PMID:11226327

Citation	Vila, M, Jackson-Lewis, V, Vukosavic, S, Djaldetti, R, Liberatore, G, Offen, D, Korsmeyer, SJ and Przedborski, S (2001) Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease. Proc. Natl. Acad. Sci. U.S.A. 98:2837-42
Abstract	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) damages dopaminergic neurons in the substantia nigra pars compacta (SNpc) as seen in Parkinson's disease. Here, we show that the pro-apoptotic protein Bax is highly expressed in the SNpc and that its ablation attenuates SNpc developmental neuronal apoptosis. In adult mice, there is an up-regulation of Bax in the SNpc after MPTP administration and a decrease in Bcl-2. These changes parallel MPTP-induced dopaminergic neurodegeneration. We also show that mutant mice lacking Bax are significantly more resistant to MPTP than their wild-type littermates. This study demonstrates that Bax plays a critical role in the MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson's disease.
Links	PubMed PMC30226 Online version:10.1073/pnas.051633998
Keywords	1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine/pharmacology; Animals; Base Sequence; DNA Primers; Dimerization; Disease Models, Animal; Dopamine/metabolism; Mesencephalon/metabolism; Mice; Mice, Inbred C57BL; Parkinson Disease/genetics; Parkinson Disease/metabolism; Parkinson Disease/pathology; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins c-bcl-2; RNA, Messenger/genetics; RNA, Messenger/metabolism; Up-Regulation; bcl-2-Associated X Protein
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