.initials: YH
authors.lastname: Suh
mesh_terms: D000367:Age Factors; D000544:Alzheimer Disease / Q000097:blood / Q000150:complications / Q000235:genetics / Q000628:therapy*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics*; D000704:Analysis of Variance; D000818:Animals; D002465:Cell Movement / Q000502:physiology; D003345:Corticosterone / Q000097:blood; D051360:Cyclin-Dependent Kinase 5 / Q000378:metabolism; D018891:Dentate Gyrus / Q000166:cytology / Q000502:physiology; D004195:Disease Models, Animal; D018450:Disease Progression; D000089622:Doublecortin Domain Proteins; D004777:Environment; D004797:Enzyme-Linked Immunosorbent Assay / Q000379:methods; D005260:Female; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006801:Humans; D018782:Maze Learning / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D055495:Neurogenesis / Q000502:physiology; D009479:Neuropeptides / Q000378:metabolism; D010446:Peptide Fragments / Q000378:metabolism; D010770:Phosphotransferases / Q000378:metabolism; D018809:Proliferating Cell Nuclear Antigen / Q000378:metabolism; D013315:Stress, Psychological / Q000503:physiopathology*; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; C492235:Cdk5r1 protein, rat; D000089622:Doublecortin Domain Proteins; D008869:Microtubule-Associated Proteins; D009479:Neuropeptides; D010446:Peptide Fragments; D018809:Proliferating Cell Nuclear Antigen; C078592:amyloid beta-protein (1-40); C075222:amyloid beta-protein (1-42); D016875:tau Proteins; D010770:Phosphotransferases; D051360:Cyclin-Dependent Kinase 5; D000071679:Glycogen Synthase Kinase 3 beta; D038362:Glycogen Synthase Kinase 3; D003345:Corticosterone