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Gabriel Liberatore

Researcher at Columbia University

Publications -  6
Citations -  1762

Gabriel Liberatore is an academic researcher from Columbia University. The author has contributed to research in topics: Substantia nigra & Pars compacta. The author has an hindex of 5, co-authored 6 publications receiving 1698 citations.

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Inducible nitric oxide synthase stimulates dopaminergic neurodegeneration in the MPTP model of Parkinson disease.

TL;DR: It is shown that after administration of MPTP to mice, there was a robust gliosis in the substantia nigra pars compacta associated with significant upregulation of inducible nitric oxide synthase (iNOS), which indicates that inhibitors of iNOS may provide protective benefit in the treatment of Parkinson disease.
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Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl- 4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease

TL;DR: In this paper, the pro-apoptotic protein Bax is shown to play a critical role in MPTP neurotoxic process and suggests that targeting Bax may provide protective benefit in the treatment of Parkinson's disease.
Journal Article

The parkinsonian toxin MPTP: action and mechanism.

TL;DR: Findings support the view that MPTP's deleterious cascade of events include mito-chondrial respiration deficit, oxidative stress, and energy failure, and that a similar scenario applies to the pathogenesis of PD.
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Developmental cell death in dopaminergic neurons of the substantia nigra of mice.

TL;DR: It is demonstrated that destruction of intrinsic striatal neurons by a local injection of quinolinic acid (QA) dramatically enhances the magnitude of SNpc apoptosis and results in a lower number of adult SNpc dopaminergic neurons.

Bax ablation prevents dopaminergic neurodegeneration in the 1-methyl-

TL;DR: It is shown that the pro-apoptotic protein Bax is highly expressed in the SNpc and that its ablation attenuates SNpc developmental neuronal apoptosis, and it is suggested that targeting Bax may provide protective benefit in the treatment of Parkinson's disease.