Evidence map›Paper›PMID 28135712›Full record

ArticleNeuroepidemiology2016

Gene-Environment Interaction in Parkinson's Disease: Coffee, ADORA2A, and CYP1A2.

Yu-Hsuan Chuang, Christina M Lill, Pei-Chen Lee, Johnni Hansen, Christina F Lassen, Lars Bertram, Naomi Greene, Janet S Sinsheimer, Beate Ritz

Open access · bronzeAbstract read
In one paragraph

Article in Neuroepidemiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
2.3field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Article
  4. Dual-Risk axis:Journal of Parkinson's disease · 2026
    Article
  5. Review
  6. Microbiome-based therapeutics for Parkinson's disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Review
  15. Article
  16. Journal of clinical medicine · 2021
    Article
  17. Beneficial Effects of Epigallocatechin-3-Molecules (Basel, Switzerland) · 2021
    Review
  18. CYP1A2 rs762551 polymorphism and risk for amyotrophic lateral sclerosis.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021
    Article
  19. Do caffeine and more selective adenosine AParkinsonism & related disorders · 2020
    Review
  20. Article
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

9 authors at 6 institutions in 6 countries.

Yu-Hsuan ChuangDepartment of Epidemiology, Fielding School of Public Health, University of California, Los Angeles (UCLA), USA.
Christina M Lill
Pei-Chen Lee
Johnni Hansen
Christina F Lassen
Lars Bertram
Naomi Greene
Janet S Sinsheimer
Beate Ritz
Danish Cancer Society · DKUniversity of California, Los Angeles · USCancer Research And Biostatistics · USInstitute for Integrative and Experimental Genomics · DEInstitute of Genetic and Biomedical Research · ITNational Taipei University of Nursing and Health Science · TW

Funding

Registry Study of Parkinsons Disease in DenmarkR01ES013717 · NIEHS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI RITZ, BEATE R. · 2006 to 2010
$4.5M
NIEHS NIH HHS R01 ES013717
6 · The paper itself

Abstract

background and purposeDrinking caffeinated coffee has been reported to provide protection against Parkinson's disease (PD). Caffeine is an adenosine A2A receptor (encoded by the gene ADORA2A) antagonist that increases dopaminergic neurotransmission and Cytochrome P450 1A2 (gene: CYP1A2) metabolizes caffeine; thus, gene polymorphisms in ADORA2A and CYP1A2 may influence the effect coffee consumption has on PD risk.

methodsIn a population-based case-control study (PASIDA) in Denmark (1,556 PD patients and 1,606 birth year- and gender-matched controls), we assessed interactions between lifetime coffee consumption and 3 polymorphisms in ADORA2A and CYP1A2 for all subjects, and incident and prevalent PD cases separately using logistic regression models. We also conducted a meta-analysis combining our results with those from previous studies.

resultsWe estimated statistically significant interactions for ADORA2A rs5760423 and heavy vs. light coffee consumption in incident (OR interaction = 0.66 [95% CI 0.46-0.94], p = 0.02) but not prevalent PD. We did not observe interactions for CYP1A2 rs762551 and rs2472304 in incident or prevalent PD. In meta-analyses, PD associations with daily coffee consumption were strongest among carriers of variant alleles in both ADORA2A and CYP1A2.

conclusionWe corroborated results from a previous report that described interactions between ADORA2A and CYP1A2 polymorphisms and coffee consumption. Our results also suggest that survivor bias may affect results of studies that enroll prevalent PD cases.

Indexed as

CoffeeGene-Environment InteractionAgedCytochrome P-450 CYP1A2DenmarkFemaleHumansMaleMiddle AgedParkinson DiseasePolymorphism, Single NucleotideReceptor, Adenosine A2ARisk FactorsCoffeeCYP1A2 protein, humanCytochrome P-450 CYP1A2Receptor, Adenosine A2A

Identifiers

PMID28135712
PMCPMC5465963
OpenAlexW2581158240

What OpenQuestion holds

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Registered trials

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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.