The Epidemiology of Parkinson's Disease

Stern, Matthew B.; Dulaney, Eugene; Gruber, Stephen B.; Golbe, Lawrence I.; Bergen, Mary; Hurtig, Howard I.; Gollomp, Steve; Stolley, Paul D.

doi:10.1001/archneur.1991.00530210029018

Cited by 110 publications

(15 citation statements)

References 39 publications

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“…Some of the studies that did undertake multivariate analysis did not include pesticide exposure in the predictive models (Behari et al 2001; McCann et al 1998; Preux et al 2000; Wong et al 1991; Zorzon et al 2002). A few studies found that pesticide exposure was not a significant risk factor after adjustment for confounding variables (Chan et al 1998; Stern et al 1991; Taylor et al 1999; Werneck and Alvarenga 1999). In contrast, pesticide exposure was shown to be a significant risk factor after adjustment in several studies (Butterfield et al 1993; Gorell et al 1998; Hertzman et al 1990; Hubble et al 1993; Liou et al 1997; Menegon et al 1998; Seidler et al 1996; Semchuk et al 1992; Zorzon et al 2002).…”

Section: Epidemiologic Evidencementioning

confidence: 99%

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

Brown

Rumsby²,

Capleton³

et al. 2006

Environ Health Perspect

385

246

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Parkinson’s disease (PD) is an idiopathic disease of the nervous system characterized by progressive tremor, bradykinesia, rigidity, and postural instability. It has been postulated that exogenous toxicants, including pesticides, might be involved in the etiology of PD. In this article we present a comprehensive review of the published epidemiologic and toxicologic literature and critically evaluate whether a relationship exists between pesticide exposure and PD. From the epidemiologic literature, there does appear to be a relatively consistent relationship between pesticide exposure and PD. This relationship appears strongest for exposure to herbicides and insecticides, and after long durations of exposure. Toxicologic data suggest that paraquat and rotenone may have neurotoxic actions that potentially play a role in the development of PD, with limited data for other pesticides. However, both the epidemiology and toxicology studies were limited by methodologic weaknesses. Particular issues of current and future interest include multiple exposures (both pesticides and other exogenous toxicants), developmental exposures, and gene–environment interactions. At present, 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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Section: Epidemiologic Evidencementioning

confidence: 99%

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

Brown

Rumsby²,

Capleton³

et al. 2006

Environ Health Perspect

385

246

View full text Add to dashboard Cite

show abstract

“…There are also a number of studies that have shown no association between PD and pesticide exposure (Behari et al 2001; Koller et al 1990; Kuopio et al 1999; McCann et al 1998; Smargiassi et al 1998; Stern et al 1991), herbicide exposure (McCann et al 1998; Smargiassi et al 1998), and fungicide exposure (Gorell et al 1998). Some studies use a broad exposure definition for pesticides, as mentioned above.…”

Section: Parkinson Diseasementioning

confidence: 99%

“…Residence in rural locations was found to be associated with PD in a number of studies (Butterfield et al 1993; Golbe et al 1990; Ho et al 1989; Koller et al 1990; McCann et al 1998; Morano et al 1994; Rajput et al 1986; Stern et al 1991; Wong et al 1991). Yet no association was found in a few other studies (Baldi et al 2003b; Behari et al 2001; Chan et al 1998; Semchuk et al 1991) and decreased risk was reported in others (Tanner et al 1989; Wang et al 1993).…”

Section: Parkinson Diseasementioning

confidence: 99%

“…A number of studies show a positive association (Koller et al 1990; Morano et al 1994; Rajput et al 1986; Smargiassi et al 1998; Wong et al 1991). However, many others found no association for drinking well water and the development of PD (Behari et al 2001; Chan et al 1998; Engel et al 2001; Gorell et al 1998; Kuopio et al 1999; Liou et al 1997; Semchuk et al 1991; Stern et al 1991; Wang et al 1993), and one found an inverse relationship (McCann et al 1998), although many of these studies may have low power to detect outcomes, and the study designs vary.…”

Section: Parkinson Diseasementioning

confidence: 99%

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Neurodegenerative Diseases: An Overview of Environmental Risk Factors

Brown

Lockwood

Sonawane

2005

Environ Health Perspect

400

226

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The population of the United States is aging, and an ever-increasing number of Americans are afflicted with neurodegenerative diseases. Because the pathogenesis of many of these diseases remains unknown, we must consider that environmental factors may play a causal role. This review provides an overview of the epidemiologic evidence for environmental etiologies for neurodegenerative diseases such as Alzheimer disease, Parkinson disease, parkinsonian syndromes (multiple system atrophy and progressive supranuclear palsy), and amyotrophic lateral sclerosis. Epidemiologic evidence for an association between environmental agents’ exposure and neurodegenerative diseases is not conclusive. However, there are indications that there may be causal links, and the need for more research is obvious.

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“…Recent studies of genetics, disease progression, drug response, and clinical manifestation have provided evidence of different pathological heterogeneity in LOPD and EOPD. Compared with LOPD, EOPD is more affected by genetic factors and the relatives of EOPD patients have a higher risk in developing PD (Stern et al, 1991). Although gait disturbance and dystonia are more common in LOPD patients, EOPD patients have higher prevalence of dyskinesia (Schrag and Schott, 2006;Wickremaratchi et al, 2009), a much slower disease progression (Inzelberg et al, 2004), and levodopa treatment effectiveness (Spica et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

ALFF and ReHo Mapping Reveals Different Functional Patterns in Early- and Late-Onset Parkinson’s Disease

Yue

Jiang²,

Shen³

et al. 2020

Front. Neurosci.

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Heterogeneity between late-onset Parkinson's disease (LOPD) and early-onset Parkinson's disease (EOPD) is mainly reflected in the following aspects including genetics, disease progression, drug response, clinical manifestation, and neuropathological change. Although many studies have investigated these differences in relation to clinical significance, the functional processing circuits and underlying neural mechanisms have not been entirely understood. In this study, regional homogeneity (ReHo) and amplitude of low-frequency fluctuation (ALFF) maps were used to explore different spontaneous brain activity patterns in EOPD and LOPD patients. Abnormal synchronizations were found in the motor and emotional circuits of the EOPD group, as well as in the motor, emotional, and visual circuits of the LOPD group. EOPD patients showed functional activity change in the visual, emotional and motor circuits, and LOPD patients only showed increased functional activity in the emotional circuits. In summary, the desynchronization process in the LOPD group was relatively strengthened, and the brain areas with changed functional activity in the EOPD group were relatively widespread. The results might point out different impairments in the synchronization and functional activity for EOPD and LOPD patients.

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The Epidemiology of Parkinson's Disease

Cited by 110 publications

References 39 publications

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

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

Neurodegenerative Diseases: An Overview of Environmental Risk Factors

ALFF and ReHo Mapping Reveals Different Functional Patterns in Early- and Late-Onset Parkinson’s Disease

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