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Neurology 2000;55:309-311
© 2000 American Academy of Neurology
Brief Communications

Glutamate decarboxylase is not genetically linked to pyridoxine-dependent seizures

Gino Battaglioli, PhD, Daniel R. Rosen, PhD, Sidney M. Gospe, Jr., MD, PhD and David L. Martin, PhD

From the Wadsworth Center (Drs. Battaglioli, Rosen, and Martin), New York State Department of Health, Albany; and the Departments of Neurology and Pediatrics (Dr. Gospe), University of California, Davis.

Address correspondence and reprint requests to Dr. Gino Battaglioli, Wadsworth Center, PO Box 509, Albany, NY 12201-0509; e-mail: battagli@ wadsworth.org

Several aspects of pyridoxine-dependent seizure (PDS) suggest a mutation affecting glutamate decarboxylase (GAD) as a possible cause. To examine the possibility of GAD linkage with PDS, the authors performed genotype analyses of three families using polymorphic markers near the GAD genes (GAD1 and GAD2). In each family, the affected siblings exhibited different genotypes for the GAD2 gene; in two families the GAD1 genotype was disparate. These findings suggest that a mutation of GAD is not directly involved in all cases of PDS.




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