| First Author | Feng Z | Year | 2003 |
| Journal | Neuroreport | Volume | 14 |
| Issue | 15 | Pages | 1927-9 |
| PubMed ID | 14561922 | Mgi Jnum | J:89629 |
| Mgi Id | MGI:3040987 | Doi | 10.1097/00001756-200310270-00009 |
| Citation | Feng Z, et al. (2003) COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice. Neuroreport 14(15):1927-9 |
| abstractText | The primary lesion in Parkinson's disease is the death of dopaminergic neurons in the substantia nigra. The role of cyclooxygenase (COX)-2 in the etiology of Parkinson's disease was explored using COX-2 gene knockout mice. Mortality after injection of 1-methyl-4-phenyl-1,2,3,6 tetrahydropyridine (MPTP, a chemical known to cause parkinsonism in humans) in heterozygous COX-2-deficient mice was lower than that in wild-type mice. The number of tyrosine hydroxylase immunoreactive neurons in the substantia nigra pars compacta of MPTP-treated wild-type mice declined to a greater extent than in heterozygous mice. Inhibition of COX-2 protein expression decreased the lesion caused by MPTP and protected the dopaminergic neurons in substantia nigra pars compacta. This result suggested that inhibition of COX-2 has potential therapeutic implications. |
