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NEUROLOGY 1996;47:251S-254S
© 1996 American Academy of Neurology

ALS therapy

Targets for the future

Jacques Hugon, MD, PhD

From the Unit of Neurobiology and Cellular Pathology, Laboratory of Histology and Cell Biology, UCNRS 1485, Faculty of Medicine, Limoges, France.
Address correspondence and reprint requests to Professor Jacques Hugon, Unit of Neurobiology and Cellular Pathology, Laboratory of Histology and Cell Biology, UCNRS 1485, Faculty of Medicine, 2 rue du Dr. Marcland, 87025 Limoges Cedex, France.

Abstract.

There are four main hypotheses about the cause of ALS:excitotoxicity linked to glutamate receptor overactivation; mutation of the superoxide dismutase gene; production of autoantibodies to calcium channels; neurofilament accumulation. The motoneuron degeneration characteristic of ALS could be caused by any one or a combination of these mechanisms. Future therapeutic approaches should be based on these mechanisms and given in combination so that different levels of the degenerative process are targeted. Protection against excitotoxicity could be achieved with a combination of pharmacologic agents having neuroprotective activity, such as antiglutamate agents (e.g., riluzole), N-methyl-D-aspartate (NMDA) and non-NMDA antagonists, free-radical scavengers, calcium-channel blockers, and neurotrophic factors. Gene transfer is a possible future approach when causative mutations are identified. Transfer of genes encoding neuroprotective agents or genetically modified cells stably expressing these agents is another possible strategy.

NEUROLOGY 1996;47(Suppl 4): S251-S254






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