Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/5755
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Type: Journal article
Title: Magnesium supplementation does not delay disease onset or increase survival in a mouse model of familial ALS
Author: Pamphlett, R.
Todd, E.
Vink, R.
McQuilty, R.
Cheema, S.
Citation: Journal of the Neurological Sciences, 2003; 216(1):95-98
Publisher: Elsevier Science BV
Issue Date: 2003
ISSN: 0022-510X
1878-5883
Statement of
Responsibility: 
Roger Pamphlett, Elizabeth Todd, Robert Vink, Robert McQuilty and Surindar S. Cheema
Abstract: Treatment of amyotrophic lateral sclerosis (ALS) with anti-glutamate agents has had some success, but the search continues for more effective glutamate blockers. Magnesium (Mg) ions inhibit the opening of some glutamate receptors, so we increased dietary Mg in a mouse model of ALS in an attempt to modify the course of the disease. From the age of 6 weeks, mutant superoxide dismutase 1 (SOD1) transgenic mice and wild-type controls had either 0, 21.5 or 43 g/l of Mg pidolate added to their drinking water. Disease onset was measured by tests for coordination and forelimb strength, and survival by standard endpoints. Mg levels in the brain were measured in wild-type mice using mass spectrometry. Mutant SOD1 mice on no added Mg became weak at about 105 days, and survived between 114 and 137 days. No difference in either time of onset of weakness, or survival, was seen in mutant SOD1 mice on different doses of Mg. No increase in wild-type brain Mg was found after supplemental Mg. From these results, it appears that a trial of oral Mg supplementation in human ALS is not warranted.
Keywords: Brain; Animals; Mice, Transgenic; Mice; Muscle Weakness; Amyotrophic Lateral Sclerosis; Disease Models, Animal; Magnesium; Superoxide Dismutase; Glutamic Acid; Receptors, N-Methyl-D-Aspartate; Excitatory Amino Acid Antagonists; Hand Strength; Treatment Failure; Survival Rate; Age of Onset; Dose-Response Relationship, Drug; Superoxide Dismutase-1
Description: Copyright © 2003 Elsevier B.V. All rights reserved.
RMID: 0020031047
DOI: 10.1016/S0022-510X(03)00216-8
Appears in Collections:Pathology publications

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