Zinc in the spinal cord of a mutant SOD1 mouse model of ALS.
Both decreases and increases in zinc have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS). We therefore examined the distribution of zinc in transgenic mutant superoxide dismutase 1 (SOD1) mice, a model for ALS. Frozen sections of spinal cord from these mice were stained for free zinc with autometallography. Zinc granules in the spinal anterior horn surrounded motor neuron cell bodies and their processes. The same distribution of zinc was seen in wildtype mice. The onset of weakness in the mutant SOD1 mice did not alter the zinc distribution. Changes in the tissue distribution of free zinc do not appear to play a role in the pathogenesis of mutant SOD1-associated ALS.
Pamphlett
Roger
R
Neuropathology Division, Department of Pathology D06, University of Sydney, NSW 2006, Australia. rogerp@med.usyd.edu.au
Kum-Jew
Stephen
S
D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D004195:Disease Models, Animal; D051379:Mice; D008822:Mice, Transgenic; D009046:Motor Neurons / Q000378:metabolism; D009154:Mutation; D016622:Silver Staining / Q000379:methods; D013116:Spinal Cord / Q000033:anatomy & histology / Q000378:metabolism* / Q000473:pathology; D013482:Superoxide Dismutase / Q000235:genetics* / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D015032:Zinc / Q000378:metabolism*
C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1; D015032:Zinc