Of mice, men and motor neurons.
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.
Newbery
Helen J
HJ
Medical Genetics Section, University of Edinburgh, Molecular Medicine Centre, Western General Hospital, Edinburgh, UK EH4 2XU.
Abbott
Catherine M
CM
D000690:Amyotrophic Lateral Sclerosis / Q000235:genetics* / Q000378:metabolism / Q000473:pathology* / Q000628:therapy; D000818:Animals; D003599:Cytoskeleton / Q000378:metabolism; D004195:Disease Models, Animal; D016228:Endothelial Growth Factors / Q000235:genetics / Q000502:physiology; D015316:Genetic Therapy / Q000639:trends; D006801:Humans; D008222:Lymphokines / Q000235:genetics / Q000502:physiology; D051379:Mice; D008817:Mice, Mutant Strains; D008822:Mice, Transgenic; D009046:Motor Neurons / Q000378:metabolism / Q000473:pathology*; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D000072105:Superoxide Dismutase-1; D042461:Vascular Endothelial Growth Factor A; D042442:Vascular Endothelial Growth Factors
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