Gene expression analysis in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mice model of Parkinson's disease using cDNA microarray: effect of R-apomorphine

Authors

  • Edna Grünblatt,

    1. Technion Faculty of Medicine, Eve Topf and US National Parkinson's Foundation Centers for Neurodegenerative Diseases,
      Bruce Rappaport Family Research Institute, Department of Pharmacology, Haifa, Israel
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  • Silvia Mandel,

    1. Technion Faculty of Medicine, Eve Topf and US National Parkinson's Foundation Centers for Neurodegenerative Diseases,
      Bruce Rappaport Family Research Institute, Department of Pharmacology, Haifa, Israel
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  • Gila Maor,

    1. Eve Topf and US National Parkinson's Foundation Centers for Neurodegenerative diseases, Bruce Rappaport Family Research Institute, Department of Cell Biology, Haifa, Israel
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  • Moussa B. H. Youdim

    1. Technion Faculty of Medicine, Eve Topf and US National Parkinson's Foundation Centers for Neurodegenerative Diseases,
      Bruce Rappaport Family Research Institute, Department of Pharmacology, Haifa, Israel
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Address correspondence and reprint requests to Professor M. B. H. Youdim, Department of Pharmacology, Technion Faculty of Medicine, P.O.B. 9697, 31096 Haifa, Israel. E-mail: youdim@tx.technion.ac.il

Abstract

To establish the possible roles of oxidative stress, inflammatory processes and other unknown mechanisms in neurodegeneration, we investigated brain gene alterations in N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mice model of Parkinson's disease using Atlas mouse cDNA expression array membrane. The expression of 51 different genes involved in oxidative stress, inflammation, glutamate and neurotrophic factors pathways as well as in still undefined processes, such as cell cycle regulators and signal transduction molecules, was differentially affected by the treatment. The present study indicates the involvement of an additional cascade of events that might act in parallel to oxidative stress and inflammation to converge eventually into a common pathway leading to neurodegeneration. The attenuation of these gene changes by R-apomorphine, an iron chelator-radical scavenger drug, supports our previous findings in vivo where R-apomorphine was neuroprotective.

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