Abstract
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 oilier 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.
Original language | English (US) |
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Pages (from-to) | 792-795 |
Number of pages | 4 |
Journal | Annals of neurology |
Volume | 48 |
Issue number | 5 |
DOIs | |
State | Published - Nov 20 2000 |
ASJC Scopus subject areas
- Neurology
- Clinical Neurology