α-Synuclein, pesticides, and Parkinson disease

Brighina, Laura; Frigerio, Roberta; Schneider, Nicole; Lesnick, Timothy G.; Andrade, Mariza de; Cunningham, John M.; Farrer, Matthew J.; Lincoln, Sarah; Checkoway, Harvey; Rocca, Walter A.; Maraganore, Demetrius M.

doi:10.1212/01.wnl.0000304049.31377.f2

Cited by 47 publications

(55 citation statements)

References 41 publications

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“…Two studies reported an interaction between the α-Synuclein Rep1 polymorphism and smoking [270,271]. One study reported an interaction between the α-Synuclein Rep1 polymorphism and pesticides, more prominent in early-onset cases [271], but another study [272] reported no such interaction. In the same sample, there was no interaction between the α-Synuclein Rep1 polymorphism and alcohol use [273].…”

Section: Susceptibility Genesmentioning

confidence: 99%

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

et al. 2011

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Section: Susceptibility Genesmentioning

confidence: 99%

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

et al. 2011

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“…Paraquat is the only herbicide substantially investigated in relation to PD, although there have been studies on the ability of atrazine to disrupt dopamine homeostasis at high concentrations [20]. A recent case-control study reported that herbicide exposure increased the risk of PD [21].…”

Section: Herbicidesmentioning

confidence: 99%

Parkinson's disease and pesticides: a toxicological perspective

Hatcher

Pennell

Miller

2008

Trends in Pharmacological Sciences

288

176

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Environmental factors have been shown to contribute to the incidence of Parkinson's disease (PD). Pesticides, which represent one of the primary classes of environmental agents associated with PD, share the common feature of being intentionally released into the environment to control or eliminate pests. Pesticides consist of multiple classes and subclasses of insecticides, herbicides, rodenticides, fungicides, fumigants and others and exhibit a vast array of chemically diverse structures. In this review we examine the evidence regarding the ability of each of the major pesticide subclasses to increase the incidence of PD. We propose that, from a toxicological perspective, it would be beneficial to identify specific subclasses, common structural features and the propensity for widespread human exposure when considering the potential role in PD, rather than using the overly broad term of 'pesticides' to describe this diverse group of chemicals. Furthermore, these chemicals and their environmentally relevant combinations should be evaluated for their ability to promote or accelerate PD and not merely for being singular causative agents.

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“…A case-control study with 833 case-control pairs further examined the possible interaction between SNCA REP1 genotypes (coding for α-synuclein), which have been shown to confer susceptibility to sporadic PD, and pesticide exposure on the risk of PD in human. This epidemiological study did not find any interaction between the SNCA REP1 genotype and herbicides, although both SNCA REP1 score (OR = 1.18; 95% CI 1.02-1.37; p = 0.03) and pesticide exposure were significantly associated with PD in younger subjects (≤ 59.8 years of age; OR = 1.80; 95% CI 1.12-2.87; p = 0.01 for all pesticides; OR = 2.46; 95% CI 1.34-4.52; p = 0.004 for herbicides) (Brighina et al 2008). Taken together, the results of the gene-environment epidemiological studies converge toward an influence of certain gene polymorphisms on the effect of exposure to at least some pesticides on PD and its onset.…”

Section: Susceptibility Genes Targeted In Parkinson's Diseasementioning

confidence: 95%