New Compound Boosts Glutamate
Transport In ALS-Affected Rodents

A compound dubbed GPI-1046, developed with MDA support in the laboratory of Jeffrey Rothstein at Johns Hopkins University in Baltimore, shows promise in increasing removal and recycling of the central nervous system chemical glutamate by boosting production of a glutamate transporter protein. Excess glutamate has been implicated as a possible factor in amyotrophic lateral sclerosis (ALS) causation or perpetuation.

Rothstein, who directs the MDA/ALS Center at Hopkins, and colleagues published their findings in the February issue of Neurobiology of Disease.

GPI-1046 improves the transport of glutamate away from nerve cells, where it can be toxic, and into surrounding cells, where it can be recycled. Mice treated with it lived 12 percent longer than an untreated group.