Pooled Analysis of Tobacco Use and Risk of Parkinson Disease

Ritz, Beate; Ascherio, Alberto; Checkoway, Harvey; Marder, Karen; Nelson, Lorene M.; Rocca, Walter A.; Ross, G. Webster; Strickland, Daniel; Eeden, Stephen K. Van Den; Gorell, Jay M.

doi:10.1001/archneur.64.7.990

Cited by 301 publications

(243 citation statements)

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“…A meta-analysis that included 11 US studies (8 case-control and three cohort studies) addressed the importance of smoking intensity versus duration, age of starting or quitting smoking, time interval after smoking cessation, and type of tobacco in relation to risk of PD [440]. The largest cohort study [430] also addressed the importance of smoking intensity versus duration.…”

Section: Meta-analysesmentioning

confidence: 99%

“…A prospective study that assessed PD mortality as the outcome reported a RR of 0.22 (95% CI 0.07-0.67) for current users of smokeless tobacco at enrollment versus never users [455]. The meta-analysis of 11 US studies mentioned above [440] reported a non-significant inverse association for chewing tobacco after adjustment for other types of smoking (OR 0.66, 95% CI 0.43-1.02) [440].…”

Section: Suggested Systemic Biases In Studies Of Smoking and Pdmentioning

confidence: 99%

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

et al. 2011

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Section: Meta-analysesmentioning

confidence: 99%

Section: Suggested Systemic Biases In Studies Of Smoking and Pdmentioning

confidence: 99%

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

et al. 2011

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“…Similarly, polymorphism in enzymes, which generate free radicals or those involved in dopamine neurotransmission such as cytochrome P450 2E1 (CYP2E1), glutathione S-transferases (GST), superoxide dismutase (MnSOD), monoamine oxidase-B (MAO-B), dopamine receptor D2 (DRD2) and dopamine transporter (DAT) which are known to interact with environmental exposures, could be implicated in the pathogenesis of PD 1,11 . GST may modify PD risk, since PD is more common among people who report the use of pesticides 12 and smokers generally have a lower risk of developing PD 13 . As many products of oxidative stress and neurotoxins are detoxified by GST enzymes, decreased (impaired) detoxification capacity may result in an increased PD risk.…”

mentioning

confidence: 99%

Nullity of GSTT1/GSTM1 related to pesticides is associated with Parkinson's disease

Pinhel

Sado

Longo

et al. 2013

Arq. Neuro-Psiquiatr.

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Parkinson's disease (PD) is a progressive neurodegenerative disorder, clinically characterized by bradykinesia, rigidity, resting tremor, and postural instability. Early symptoms of PD are primarily due to the selective degeneration of dopaminergic neurons of the substantia nigra, innervating the neostriatum. The primary cause of PD is unknown, however, mitochondrial failure, oxidative stress and genetic factors, responsible for neurodegeneration in the substantia nigra are investigated hypotheses for the etiology of idiopathic PD 1 . The progression of cell loss is thought to occur over a somewhat protracted period of time in a defined spatiotemporal manner, and the onset of PD symptoms is typically ABSTRACTGenetic and environmental factors affect the pathogenesis of Parkinson's disease (PD). Genetic variants of the enzyme glutathione S-transferases (GST) may be related to the disease. This study aimed to evaluate the influence of genetic variants of GST (GSTT1/GSTM1) and their association with the exposure to environmental toxins in PD patients. We studied 254 patients with PD and 169 controls. The GSTM1/GSTT1 variants were analyzed by polymerase chain reaction. We applied the Fisher's exact test and the χ 2 test for statistical analysis (p<0.05). The present and absence for GSTT1 and GSTM1 were similar in patients and controls. The null for GSTT1 and GSTM1 (0/0) and exposure to pesticides prevailed in patients (18%) compared to controls (13%, p=0.014). This study suggests the association between PD and previous exposure to pesticides, whose effect may be enhanced in combination with null for GSTT1/GSTM1.Key words: Parkinson disease, glutathione transferase, polymorphism genetic, xenobiotics. RESUMOFatores genéticos e ambientais influenciam a patogênese da doença de Parkinson (DP). Variantes genéticas das enzimas glutationa S-transferases (GST) parecem estar envolvidas com a doença. Os objetivos deste estudo foram avaliar a influência de variantes genéticas de GST (GSTT1/GSTM1) e sua associação com exposição a toxinas ambientais em pacientes com DP. Foram estudados 254 pacientes com DP e 169 controles. As variantes para GSTM1/GSTT1 foram analisadas por reação em cadeia da polimerase. Para análise estatística foram aplicados os testes de Fisher e do χ 2 (p<0,05). Tanto a presença quanto a nulidade para GSTT1 e GSTM1 foram semelhantes em pacientes e controles. A nulidade para GSTT1 e GSTM1 (0/0) e contato com agrotóxicos prevaleceu nos pacientes (18%) em relação aos controles (13%, p=0,014). Este estudo sugere associação entre DP e contato prévio com agrotóxicos, cujo efeito parece potencializado em combinação com nulidade para GSTT1/GSTM1. Palavras-Chave: doença de Parkinson, glutationa transferase, polimorfismo genético, xenobióticos.

