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

Abstract

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 possible risk or protection factors, consistent findings are few. There is compelling evidence for protective effects of smoking and coffee, but the biologic mechanisms for these possibly causal relations are poorly understood. Uric acid also seems to be associated with lower PD risk. Evidence that one or several pesticides increase PD risk is suggestive but further research is needed to identify specific compounds that may play a causal role. Evidence is limited on the role of metals, other chemicals and magnetic fields. Important methodological limitations include crude classification of exposure, low frequency and intensity of exposure, inadequate sample size, potential for confounding, retrospective study designs and lack of consistent diagnostic criteria for PD. Studies that assessed possible shared etiological components between PD and other diseases show that REM sleep behavior disorder and mental illness increase PD risk and that PD patients have lower cancer risk, but methodological concerns exist. Future epidemiologic studies of PD should be large, include detailed quantifications of exposure, and collect information on environmental exposures as well as genetic polymorphisms.

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  • Authors+Show Affiliations

    ,

    Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. karin.wirdefeldt@ki.se

    , , ,

    Source

    European journal of epidemiology 26 Suppl 1: 2011 Jun pg S1-58

    MeSH

    Age Factors
    Alcohol Drinking
    Comorbidity
    Diagnosis, Differential
    Diet
    Environmental Exposure
    Genetic Predisposition to Disease
    Humans
    Magnetics
    Metals
    Occupational Exposure
    Organic Chemicals
    Parkinson Disease
    Pesticides
    Polymorphism, Genetic
    Residence Characteristics
    Sex Factors
    Smoking
    Water Supply

    Pub Type(s)

    Journal Article
    Research Support, Non-U.S. Gov't
    Review

    Language

    eng

    PubMed ID

    21626386

    Citation

    Wirdefeldt, Karin, et al. "Epidemiology and Etiology of Parkinson's Disease: a Review of the Evidence." European Journal of Epidemiology, vol. 26 Suppl 1, 2011, pp. S1-58.
    Wirdefeldt K, Adami HO, Cole P, et al. Epidemiology and etiology of Parkinson's disease: a review of the evidence. Eur J Epidemiol. 2011;26 Suppl 1:S1-58.
    Wirdefeldt, K., Adami, H. O., Cole, P., Trichopoulos, D., & Mandel, J. (2011). Epidemiology and etiology of Parkinson's disease: a review of the evidence. European Journal of Epidemiology, 26 Suppl 1, pp. S1-58. doi:10.1007/s10654-011-9581-6.
    Wirdefeldt K, et al. Epidemiology and Etiology of Parkinson's Disease: a Review of the Evidence. Eur J Epidemiol. 2011;26 Suppl 1:S1-58. PubMed PMID: 21626386.
    * Article titles in AMA citation format should be in sentence-case
    TY - JOUR T1 - Epidemiology and etiology of Parkinson's disease: a review of the evidence. AU - Wirdefeldt,Karin, AU - Adami,Hans-Olov, AU - Cole,Philip, AU - Trichopoulos,Dimitrios, AU - Mandel,Jack, Y1 - 2011/05/28/ PY - 2010/09/29/received PY - 2011/04/05/accepted PY - 2011/6/1/entrez PY - 2011/6/3/pubmed PY - 2011/8/6/medline SP - S1 EP - 58 JF - European journal of epidemiology JO - Eur. J. Epidemiol. VL - 26 Suppl 1 N2 - 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 possible risk or protection factors, consistent findings are few. There is compelling evidence for protective effects of smoking and coffee, but the biologic mechanisms for these possibly causal relations are poorly understood. Uric acid also seems to be associated with lower PD risk. Evidence that one or several pesticides increase PD risk is suggestive but further research is needed to identify specific compounds that may play a causal role. Evidence is limited on the role of metals, other chemicals and magnetic fields. Important methodological limitations include crude classification of exposure, low frequency and intensity of exposure, inadequate sample size, potential for confounding, retrospective study designs and lack of consistent diagnostic criteria for PD. Studies that assessed possible shared etiological components between PD and other diseases show that REM sleep behavior disorder and mental illness increase PD risk and that PD patients have lower cancer risk, but methodological concerns exist. Future epidemiologic studies of PD should be large, include detailed quantifications of exposure, and collect information on environmental exposures as well as genetic polymorphisms. SN - 1573-7284 UR - https://www.unboundmedicine.com/medline/citation/21626386/Epidemiology_and_etiology_of_Parkinson's_disease:_a_review_of_the_evidence_ L2 - https://doi.org/10.1007/s10654-011-9581-6 DB - PRIME DP - Unbound Medicine ER -