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Etiology of Parkinson's Disease

Published online by Cambridge University Press:  02 December 2014

Zhigao Huang ,
Raúl de la Fuente-Fernández  and
A. Jon Stoessl
Zhigao Huang
Affiliation:
Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada
Raúl de la Fuente-Fernández
Affiliation:
Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada
A. Jon Stoessl
Affiliation:
Pacific Parkinson's Research Centre, University of British Columbia, Vancouver, BC, Canada
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Abstract

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There is growing recognition that Parkinson's disease (PD) is likely to arise from the combined effects of genetic predisposition as well as largely unidentified environmental factors. The relative contribution of each varies from one individual to another. Even in situations where more than one family member is affected, the predominant influence may be environmental. Although responsible for only a small minority of cases of PD, recently identified genetic mutations have provided tremendous insights into the basis for neurodegeneration and have led to growing recognition of the importance of abnormal protein handling in Parkinson's as well as other neurodegenerative disorders. Abnormal protein handling may increase susceptibility to oxidative stress; conversely, numerous other factors, including oxidative stress and impaired mitochondrial function can lead to impaired protein degradation. A limited number of environmental factors are known to be toxic to the substantia nigra; in contrast, some factors such as caffeine intake and cigarette smoking may protect against the development of PD, although the mechanisms are not established. We review the various genetic and environmental factors thought to be involved in PD, as well as the mechanisms that contribute to selective nigral cell death.

Résumé

RÉSUMÉ

L’opinion qui préut actuellement est que la maladie de Parkinson rélte de l’interaction entre une présposition gétique et des facteurs environnementaux qui demeurent en grande partie inconnus. La contribution relative de chacun varie d’un individu à’autre. Mê dans les familles oùs d’un membre est atteint, l’influence préminante peut êe environnementale. Bien qu’elles soient en cause dans seulement une minoritée cas de la maladie, des mutations gétiques identifié rémment ont fourni des indices préeux sur l’éologie de la dénéscence neuronale et ont permis de reconnaîe l’importance d’un mébolisme protéue anormal dans la maladie de Parkinson ainsi que dans d’autres maladies neurodénétrices. Un mébolisme protéue anormal peut augmenter la susceptibilitéu stress oxydatif; à’inverse, plusieurs autres facteurs, dont le stress oxydatif et une fonction mitochondriale altée, peuvent induire une altétion de la déadation protéue. On connaîl’effet toxique d’un certain nombre de facteurs environnementaux sur la substance noire; par contre, certains facteurs tels la consommation de cafée et le tabagisme pourraient protér de la maladie de Parkinson, bien que les ménismes n’en soient pas éblis. Nous revoyons les diffénts facteurs gétiques et environnementaux qu’on pense impliquédans la maladie de Parkinson ainsi que les ménismes qui contribuent àa mort séctive de cellules de la substance noire.

Type
Research Article
Information
Canadian Journal of Neurological Sciences , Volume 30 , supplement S1: A Peer-Reviewed Supplement to the Canadian Journal of Neurological Sciences , February 2003 , pp. S10 - S18
Copyright
Copyright © The Canadian Journal of Neurological 2003

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