Evidence map›Paper›PMID 17449559›Full record

ArticleOccupational and environmental medicine2007

Gene-environment interactions in parkinsonism and Parkinson's disease: the Geoparkinson study.

F D Dick, G De Palma, A Ahmadi, A Osborne, N W Scott, G J Prescott, J Bennett, S Semple, S Dick, P Mozzoni and 8 more

Open access · greenAbstract readMulticenter Study
In one paragraph

Article in Occupational and environmental medicine, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 5 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 5 pooled it
25.0field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

51 citing papers in PubMed, 5 syntheses or guidelines pooled it, 104 citations in OpenAlex.

  1. Pooled it
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  3. Glutathione S-transferase T1 and M1 null genotypes and Parkinson's disease risk: evidence from an updated meta-analysis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2015
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  9. Preventing Parkinson's Disease: An Environmental Agenda.Journal of Parkinson's disease · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

18 authors at 5 institutions in 5 countries.

F D DickDepartment of Environmental and Occupational Medicine, University of Aberdeen, UK. f.dick@abdn.ac.uk
G De Palma
A Ahmadi
A Osborne
N W Scott
G J Prescott
J Bennett
S Semple
S Dick
P Mozzoni
N Haites
S Bezzina Wettinger
A Mutti
M Otelea
A Seaton
P Soderkvist
A Felice
Geoparkinson Study Group
University of Aberdeen · GBUniversity of Parma · ITLinköping University · SEUniversity of Malta · MTSpitalul Clinic Colentina · RO

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesTo investigate associations of Parkinson's disease (PD) and parkinsonian syndromes with polymorphic genes that influence metabolism of either foreign chemical substances or dopamine and to seek evidence of gene-environment interaction effects that modify risk.

methodsA case-control study of 959 prevalent cases of parkinsonism (767 with PD) and 1989 controls across five European centres. Occupational hygienists estimated the average annual intensity of exposure to solvents, pesticides and metals, (iron, copper, manganese), blind to disease status. CYP2D6, PON1, GSTM1, GSTT1, GSTM3, GSTP1, NQO1, CYP1B1, MAO-A, MAO-B, SOD 2, EPHX, DAT1, DRD2 and NAT2 were genotyped. Results were analysed using multiple logistic regression adjusting for key confounders.

resultsThere was a modest but significant association between MAO-A polymorphism in males and disease risk (G vs T, OR 1.30, 95% CI 1.02 to 1.66, adjusted). The majority of gene-environment analyses did not show significant interaction effects. There were possible interaction effects between GSTM1 null genotype and solvent exposure (which were stronger when limited to PD cases only).

conclusionsMany small studies have reported associations between genetic polymorphisms and PD. Fewer have examined gene-environment interactions. This large study was sufficiently powered to examine these aspects. GSTM1 null subjects heavily exposed to solvents appear to be at increased risk of PD. There was insufficient evidence that the other gene-environment combinations investigated modified disease risk, suggesting they contribute little to the burden of PD.

Indexed as

Case-Control StudiesEnvironmental ExposureEuropeFemaleGenetic Predisposition to DiseaseGenotypeHumansMaleOdds RatioParkinson DiseasePolymorphism, GeneticRisk FactorsSex Distribution

Identifiers

PMID17449559
PMCPMC2078383
OpenAlexW2106335169

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.