Epidemiology and etiology of Parkinson’s disease: a review of the evidence

  title={Epidemiology and etiology of Parkinson’s disease: a review of the evidence},
  author={Karin Wirdefeldt and Hans-Olov Adami and Philip A. Cole and Dimitrios Trichopoulos and Jack S. Mandel},
  journal={European Journal of Epidemiology},
The etiology of Parkinson’s disease (PD) is not well understood but likely to involve both genetic and environmental factors. Incidence and prevalence estimates vary to a large extent—at least partly due to methodological differences between studies—but are consistently higher in men than in women. Several genes that cause familial as well as sporadic PD have been identified and familial aggregation studies support a genetic component. Despite a vast literature on lifestyle and environmental… 

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The main focus of the research described in this thesis was on studying associations between occupational exposures and PD risk, and observed a strong inverse association of cigarette smoking with PD risk.

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Enough evidence exists to suggest that age has a causal relationship to PD, and significant evidence exists that gender, tobacco use, and caffeine consumption are also associated with the development of PD.

Can Parkinson’s disease be prevented? : epidemiological evidence on lifestyle factors

The results from prospective cohort studies suggest that lifestyle factors can influence future risk of Parkinson's disease, and interventions on these lifestyle factors may have the possibility to prevent the disease eventually.

Genetic Profile, Environmental Exposure, and Their Interaction in Parkinson's Disease

This review summarizes the current knowledge on causal mutation for Parkinson's disease, susceptibility factors increasing disease risk, and the genetic factors that modify the impact of environmental exposure.

Paths from Pesticides to Parkinson's

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More attention should be made on examining what factors determine prognosis and using epidemiological and qualitative methods to determine the needs of patients with PD, and any postulated factor must be found commonly in developed countries.

The Role of Early Life Environmental Risk Factors in Parkinson Disease: What Is the Evidence?

  • G. Logroscino
  • Medicine, Psychology
    Environmental health perspectives
  • 2005
Much evidence indicates that risk factors that have a long latency or a slow effect could be important for late-onset PD, and smoking and coffee drinking have consistently been identified to have protective associations.

Epidemiologic studies of environmental exposures in Parkinson's disease

Pesticides and Parkinson’s Disease—Is There a Link?

The weight of evidence is sufficient to conclude that a generic association between pesticide exposure and PD exists but is insufficient for concluding that this is a causal relationship or that such a relationship exists for any particular pesticide compound or combined pesticide and other exogenous toxicant exposure.

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It is suggested that smoking and family history interact synergistically on a multiplicative scale in determining the risk of PD in individuals older than 75 years.

Environmental factors and Parkinson's disease: a case-control study in the Tuscany region of Italy.

Environmental Factors in the Etiology of Parkinson's Disease

In 35 PD patients and 19 age-matched controls, no significant differences in debrisoquine metabolism were found, although a trend to impaired metabolism was noted in patients with disease onset ≤40, and patients with PD onset ≤age 47 were significantly more likely to have lived in rural areas and to have drunk well water.

The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients.

It is suggested that the risk of developing Parkinson's disease is influenced by a variety of factors, and smoking was inversely associated with PD, as has been previously reported.

Environmental Risk Factors for Parkinson's Disease

Two studies suggest that, on a population level, a major genetic contribution to Parkinson’s disease is unlikely to be made by a single gene.