Evidence map›Paper›PMID 29856137›Full record

ArticleBrain and behavior2018

Taq1A polymorphism and medication effects on inhibitory action control in Parkinson disease.

Katherine E McDonell, Nelleke C van Wouwe, Madaline B Harrison, Scott A Wylie, Daniel O Claassen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain and behavior, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
2.4field-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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 18 citations in OpenAlex.

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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

5 authors at 3 institutions in 1 country.

Katherine E McDonellDepartment of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee.ORCID 0000-0003-4620-3850
Nelleke C van WouweDepartment of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee.
Madaline B HarrisonDepartment of Neurology, University of Virginia, Charlottesville, Virginia.
Scott A WylieDepartment of Neurosurgery, University of Louisville, Louisville, KY, United States.
Daniel O ClaassenDepartment of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee.
Vanderbilt University Medical Center · USUniversity of Louisville · USUniversity of Virginia · US

Funding

Neurocognitive Mechanisms of Inhibition Deficits in Parkinson's DiseaseK23AG028750 · NIA · VANDERBILT UNIVERSITY · PI WYLIE, SCOTT A · 2009 to 2013
$791k
NIA NIH HHS K23 AG028750
6 · The paper itself

Abstract

backgroundDopamine therapy in Parkinson disease (PD) can have differential effects on inhibitory action control, or the ability to inhibit reflexive or impulsive actions. Dopamine agonist (DAAg) medications, which preferentially target D2 and D3 receptors, can either improve or worsen control of impulsive actions in patients with PD. We have reported that the direction of this effect depends on baseline levels of performance on inhibitory control tasks. This observation suggests that there may exist certain biologic determinants that contribute to these patient-specific differences. We hypothesized that one important factor might be functional polymorphisms in D2-like receptor genes.

aimThe goal of this study was to determine whether the direction of DAAg effects on inhibitory control depends on functional polymorphisms in the DRD2 and DRD3 genes.

methodsTwenty-eight patients with PD were genotyped for known functional polymorphisms in DRD2 (rs6277 and rs1800497) and DRD3 (rs6280) receptors. These patients then completed the Simon conflict task both on and off DAAg therapy in a counterbalanced manner.

resultsWe found that patients with the rs1800497 Taq1A (A1) polymorphism (A1/A1 or A1/A2: 11 subjects) showed improved proficiency to suppress impulsive actions when on DAAg; conversely, patients with the A2/A2 allele (14 patients) became less proficient at suppressing incorrect response information on DAAg therapy (Group × Medication, F(1, 23) = 5.65, p < 0.05). Polymorphisms in rs6277 and rs6280 were not associated with a differential medication response.

conclusionThese results suggest that certain DRD polymorphisms may determine the direction of DAAg effects on critical cognitive control processes impaired in PD. Our findings have implications for understanding pharmacogenomics interactions on a larger scale and the role these may play in the wide variability of treatment effects seen in the PD population.

Indexed as

AllelesDopamine AgonistsFemaleGenotypeHumansImpulsive BehaviorMaleMiddle AgedParkinson DiseasePolymorphism, GeneticReceptors, Dopamine D2Dopamine AgonistsDRD2 protein, humanReceptors, Dopamine D2dopamine agonistdopamine receptorgenetic polymorphismimpulse control disorderParkinson disease

Identifiers

PMID29856137
PMCPMC6043698
OpenAlexW2806186290

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LicenceCC BY
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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.