Recombinant Human Erythropoietin Suppresses Symptom Onset and Progression of G93a-sod1 Mouse Model of Als by Preventing Motor Neuron Death and Inflammation.
From: Department of Neurology, College of Medicine, Hanyang University, Seoul, Korea.
The European journal of neuroscience
- Publish Date: Apr 2007
- ISSN: 0953-816X
- Volume: 25
- Issue: 7
- Pages: 1923-30
- Medium: Print
- Language: English
- Citation (JAMA): Koh Seong-Ho, Kim Youngchul, Kim Hyun Young, et al. Recombinant Human Erythropoietin Suppresses Symptom Onset and Progression of G93a-sod1 Mouse Model of Als by Preventing Motor Neuron Death and Inflammation.. Eur. J. Neurosci. Apr 2007;25:1923-30
Abstract
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 imu 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.
Mesh Headings (Keywords): Amyotrophic Lateral Sclerosis, Animals, Dinoprostone, Disease Models, Animal, Disease Progression, Erythropoietin, Recombinant, Humans, Inflammation, Mice, Mice, Transgenic, Motor Neurons, Rotarod Performance Test, Spinal Cord, Superoxide Dismutase, Survival Rate
Check for Full Text / PubMed Unique Identifier (PMID): 17439481
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