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Recombinant human erythropoietin suppresses symptom onset and progression of G93A‐SOD1 mouse model of ALS by preventing motor neuron death and inflammation
Author(s) -
Koh SeongHo,
Kim Youngchul,
Kim Hyun Young,
Won Cho Goang,
Kim Kyung Sook,
Kim Seung H.
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05471.x
Subject(s) - erythropoietin , neuroprotection , inflammation , amyotrophic lateral sclerosis , medicine , programmed cell death , sod1 , cytokine , pharmacology , immunology , neuroscience , apoptosis , biology , disease , biochemistry
Multifactorial pathogenic mechanisms, including inflammation, attenuated survival signals and enhanced death signals, are involved in amyotrophic lateral sclerosis (ALS). Erythropoietin (EPO) has recently been highlighted as a cytokine with various potent neuroprotective effects, including reduction of inflammation, enhancement of survival signals and prevention of neuronal cell death. This study was undertaken to evaluate the effect of recombinant human EPO (rhEPO) on ALS model mice. We treated 96 ALS model mice with vehicle only, or 1, 2.5 or 5 iµ of rhEPO/g of mouse once every other week after they were 60 days old. The treatment significantly prolonged symptom onset and life span, preserved more motor neurons, enhanced survival signals, and attenuated inflammatory signals in a dose‐dependent manner. These data suggest that treatment with rhEPO represents a potential therapeutic strategy for ALS.