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Erythropoietin improves memory function with reducing endothelial dysfunction and amyloid‐beta burden in Alzheimer’s disease models
Author(s) -
Lee SoonTae,
Chu Kon,
Park JungEun,
Jung KeunHwa,
Jeon Daejong,
Lim JiYoun,
Lee Sang Kun,
Kim Manho,
Roh JaeKyu
Publication year - 2012
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.2011.07534.x
Subject(s) - erythropoietin , synaptophysin , endocrinology , angiogenesis , medicine , hippocampus , amyloid beta , amyloid precursor protein , rage (emotion) , pathogenesis , alzheimer's disease , erythropoietin receptor , neuroscience , disease , biology , immunohistochemistry
J. Neurochem. (2012) 120 , 115–124. Abstract Neurovascular degeneration contributes to the pathogenesis of Alzheimer’s disease (AD). Because erythropoietin (EPO) promotes endothelial regeneration, we investigated the therapeutic effects of EPO in animal models of AD. In aged Tg2576 mice, EPO receptors (EPORs) were expressed in the cortex and hippocampus. Tg2576 mice were treated with daily injection of EPO (5000 IU/kg/day) for 5 days. At 14 days, EPO improved contextual memory as measured by fear‐conditioning test. EPO enhanced endothelial proliferation and the level of synaptophysin expression in the brain. EPO also increased capillary density, and decreased the level of the receptor for advanced glycation endproducts (RAGE) in the brain, while decreasing in the amount of amyloid plaque and amyloid‐β (Aβ). In cultured human endothelial cells, EPO enhanced angiogenesis and suppressed the expression of the RAGE. These results show that EPO improves memory and ameliorates endothelial degeneration induced by Aβ in AD models. This pre‐clinical evidence suggests that EPO may be useful for the treatment of AD.