title: Of mice, men and motor neurons.
abstract: The use of mouse models has been of particular importance in studying the pathogenesis of amyotrophic lateral sclerosis. Here, we describe both transgenic and classical mutants for which the genetic lesion is known. We draw attention, wherever possible, to pathological factors common to multiple models.
authors.affiliation: Medical Genetics Section, University of Edinburgh, Molecular Medicine Centre, Western General Hospital, EH4 2XU., Edinburgh, UK.
authors.forename: H J
authors.initials: HJ
authors.lastname: Newbery
authors.forename: C M
authors.initials: CM
authors.lastname: Abbott
mesh_terms: D000690:Amyotrophic Lateral Sclerosis / Q000201:enzymology / Q000235:genetics; D000818:Animals; D004195:Disease Models, Animal; D016228:Endothelial Growth Factors / Q000235:genetics; D006801:Humans; D008222:Lymphokines / Q000235:genetics; D051379:Mice; D018345:Mice, Knockout; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D016472:Motor Neuron Disease / Q000201:enzymology / Q000235:genetics*; D013482:Superoxide Dismutase / Q000235:genetics; D000072105:Superoxide Dismutase-1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
chemical_list: D016228:Endothelial Growth Factors; D008222:Lymphokines; C000606290:SOD1 protein, human; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors; C000606291:Sod1 protein, mouse; D013482:Superoxide Dismutase; D000072105:Superoxide Dismutase-1