Quinone formation as dopaminergic neuron-specific oxidative stress in the pathogenesis of sporadic parkinson's disease and neurotoxin-induced parkinsonism

Masato Asanuma, Ikuko Miyazaki, Francisco J. Diaz-Corrales, Norio Ogawa

Research output: Contribution to journalReview article

57 Citations (Scopus)

Abstract

Parkinson's disease (PD) is a progressive neurodegenerative disease characterized by dopaminergic neuron-specific degeneration in the substantia nigra. A number of gene mutations and deletions have been reported to play a role in the pathogenesis of familial PD. Moreover, a number of pathological and pharmacological studies on sporadic PD and dopaminergic neurotoxin-induced parkinsonism have hypothesized that mitochondrial dysfunction, inflammation, oxidative stress, and dysfunction of the ubiquitin-proteasome system all play important roles in the pathogenesis and progress of PD. However, these hypotheses do not yet fully explain the mechanisms of dopaminergic neuron-specific cell loss in PD. Recently, the neurotoxicity of dopamine quinone formation by auto-oxidation of dopamine has been shown to cause specific cell death of dopaminergic neurons in the pathogenesis of sporadic PD and dopaminergic neurotoxin-induced parkinsonism. Furthermore, this quinone formation is closely linked to other representative hypotheses in the pathogenesis of PD. In this article, we mainly review recent studies on the neurotoxicity of quinone formation as a dopaminergic neuron-specific oxidative stress and its role in the etiology of PD, in addition to several neuroprotective approaches against dopamine quinone-induced toxicity.

Original languageEnglish
Pages (from-to)221-233
Number of pages13
JournalActa medica Okayama
Volume58
Issue number5
Publication statusPublished - Oct 1 2004

Keywords

  • Dopamine quinone
  • Neurotoxin
  • Oxidative stress
  • Parkinson's disease
  • Quinoprotein

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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