title: Erythropoietin attenuates Alzheimer-like memory impairments and pathological changes induced by amyloid β42 in mice.
abstract: Amyloid beta (Aβ) is a key molecule in the neurodegenerative progression of Alzheimer׳s disease (AD). It is critical to develop a treatment that can arrest the Aβ-induced pathologic progression of AD. Erythropoietin (EPO) has various protective effects in the nervous system. However, the effect of EPO on Aβ-induced Alzheimer-like cognitive deficits and pathological changes remains unclear. In the present study, we observed that the treatment of mice with EPO (1000 IU/kg) attenuated Aβ42-induced cognitive deficits and tau hyperphosphorylation at multiple AD-related sites through the regulation of glycogen synthase kinase-3β (GSK-3β). We also observed that EPO attenuated the Aβ42-induced mitochondrial dysfunction and apoptosis in brain. These results indicate a potential role for EPO in AD therapy.
authors.affiliation: Department of Pathophysiology, Henan Medical College, Zhengzhou 451191, PR China.
authors.forename: Yi-Pei
authors.initials: YP
authors.lastname: Li
authors.affiliation: Department of Nutrition, Henan Medical College, Zhengzhou 451191, PR China.
authors.forename: Guo-Jun
authors.initials: GJ
authors.lastname: Yang
authors.affiliation: Department of Pathophysiology, Basic Medical College, Zhengzhou University, Zhengzhou 450001, PR China.
authors.forename: Li
authors.initials: L
authors.lastname: Jin
authors.affiliation: Department of Pathophysiology, Henan Medical College, Zhengzhou 451191, PR China.
authors.forename: Hong-Mei
authors.initials: HM
authors.lastname: Yang
authors.affiliation: Department of Pathophysiology, Henan Medical College, Zhengzhou 451191, PR China.
authors.forename: Jie
authors.initials: J
authors.lastname: Chen
authors.affiliation: Department of Basic Medicine, Wuxi Medical School, Jiangnan University, Wuxi 214122, PR China. Electronic address: chaigaoshang@jiangnan.edu.cn.
authors.forename: Gao-Shang
authors.initials: GS
authors.lastname: Chai
authors.affiliation: Department of Pathophysiology, Henan Medical College, Zhengzhou 451191, PR China; The Institute of Gerontology, Henan Medical College, Zhengzhou 451191, PR China. Electronic address: kyk02@126.com.
authors.forename: Li
authors.initials: L
authors.lastname: Wang
mesh_terms: D016229:Amyloid beta-Peptides / Q000633:toxicity*; D000818:Animals; D001362:Avoidance Learning / Q000187:drug effects; D004195:Disease Models, Animal; D042967:Electron Transport Complex I / Q000378:metabolism; D004921:Erythropoietin / Q000627:therapeutic use*; D038362:Glycogen Synthase Kinase 3 / Q000378:metabolism; D000071679:Glycogen Synthase Kinase 3 beta; D006624:Hippocampus / Q000187:drug effects* / Q000473:pathology; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D018782:Maze Learning / Q000187:drug effects; D053078:Membrane Potential, Mitochondrial / Q000187:drug effects; D008569:Memory Disorders / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D051379:Mice; D008810:Mice, Inbred C57BL; D018384:Oxidative Stress / Q000187:drug effects; D010446:Peptide Fragments / Q000633:toxicity*; D010766:Phosphorylation / Q000187:drug effects; D013482:Superoxide Dismutase / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D016875:tau Proteins; D004921:Erythropoietin; D008315:Malondialdehyde; D013482:Superoxide Dismutase; D000071679:Glycogen Synthase Kinase 3 beta; C000605507:Gsk3b protein, mouse; D038362:Glycogen Synthase Kinase 3; D042967:Electron Transport Complex I
keywords: Alzheimer׳s disease; Amyloid β; Apoptosis; Erythropoietin; Tau