Evidence map›Paper›PMID 28320167›Full record

ArticleJournal of the neurological sciences2017

Caffeine, creatine, GRIN2A and Parkinson's disease progression.

David K Simon, Cai Wu, Barbara C Tilley, Katja Lohmann, Christine Klein, Haydeh Payami, Anne-Marie Wills, Michael J Aminoff, Jacquelyn Bainbridge, Richard Dewey and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the neurological sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
3.0field-weighted citation impact, top 9% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Designing the First Trials for Parkinson's Prevention.Journal of Parkinson's disease · 2024
    Review
  5. Article
  6. Review
  7. The Impact of Environmental Factors on Monogenic Mendelian Diseases.Toxicological sciences : an official journal of the Society of Toxicology · 2021
    Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Selected health and lifestyle factors, cytosine-adenine-guanine status, and phenoconversion in Huntington's disease.Movement disorders : official journal of the Movement Disorder Society · 2018
    Article
  13. Review
  14. The emerging science of precision medicine and pharmacogenomics for Parkinson's disease.Movement disorders : official journal of the Movement Disorder Society · 2017
    Review
  15. Identification of a Novel Mutation inAnnals of Indian Academy of Neurology
    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

20 authors at 16 institutions in 3 countries.

David K SimonDepartment of Neurology, Beth Israel Deaconess Medical Center, Harvard Medical School, 330 Brookline Avenue, Boston, MA 02215, USA. Electronic address: dsimon1@bidmc.harvard.edu.
Cai WuDepartment of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Cai.Wu@uth.tmc.edu.
Barbara C TilleyDepartment of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Barbara.C.Tilley@uth.tmc.edu.
Katja LohmannInstitute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: katja.lohmann@neuro.uni-luebeck.de.
Christine KleinInstitute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: christine.klein@neuro.uni-luebeck.de.
Haydeh PayamiDepartment of Neurology, University of Alabama at Birmingham, Birmingham, AL 35233, USA; Center for Genomic Medicine, HudsonAlpha Institute for Biotechnology, Huntsville, AL 35806, USA. Electronic address: haydehpayami@uabmc.edu.
Anne-Marie WillsDepartment of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: AWILLS@mgh.harvard.edu.
Michael J AminoffDepartment of Neurology, University of California, San Francisco, USA. Electronic address: Michael.Aminoff@ucsf.edu.
Jacquelyn BainbridgeUniversity of Colorado, Anschutz Medical Campus, Skaggs School of Pharmacy and Pharmaceutical Sciences, Department of Clinical Pharmacy and Neurology, Aurora, CO, USA. Electronic address: Jacci.Bainbridge@ucdenver.edu.
Richard DeweyUniversity of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: richard.dewey@utsouthwestern.edu.
Robert A HauserDepartment of Neurology, University of South Florida, Tampa, FL, USA. Electronic address: rhauser@health.usf.edu.
Susen SchaakeInstitute of Neurogenetics, University of Luebeck, 23538 Luebeck, Germany. Electronic address: susen.schaake@neuro.uni-luebeck.de.
Jay S SchneiderDepartment of Pathology, Anatomy and Cell Biology, Parkinson's Disease Research Unit, Thomas Jefferson University, Philadelphia, PA 19107, USA. Electronic address: Jay.Schneider@jefferson.edu.
Saloni SharmaClinical Trials Coordination Center, University of Rochester Medical Center, Rochester, NY 14642, USA. Electronic address: saloni.sharma@chet.rochester.edu.
Carlos SingerDepartment of Neurology, Miller School of Medicine, University of Miami, Miami, FL, USA. Electronic address: csinger@med.miami.edu.
Caroline M TannerParkinson's Disease Research Education and Clinical Center, San Francisco Veteran's Affairs Medical Center, Department of Neurology, University of California, San Francisco, CA, USA. Electronic address: Caroline.Tanner@ucsf.edu.
Daniel TruongThe Parkinson's and Movement Disorder Institute, Fountain Valley, CA, USA. Electronic address: dtruong@pmdi.org.
Peng WeiDepartment of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Peng.Wei@uth.tmc.edu.
Pei Shieen WongUniversity of Colorado, Anschutz Medical Campus, Skaggs School of Pharmacy and Pharmaceutical Sciences, Department of Clinical Pharmacy and Neurology, Aurora, CO, USA; Singapore General Hospital, Singapore 169608, Singapore. Electronic address: pei.wong@ucdenver.edu.
Tianzhong YangDepartment of Biostatistics, University of Texas Health Science Center School of Public Health at Houston, Houston, TX 77030, USA. Electronic address: Tianzhong.Yang@uth.tmc.edu.
Institute for Integrative and Experimental Genomics · DEThe University of Texas Health Science Center at Houston · USBeth Israel Deaconess Medical Center · USHarvard University · USParkinson's and Movement Disorder Institute · USSan Francisco VA Medical Center · USSingapore General Hospital · SGSouthwestern Medical Center · USThe University of Texas Health Science Center · USThomas Jefferson University · USUniversity of Alabama at Birmingham · USUniversity of California, San Francisco · USUniversity of Colorado Anschutz Medical Campus · USUniversity of Miami · USUniversity of Rochester Medical Center · USUniversity of South Florida · US

Funding

Pharmacogenomics of Parkinson's DiseaseR01NS067469 · NINDS · WADSWORTH CENTER · PI PAYAMI, HAYDEH · 2010 to 2014
$2.5M
Clinical Center for Neuroprotection in Parkinson's DiseaseU10NS044545 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI DEWEY, RICHARD B · 2002 to 2013
$1.0M
Parkinson Disease Neuroprotection Clinical TrialU10NS044482 · NINDS · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SIMON, DAVID K. · 2002 to 2013
$955k
NINDS NIH HHS R01 NS067469NINDS NIH HHS U10 NS044482NINDS NIH HHS U10 NS044545
6 · The paper itself

Abstract

Caffeine is neuroprotective in animal models of Parkinson's disease (PD) and caffeine intake is inversely associated with the risk of PD. This association may be influenced by the genotype of GRIN2A, which encodes an NMDA-glutamate-receptor subunit. In two placebo-controlled studies, we detected no association of caffeine intake with the rate of clinical progression of PD, except among subjects taking creatine, for whom higher caffeine intake was associated with more rapid progression. We now have analyzed data from 420 subjects for whom DNA samples and caffeine intake data were available from a placebo-controlled study of creatine in PD. The GRIN2A genotype was not associated with the rate of clinical progression of PD in the placebo group. However, there was a 4-way interaction between GRIN2A genotype, caffeine, creatine and the time since baseline. Among subjects in the creatine group with high levels of caffeine intake, but not among those with low caffeine intake, the GRIN2A T allele was associated with more rapid progression (p=0.03). These data indicate that the deleterious interaction between caffeine and creatine with respect to rate of progression of PD is influenced by GRIN2A genotype. This example of a genetic factor interacting with environmental factors illustrates the complexity of gene-environment interactions in the progression of PD.

Indexed as

AgedCaffeineCreatineDisease ProgressionFemaleGene-Environment InteractionGenetic Predisposition to DiseaseGenotypeHumansLongitudinal StudiesMaleMiddle AgedParkinson DiseasePolymorphism, Single NucleotideReceptors, N-Methyl-D-AspartateCaffeineCreatineReceptors, N-Methyl-D-AspartateCaffeineCoffeeCreatineGRIN2AParkinson's diseaseProgression

Identifiers

PMID28320167
PMCPMC5386398
OpenAlexW2588110024

What OpenQuestion holds

Textmetadata
LicenceTDM
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.