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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
Author(s) -
Grünblatt Edna,
Mandel Silvia,
Maor Gila,
Youdim Moussa B. H.
Publication year - 2001
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2001.00397.x
Subject(s) - neurodegeneration , neuroprotection , oxidative stress , mptp , gene expression , biology , parkinson's disease , apomorphine , microarray analysis techniques , inflammation , microbiology and biotechnology , pharmacology , neuroscience , gene , medicine , dopaminergic , biochemistry , immunology , disease , dopamine
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.