Absence of dopaminergic neuronal degeneration and oxidative damage in aged DJ-I-deficient mice

hiroo yamaguchi, Jie Shen

    Research output: Contribution to journalArticle

    54 Citations (Scopus)

    Abstract

    Parkinson's disease is the most common movement disorder characterized by dopaminergic dysfunction and degeneration. Loss-of-function mutations in the DJ-I gene have been linked to autosomal recessive forms of early-onset familial Parkinson's disease. DJ-I is thought to play roles in protection of cells against oxidative stress and in maintenance of the normal dopaminergic function in the nigrostriatal pathway. Here we investigate the consequence of both DJ-I inactivation and aging in mice. We found that DJ-I-I- mice at the age of 24-27 months have normal numbers of dopaminergic neurons in the substantia nigra and normal levels of dopamine and its major metabolites in the striatum. The number of noradrenergic neurons in the locus coeruleus is also unchanged in DJ-I-I- mice. Moreover, there is no accumulation of oxidative damage or inclusion bodies in aged DJ-I-I- brains. Together, these results indicate that loss of DJ-I function alone is insufficient to cause nigral degeneration and oxidative damage in the life span of mice.

    Original languageEnglish
    Article number10
    JournalMolecular Neurodegeneration
    Volume2
    Issue number1
    DOIs
    Publication statusPublished - Jun 20 2007

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    Substantia Nigra
    Parkinson Disease
    Adrenergic Neurons
    Cytoprotection
    Locus Coeruleus
    Dopaminergic Neurons
    Inclusion Bodies
    Movement Disorders
    Dopamine
    Oxidative Stress
    Maintenance
    Mutation
    Brain
    Genes

    All Science Journal Classification (ASJC) codes

    • Molecular Biology
    • Clinical Neurology
    • Cellular and Molecular Neuroscience

    Cite this

    Absence of dopaminergic neuronal degeneration and oxidative damage in aged DJ-I-deficient mice. / yamaguchi, hiroo; Shen, Jie.

    In: Molecular Neurodegeneration, Vol. 2, No. 1, 10, 20.06.2007.

    Research output: Contribution to journalArticle

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