Erythropoietin attenuates Alzheimer-like memory impairments and pathological changes induced by amyloid β42 in mice

• Published in: Brain research 2015-08, Vol.1618, p.159-167
• Main Authors: Li, Yi-pei, Yang, Guo-jun, Jin, Li, Yang, Hong-mei, Chen, Jie, Chai, Gao-shang, Wang, Li
• Format: Article
• Language: English
• Subjects: Alzheimer׳s disease; Amyloid beta-Peptides - toxicity; Amyloid β; Animals; Apoptosis; Avoidance Learning - drug effects; Disease Models, Animal; Electron Transport Complex I - metabolism; Erythropoietin; Erythropoietin - therapeutic use; Glycogen Synthase Kinase 3 - metabolism; Glycogen Synthase Kinase 3 beta; Hippocampus - drug effects; Hippocampus - pathology; Male; Malondialdehyde - metabolism; Maze Learning - drug effects; Membrane Potential, Mitochondrial - drug effects; Memory Disorders - chemically induced; Memory Disorders - drug therapy; Memory Disorders - pathology; Mice; Mice, Inbred C57BL; Neurology; Oxidative Stress - drug effects; Peptide Fragments - toxicity; Phosphorylation - drug effects; Superoxide Dismutase - metabolism; Tau; tau Proteins - metabolism
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/j.brainres.2015.05.031

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.