European Journal of Epidemiology

, 26:1

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

Authors

    • Department of Medical Epidemiology and BiostatisticsKarolinska Institutet
    • Department of Clinical NeuroscienceKarolinska Institutet
  • Hans-Olov Adami
    • Department of Medical Epidemiology and BiostatisticsKarolinska Institutet
    • Department of EpidemiologyHarvard School of Public Health
  • Philip Cole
    • School of Public HealthUniversity of Alabama at Birmingham
  • Dimitrios Trichopoulos
    • Department of EpidemiologyHarvard School of Public Health
  • Jack Mandel
    • Dalla Lana School of Public HealthUniversity of Toronto
Supplement

DOI: 10.1007/s10654-011-9581-6

Cite this article as:
Wirdefeldt, K., Adami, H., Cole, P. et al. Eur J Epidemiol (2011) 26: 1. doi:10.1007/s10654-011-9581-6

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.

Keywords

Parkinson diseaseEpidemiologyRisk factor

Abbreviations

AHS

Agricultural Health Study

BMI

Body mass index

CI

Confidence interval

DDE

Dichlorodiphenyldichloroethylene

DDT

Dichlorodiphenyltrichloroethane

DLB

Dementia with Lewy bodies

GIS

Geographical information system

GWAS

Genome-wide association study

HDL

High-density lipoprotein

HR

Hazard ratio

IOM

Institute of Medicine

JEM

Job exposure matrix

LDL

Low-density lipoprotein

LPS

Lipopolysacharide

MSA

Multiple system atrophy

MET

Metabolic equivalent task

MPTP

1-methyl-4-phenyl-1, 2, 3, 6,-tetrahydropiridine

NAS–NRC

National Academy of Sciences–National Research Council

NSAID

Non-steroid anti-inflammatory drugs

OR

Odds ratio

PD

Parkinson’s disease

PET

Positron emission tomography

PMR

Proportionate mortality ratio

POR

Prevalence odds ratio

PSP

Progressive supranuclear palsy

RBD

REM sleep behavior disorder

RR

Relative risk

SPECT

Single photon emission computed tomography

SIR

Standardized incidence ratio

SHR

Standardized hospitalization ratio

SMR

Standardized mortality ratio

TIA

Transient ischaemic attack

Supplementary material

10654_2011_9581_MOESM1_ESM.doc (44 kb)
Supplementary material 1 (DOC 44 kb)
10654_2011_9581_MOESM2_ESM.doc (27 kb)
Supplementary material 2 (DOC 27 kb)
10654_2011_9581_MOESM3_ESM.xls (180 kb)
Supplementary material 3 (XLS 172 kb)

Copyright information

© Springer Science+Business Media B.V. 2011