Erythropoietin improves memory function with reducing endothelial dysfunction and amyloid-beta burden in Alzheimers disease models

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Neurovascular degeneration contributes to the pathogenesis of Alzheimers 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-beta (A beta). 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 A beta in AD models. This pre-clinical evidence suggests that EPO may be useful for the treatment of AD.
Publisher
WILEY-BLACKWELL
Issue Date
2012-01
Language
English
Article Type
Article
Keywords

RECOMBINANT-HUMAN-ERYTHROPOIETIN; BLOOD-BRAIN-BARRIER; AMYOTROPHIC-LATERAL-SCLEROSIS; CIRCULATING ANGIOGENIC CELLS; ACTIVATED PROTEIN-KINASE; LONG-TERM POTENTIATION; MOUSE MODEL; RECEPTOR EXPRESSION; STATUS-EPILEPTICUS; CEREBRAL-ISCHEMIA

Citation

JOURNAL OF NEUROCHEMISTRY, v.120, no.1, pp.115 - 124

ISSN
0022-3042
DOI
10.1111/j.1471-4159.2011.07534.x
URI
http://hdl.handle.net/10203/98589
Appears in Collection
BiS-Journal Papers(저널논문)
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