Monday, September 21, 1998
Superoxide dismutase (SOD) has been an enzyme in search of a disease
for a long time. It has been largely unsuccessful as a therapeutic in conditions thought
to involve oxidative damage (such as brain trauma). But a link between mutations in the
gene encoding SOD1 and amyotrophic lateral sclerosis (ALS) was thought to provide an
opportunity to apply the protein beneficially.
Last week, however, research published in Science by Cephalon Inc. (CEPH, West Chester, Penn.) and colleagues showed that mutations in SOD1 cause ALS in
mice through a toxic property of the mutant enzyme rather