COX-2-deficient mice are less prone to MPTP-neurotoxicity than wild-type mice

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Abstract
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 I -methyl-4-phanyl-l,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. © 2003 Lippincott Williams & Wilkins.link_to_subscribed_fulltex