ABSTRACT
Much is known about the pathogenesis of amyotrophic lateral sclerosis (ALS); that is, how the disease comes about in molecular terms. Virtually all the information has come from studies of the transgenic mouse bearing mutations of superoxide dismutase 1 (SOD1). The process seems to be similar in mice and humans. In contrast, little is known about the etiology of non-genetic or sporadic human ALS. Bruijn et al. (1) suggest that the cause sets off the same cascade of pathophysiology in the SOD1 transgenic mouse and in humans, differing only in that one cause is a mutation and other causes are not yet clearly identified.
