ALS-Related Findings Reported at Meeting

At the 36th annual meeting of the Society of Neuroscience, held this week in Atlanta, scientists noted two possible toxins they believe should be pursued for their possible role in amyotrophic lateral sclerosis (ALS) and reported that blocking a protein that inhibits muscle growth delays the onset of ALS symptoms in mice with an ALS-causing genetic mutation.

A group from the University of British Columbia in Vancouver, Canada, reported that aluminum salts used in anthrax vaccinations during the Persian Gulf War of 1991 might be playing a role in the increased incidence of ALS in Gulf War veterans. Mice treated with an aluminum-based compound used in the vaccines developed motor dysfunction, lost motor neurons (the cells involved in ALS) and showed signs of nervous system inflammation.

Another Canadian group, with scientists from the University of British Columbia and McGill University in Montreal, reported they’ve identified the likely toxins in cycad seeds, long associated with excessive numbers of ALS cases on Guam. They say the culprits are molecules called sterol glucosides. Mice fed these molecules for 10 weeks lost 30 percent to 45 percent of their spinal cord motor neurons.

Researchers from the University of Southern California in Los Angeles reported that mice bred with a genetic mutation in the SOD1 gene known to cause ALS and also bred not to produce a protein called myostatin, known to limit muscle growth, fared better than mice with the SOD1 mutation but with intact myostatin genes. The mice without myostatin did better than the other mice on tests of motor function, and they showed better preservation of nerve and muscle cells at various time points. Life span in the male mice didn’t increase, but two female mice showed an average increase in life span of 21 percent compared to a myostatin-producing littermate. A medication to block myostatin is in clinical trials for adult forms of muscular dystrophy.