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NEUROLOGY 1996;47:40S-46S
© 1996 American Academy of Neurology

Autoimmunity and ALS

R. G. Smith, MD, PhD, L. Siklos, PhD, M. E. Alexianu, MD, PhD, J. I. Engelhardt, MD, D. R. Mosier, MD, PhD, L. Colom, MD, PhD, A. Habib Mohamed, PhD and S. H. Appel, MD

From the Department of Neurology, (Drs. Smith, Alexianu, Mosier, Colom, Habib Mohamed, and Appel), Baylor College of Medicine, Houston, TX; the Department of Neurology and Psychiatry, (Dr. Engelhardt) Albert Szent-Gyorgyi Medical University, Szeged, Hungary; and the Institute of Biophysics (Dr. Siklos), Biological Research Center, Szeged, Hungary.
Address correspondence and reprint requests to Dr Appel, Chairman, Dept. of Neurology NB-302, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030.

Abstract.

Significant evidence has accrued suggesting that antibodies to voltage-gated calcium channel are observed in at least some patients with sporadic ALS (SALS) and that such antibodies alter the function of these ion channels in vitro and in vivo. Further, passive transfer of these immunoglobulin-containing fractions into mice produces changes at the neuromuscular junction that are very similar to changes observed in patients with SALS. These changes reflect local alterations in intracellular Ca (2+) homeostasis and, in animal models, may also evidence early changes of motoneuron injury, such as Golgi apparatus swelling and fragmentation. Although not yet documented to induce motoneuron death in vivo, SALS immunoglobulins induce Ca2+-dependent apoptosis in a differentiated motoneuron hybrid cell line via a mechanism that involves oxidative injury. SALS immunoglobulin-mediated apoptosis in these cells is regulated by the presence of the same calcium-binding proteins that may modulate selective motoneuron vulnerability in SALS.

NEUROLOGY 1996;47(Suppl 2): S40-S46






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