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May 14, 2007
 |  BioCentury  |  Tools & Techniques

ALS: Sodden dance

While it has been known for some time that a mutation in the superoxide dismutase 1 gene plays a role in some cases of amyotrophic lateral sclerosis, just how it works has been a mystery. A pair of articles published in Nature Neuroscience last month point an accusatory finger at glial cells with mutant SOD1 in the degeneration of neurons associated with the disease.

One group uncovered an SOD1-mediated pathway associated with neurotoxicity, while the other described an embryonic stem cell-based model that could be useful for screening ALS candidates.

Last week, a third group published a paper in Nature Medicine describing the design of an antibody that recognizes only misfolded forms of SOD1, which they say can be used as a tool for further study of ALS.

The progressive neurodegenerative disease is characterized by the deterioration of motor neurons in the brain and spinal cord that leads to lack of motor control, muscular atrophy and eventually death. Addressing the disease pharmacologically has proven difficult, as most cases are sporadic, meaning the patient has no familial history of the disease and it can't be linked to any particular genetic defect.

According to Serge Przedborski, professor of neurology and pathology at...

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