Document Information


PMID 14720207  (  )
Title Additive neuroprotective effects of creatine and cyclooxygenase 2 inhibitors in a transgenic mouse model of amyotrophic lateral sclerosis.
Abstract There is substantial evidence implicating both inflammation and mitochondrial dysfunction in amyotrophic lateral sclerosis (ALS) pathogenesis. We investigated the therapeutic effects of cyclooxygenase 2 (COX-2) inhibitors both alone and in combination with creatine in the G93A transgenic mouse model of ALS. Oral administration of either celecoxib or rofecoxib significantly improved motor performance, attenuated weight loss and extended survival. The administration of COX-2 inhibitors significantly reduced prostaglandin E2 levels at 110 days of age. The combination of creatine with COX-2 inhibitors produced additive neuroprotective effects and extended survival by approximately 30%. The COX-2 inhibitors significantly protected against depletion of anterior horn motor neurons and creatine with COX-2 inhibitors showed greater protection than COX-2 inhibitors alone. These results suggest that combinations of therapies targeting different disease mechanisms may be a useful strategy in the treatment of ALS. Hospital-Weill Medical College of Cornell University, New York, New York 10021, USA.

NOTE: Color highlight is limited to the abstract and SciMiner text-mining mode. If you see much more identified targets below from "Targets by SciMiner Summary" and "Targets by SciMiner Full list", they may have been identified from the full text.



Targets by SciMiner Summary

HUGO ID Symbol Target Name #Occur ActualStr
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)10COX-2 | cox 2 |

 


Targets by SciMiner Full list

HUGO ID Symbol Name ActualStr Score FlankingText
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3We investigated the therapeutic effects of cyclooxygenase 2 (COX-2) COX-2 inhibitors both alone and in combination with creatine in the
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3The administration of COX-2 inhibitors significantly reduced prostaglandin E2 levels at 110 days of
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3The combination of creatine with COX-2 inhibitors produced additive neuroprotective effects and extended survival by approximately
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3The COX-2 inhibitors significantly protected against depletion of anterior horn motor neurons
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3against depletion of anterior horn motor neurons and creatine with COX-2 inhibitors showed greater protection than COX-2 inhibitors alone
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)COX-21.3neurons and creatine with COX-2 inhibitors showed greater protection than COX-2 inhibitors alone
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)cox 21.0we investigated the therapeutic effects of cyclooxygenase 2 cox 2 inhibitors both alone and in combination with creatine in the g93a transgenic mouse model of als.
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)cox 21.0the administration of cox 2 inhibitors significantly reduced prostaglandin e2 levels at 110 days of age.
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)cox 21.0the combination of creatine with cox 2 inhibitors produced additive neuroprotective effects and extended survival by approximately 30%.
9605PTGS2prostaglandin-endoperoxide synthase 2 (prostaglandin G/H synthase and cyclooxygenase)cox 21.0the cox 2 inhibitors significantly protected against depletion of anterior horn motor neurons and creatine with cox 2 inhibitors showed greater protection than cox 2 inhibitors alone.