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• W2056546282 abstract "Parkinson's disease (PD) is a neurodegenerative disorder of uncertain pathogenesis characterized by the loss of the nigrostriatal dopaminergic neurons, which can be modeled by the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). Increased expression of cyclooxygenase type 2 (COX-2) and production of prostaglandin E 2 have been implicated in neurodegeneration in several pathological settings. Here we show that COX-2, the rate-limiting enzyme in prostaglandin E 2 synthesis, is up-regulated in brain dopaminergic neurons of both PD and MPTP mice. COX-2 induction occurs through a JNK/c-Jun-dependent mechanism after MPTP administration. We demonstrate that targeting COX-2 does not protect against MPTP-induced dopaminergic neurodegeneration by mitigating inflammation. Instead, we provide evidence that COX-2 inhibition prevents the formation of the oxidant species dopamine-quinone, which has been implicated in the pathogenesis of PD. This study supports a critical role for COX-2 in both the pathogenesis and selectivity of the PD neurodegenerative process. Because of the safety record of the COX-2 inhibitors, and their ability to penetrate the blood–brain barrier, these drugs may be therapies for PD." @default.
• W2056546282 created "2016-06-24" @default.
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• W2056546282 date "2003-04-17" @default.
• W2056546282 modified "2023-10-10" @default.
• W2056546282 title "Cyclooxygenase-2 is instrumental in Parkinson's disease neurodegeneration" @default.
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• W2056546282 doi "https://doi.org/10.1073/pnas.0837397100" @default.
• W2056546282 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/154369" @default.
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