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Ann Clin Neurophysiol > Volume 7(2); 2005 > Article
Ann Clin Neurophysiol. 2005; 7(2): 101-106.
Neuroprotective Effects of Multi-vitamin Therapy in Transgenic Mouse Model of Amyotrophic Lateral Sclerosis
Ju-Hong Min, Jong-Ha Park, Ae-shin Cho, Mi-Yeon Kim, and Yoon-Ho Hong
Copyright © 2005 The Korean Society of Clinical Neurophysiology
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
Background: There is no currently effective treatment for amyotrophic lateral sclerosis (ALS), although this disorder is a progressive neurodegenerative disease resulting in death within several years. Because recent evidence suggests that homocysteine (HC) is highly related to neurodegenerative disorders with aging, we tried to elucidate the effects of multi-vitamin therapy on G93A SOD1 transgenic mice.
Methods: We treated this murine model of ALS with multi-vitamin (folic acid 1.97 mg/day, pyridoxine 0.98 mg/day, cyanocobalamin 0.1 mg/day) from 45 days of age, per oral. We performed the rotarod test from postnatal 10th week,weekly.
Results: We found that multi-vitamin reinforcement significantly prolonged average lifespan and delayed disease onset with improvement of motor performance. However, it did not significantly slow disease progression and statistical differences of weight loss were not observed between in transgenic mice and controls.
Conclusions: These results suggest that multi-vitamin can be a potent therapeutic strategy for familial forms of ALS.
Key words: ALS, Copper/zinc superoxide dismutase, SOD1, Vitamin, Homocysteine, Transgenic mice
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