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

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.... Full description

Journal Title: European journal of epidemiology 2011-01-01, Vol.26 (Suppl 1), p.S1-S58
Main Author: Wirdefeldt, Karin
Other Authors: Adami, Hans-Olov , Cole, Philip , Trichopoulos, Dimitrios , Mandel, Jack
Format: Electronic Article Electronic Article
Language: English
Subjects:
Publisher: Dordrecht: Springer
ID: ISSN: 0393-2990
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title: Epidemiology and etiology of Parkinson's disease: a review of the evidence
format: Article
creator:
  • Wirdefeldt, Karin
  • Adami, Hans-Olov
  • Cole, Philip
  • Trichopoulos, Dimitrios
  • Mandel, Jack
subjects:
  • Age Factors
  • Alcohol Drinking - adverse effects
  • Biological and medical sciences
  • Biometry
  • Cancer
  • Cardiology
  • Case control studies
  • Causes and theories of causation
  • Cigarette smoking
  • Comorbidity
  • Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
  • Development and progression
  • Diagnosis, Differential
  • Diet
  • Disease risk
  • Diseases
  • Environmental Exposure - adverse effects
  • Epidemiology
  • General aspects
  • Genetic mutation
  • Genetic Predisposition to Disease
  • Genetics
  • Humans
  • Infectious Diseases
  • Life Sciences
  • Magnetic fields
  • Magnetics
  • Medical sciences
  • Medicin och hälsovetenskap
  • Medicine
  • Medicine & Public Health
  • Metals - toxicity
  • Miscellaneous
  • Nervous system diseases
  • Neurology
  • Neurosciences
  • Occupational Exposure - adverse effects
  • Oncology
  • Oncology, Experimental
  • Organic Chemicals - toxicity
  • Parkinson disease
  • Parkinson Disease - epidemiology
  • Parkinson Disease - etiology
  • Parkinson Disease - genetics
  • Parkinson's disease
  • Parkinsonian disorders
  • Parkinsons disease
  • Pesticides
  • Pesticides - toxicity
  • Polymorphism
  • Polymorphism, Genetic
  • Public Health
  • Public health. Hygiene
  • Public health. Hygiene-occupational medicine
  • Residence Characteristics
  • Risk factor
  • Risk factors
  • Santé publique et épidémiologie
  • Sex Factors
  • Sleep
  • Smoking - adverse effects
  • Supplement
  • Uric acid
  • Water Supply
ispartof: European journal of epidemiology, 2011-01-01, Vol.26 (Suppl 1), p.S1-S58
description: 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 epidemiologie studies of PD should be large, include detailed quantifications of exposure, and collect information on environmental exposures as well as genetic polymorphisms.
language: eng
source:
identifier: ISSN: 0393-2990
fulltext: no_fulltext
issn:
  • 0393-2990
  • 1573-7284
  • 1573-7284
url: Link


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descriptionThe 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 epidemiologie 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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subjectAge Factors ; Alcohol Drinking - adverse effects ; Biological and medical sciences ; Biometry ; Cancer ; Cardiology ; Case control studies ; Causes and theories of causation ; Cigarette smoking ; Comorbidity ; Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases ; Development and progression ; Diagnosis, Differential ; Diet ; Disease risk ; Diseases ; Environmental Exposure - adverse effects ; Epidemiology ; General aspects ; Genetic mutation ; Genetic Predisposition to Disease ; Genetics ; Humans ; Infectious Diseases ; Life Sciences ; Magnetic fields ; Magnetics ; Medical sciences ; Medicin och hälsovetenskap ; Medicine ; Medicine & Public Health ; Metals - toxicity ; Miscellaneous ; Nervous system diseases ; Neurology ; Neurosciences ; Occupational Exposure - adverse effects ; Oncology ; Oncology, Experimental ; Organic Chemicals - toxicity ; Parkinson disease ; Parkinson Disease - epidemiology ; Parkinson Disease - etiology ; Parkinson Disease - genetics ; Parkinson's disease ; Parkinsonian disorders ; Parkinsons disease ; Pesticides ; Pesticides - toxicity ; Polymorphism ; Polymorphism, Genetic ; Public Health ; Public health. Hygiene ; Public health. Hygiene-occupational medicine ; Residence Characteristics ; Risk factor ; Risk factors ; Santé publique et épidémiologie ; Sex Factors ; Sleep ; Smoking - adverse effects ; Supplement ; Uric acid ; Water Supply
ispartofEuropean journal of epidemiology, 2011-01-01, Vol.26 (Suppl 1), p.S1-S58
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descriptionThe 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 epidemiologie 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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0Age Factors
1Alcohol Drinking - adverse effects
2Biological and medical sciences
3Biometry
4Cancer
5Cardiology
6Case control studies
7Causes and theories of causation
8Cigarette smoking
9Comorbidity
10Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
11Development and progression
12Diagnosis, Differential
13Diet
14Disease risk
15Diseases
16Environmental Exposure - adverse effects
17Epidemiology
18General aspects
19Genetic mutation
20Genetic Predisposition to Disease
21Genetics
22Humans
23Infectious Diseases
24Life Sciences
25Magnetic fields
26Magnetics
27Medical sciences
28Medicin och hälsovetenskap
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30Medicine & Public Health
31Metals - toxicity
32Miscellaneous
33Nervous system diseases
34Neurology
35Neurosciences
36Occupational Exposure - adverse effects
37Oncology
38Oncology, Experimental
39Organic Chemicals - toxicity
40Parkinson disease
41Parkinson Disease - epidemiology
42Parkinson Disease - etiology
43Parkinson Disease - genetics
44Parkinson's disease
45Parkinsonian disorders
46Parkinsons disease
47Pesticides
48Pesticides - toxicity
49Polymorphism
50Polymorphism, Genetic
51Public Health
52Public health. Hygiene
53Public health. Hygiene-occupational medicine
54Residence Characteristics
55Risk factor
56Risk factors
57Santé publique et épidémiologie
58Sex Factors
59Sleep
60Smoking - adverse effects
61Supplement
62Uric acid
63Water Supply
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titleEpidemiology and etiology of Parkinson's disease: a review of the evidence
authorWirdefeldt, Karin ; Adami, Hans-Olov ; Cole, Philip ; Trichopoulos, Dimitrios ; Mandel, Jack
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1Alcohol Drinking - adverse effects
2Biological and medical sciences
3Biometry
4Cancer
5Cardiology
6Case control studies
7Causes and theories of causation
8Cigarette smoking
9Comorbidity
10Degenerative and inherited degenerative diseases of the nervous system. Leukodystrophies. Prion diseases
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12Diagnosis, Differential
13Diet
14Disease risk
15Diseases
16Environmental Exposure - adverse effects
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18General aspects
19Genetic mutation
20Genetic Predisposition to Disease
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57Santé publique et épidémiologie
58Sex Factors
59Sleep
60Smoking - adverse effects
61Supplement
62Uric acid
63Water Supply
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abstractThe 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 epidemiologie 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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