JaLCDOI 10.18926/AMO/32105
FullText URL fulltext.pdf
Author Asanuma, Masato| Miyazaki, Ikuko| Diaz-Corrales, Francisco J| Ogawa, Norio|
Abstract <p>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.</p>
Keywords dopamine quinone quinoprotein Parkinson’sdisease oxidative stress neurotoxin
Amo Type Article
Published Date 2004-10
Publication Title Acta Medica Okayama
Volume volume58
Issue issue5
Publisher Okayama University Medical School
Start Page 221
End Page 233
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language 英語
File Version publisher
Refereed True
PubMed ID 15666991
Web of Sience KeyUT 000224708800001