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“…Furthermore, GSTs may modify PD risk by metabolizing some chemical compounds in tobacco smoke, since cigarette smokers generally have a lower risk of developing PD [22]. GST polymorphisms may account for different abilities to metabolize components of cigarette smoke, and thus alter an individual's susceptibility to PD.…”

mentioning

confidence: 99%

Glutathione S-transferase mu, omega, pi, and theta class variants and smoking in Parkinson's disease

Wahner

Glatt

Bronstein

et al. 2007

Neuroscience Letters

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GSTs are a family of inducible phase II enzymes that may play a neuroprotective role in Parkinson's disease (PD). GSTs may also modify PD risk by metabolizing compounds in cigarettes, as cigarette smoking is generally found to be associated with a decrease in PD risk. Using a population-based case control study design, we examined polymorphisms of the mu, omega, pi, and theta classes of GST to elucidate the main effects and smoking-GST interactions on PD risk. From three rural California counties, we recruited 289 incident idiopathic PD cases, clinically confirmed by our study neurologist, and 270 population controls, marginally matched by age, gender, and race.We assessed main gene polymorphism associations and evaluated interactions between smoking and GST polymorphisms as departures from a multiplicative scale adjusting for age, gender, and race. We also restricted analyses to Caucasian subjects to address the potential for population stratification (n=235 cases, 220 controls).Among Caucasians, we observed a risk reduction in subjects carrying at least one variant allele for GSTO1 (OR= 0.68, 95% CI: 0.47-0.98) and also GSTO2 (OR= 0.64, 95% CI: 0.44-0.93); both genes were in strong linkage disequilibrium. No main gene effects were observed for the remaining polymorphisms. We noted a multiplicative interaction between ever having smoked regularly and GSTO1 (OR interaction = 0.55, 95% CI: 0.33-0.92) and GSTO2 (OR interaction = 0.54, 95% CI: 0.32-0.90). Results were similar when combining all races. These findings and the paucity of similar studies suggests a need for further inquiry into the association between GSTs, smoking, and PD risk. KeywordsGene-environment interaction; Glutathione-S-transferase; Parkinson's disease; SmokingThe death of dopaminergic neurons in the midbrain is a characteristic feature of Parkinson's disease (PD). Glutathione-S-transferases (GSTs), a family of inducible phase II enzymes with cytoprotective properties, are hypothesized to protect against neurodegeneration. GSTs may Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. . The small number of studies that previously explored interactions between GST gene polymorphisms and smoking in PD were inconclusive and subject to limitations in study design and sample size [3,4,13]. Here we present the first population-based case control study to examine the interaction between several GST polymorphisms and smoking in PD. NIH Public AccessWe concentrated on polymorphisms in four of eight classes of cytoplasmic mammalian GSTs (mu, omega, pi, theta). These classes and their respective gene polymorphi...

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Pooled Analysis of Tobacco Use and Risk of Parkinson Disease

Cited by 301 publications

References 34 publications

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

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

Nullity of GSTT1/GSTM1 related to pesticides is associated with Parkinson's disease

Glutathione S-transferase mu, omega, pi, and theta class variants and smoking in Parkinson's disease

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