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Neurology 2002;59:1464-1466
© 2002 American Academy of Neurology
Brief Communications

SMN1 gene study in three families in which ALS and spinal muscular atrophy co-exist

P. Corcia, MD, J. Khoris, MD, P. Couratier, MD PhD, V. Mayeux-Portas, PhD, E. Bieth, MD PhD, B. de Toffol, MD PhD, A. Autret, MD, J.P. Müh, MD PhD, C. Andres, MD PhD and W. Camu, MD PhD

From the INSERM U316 (Drs. Corcia, Müh, and Andres), Tours; Department of Neurology (Drs. Corcia, de Toffol, and Autret), CHRU Bretonneau, Tours; Department of Neurology and the Genetic Unit on Motor Neuron Diseases (Drs. Khoris, Mayeux-Portas, and Camu), INSERM U336, Montpellier; Department of Neurology (Dr. Couratier), CHRU Dupuytren, Limoges; Department of Medical Genetics (Dr. Bieth), CHRU Purpan, Toulouse, France.

Address correspondence and reprint requests to Dr. P. Corcia, Clinique Neurologique, CHRU Bretonneau, 2 Boulevard Tonnellé, 37044 Tours Cedex, France; e-mail: corcia{at}med.univ-tours.fr

Spinal muscular atrophy (SMA) is caused by SMN1 gene deletions or mutations, and ALS is the most frequent motor neuron condition in adults. The authors describe three families in which ALS and SMA coexist. The authors found that no SOD1 mutation was found within these families; all three ALS cases had at least two SMN1 copies; and an abnormal SMN1 gene locus did not explain the co-occurrence of these two motor neuron disorders in these families.






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