sc-236 and Amyotrophic-Lateral-Sclerosis

The pathogenesis of motor neuron loss in amyotrophic lateral sclerosis (ALS) is thought to involve both glutamate-mediated excitotoxicity and oxidative damage due to the accumulation of free radicals and other toxic molecules. Cyclooxygenase-2 (COX-2) may play a key role in these processes by producing prostaglandins, which trigger astrocytic glutamate release, and by inducing free radical formation. We tested the effects of COX-2 inhibition in an organotypic spinal cord culture model of ALS. The COX-2 inhibitor (SC236) provided significant protection against loss of spinal motor neurons in this system, suggesting that it may be useful in the treatment of ALS.

Topics: Amyotrophic Lateral Sclerosis; Animals; Cyclooxygenase 2; Disease Models, Animal; Isoenzymes; Motor Neurons; Organ Culture Techniques; Prostaglandin-Endoperoxide Synthases; Pyrazoles; Rats; Spinal Cord; Sulfonamides