title: Magnesium supplementation does not delay disease onset or increase survival in a mouse model of familial ALS.
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.
authors: Department of Pathology D06, The University of Sydney, New South Wales 2006, Sydney, Australia. rogerp@med.usyd.edu.au
authors: Roger
authors: R
authors: Pamphlett
authors: Elizabeth
authors: E
authors: Todd
authors: Robert
authors: R
authors: Vink
authors: Robert
authors: R
authors: McQuilty
authors: Surindar S
authors: SS
authors: Cheema
mesh_terms: D017668:Age of Onset; D000690:Amyotrophic Lateral Sclerosis / Q000378:metabolism / Q000517:prevention & control / Q000628:therapy*; D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology* / Q000627:therapeutic use; D018698:Glutamic Acid / Q000378:metabolism*; D018737:Hand Strength; D008274:Magnesium / Q000494:pharmacology* / Q000627:therapeutic use; D051379:Mice; D008822:Mice, Transgenic; D018908:Muscle Weakness / Q000188:drug therapy / Q000209:etiology / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000378:metabolism; D013482:Superoxide Dismutase / Q000172:deficiency / Q000235:genetics; D000072105:Superoxide Dismutase-1; D015996:Survival Rate; D017211:Treatment Failure
chemical_list: D018691:Excitatory Amino Acid Antagonists; D016194:Receptors, N-Methyl-D-Aspartate; C000606290:SOD1 protein, human; D018698:Glutamic Acid; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D008274:Magnesium