Evidence map›Paper›PMID 29249680›Full record

ArticleParkinsonism & related disorders2018

Dopaminergic polymorphisms associated with medication responsiveness of gait in Parkinson's disease.

Nathaniel S Miller, Kelvin L Chou, Nicolaas I Bohnen, Martijn L T M Müller, Rachael D Seidler

Open access · greenAbstract read
In one paragraph

Article in Parkinsonism & related disorders, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 18% 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, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
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  6. Freezing of gait: overview on etiology, treatment, and future directions.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 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

5 authors at 2 institutions in 1 country.

Nathaniel S MillerPsychology Department, University of Michigan, 303 East Kearsley Street, Flint, MI 48502-1950, United States. Electronic address: natmille@umich.edu.
Kelvin L ChouDepartment of Neurology, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States; Department of Neurosurgery, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States; University of Michigan, Morris K. Udall Center of Excellence for Parkinson's Disease Research, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States. Electronic address: klchou@med.umich.edu.
Nicolaas I BohnenUniversity of Michigan, Morris K. Udall Center of Excellence for Parkinson's Disease Research, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States; Department of Radiology, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States; Neurology Service and GRECC, VAAAHS, University of Michigan, 2215 Fuller Road, Ann Arbor, MI 48109-5030, United States. Electronic address: nbohnen@umich.edu.
Martijn L T M MüllerUniversity of Michigan, Morris K. Udall Center of Excellence for Parkinson's Disease Research, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States; Department of Radiology, University of Michigan, 1500 East Medical Center Drive, Ann Arbor, MI 48109-5030, United States. Electronic address: mtmuller@umich.edu.
Rachael D SeidlerSchool of Kinesiology, University of Michigan, 1402 Washington Heights, Ann Arbor, MI 48109-2013, United States; Department of Applied Physiology & Kinesiology, College of Health and Human Performance, University of Michigan, 1864 Stadium Road, Gainesville, FL 32611, United States. Electronic address: rachaelseidler@ufl.edu.
University of Michigan · USUniversity of Michigan–Flint · US

Funding

Michigan Institute for Clinical and Health Research (MICHR)UL1TR002240 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LUMENG, JULIE C, MASHOUR, GEORGE ALEXANDER · 2017 to 2022
$54.9M
Michigan Institute for Clinical and Health Research (MCHR)UL1TR000433 · NCATS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI MASHOUR, GEORGE ALEXANDER · 2012 to 2016
$49.9M
Research Education CoreP30AG024824 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Neil Alexander · 2004 to 2026
$29.2M
Public Outreach and Education CoreP50NS091856 · NINDS · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ALBIN, ROGER L · 2014 to 2019
$10.1M
NCATS NIH HHS UL1 TR000433NCATS NIH HHS UL1 TR002240NIA NIH HHS P30 AG024824NINDS NIH HHS P50 NS091856
6 · The paper itself

Abstract

backgroundGait dysfunction is a common symptom of Parkinson's disease that can cause significant disability and put patients at risk for falls. These symptoms show variable responsiveness to dopaminergic therapy.

objectiveTo determine whether dopaminergic (rs1076560 DRD2 G > T and rs4680 catechole-o-methyltranspherase (COMT) Val158Met) or brain derived neurotrophic factor (rs6265 BDNF Val66Met) genetic polymorphisms are associated with gait function and medication responsiveness in Parkinson's disease.

methodGait function was evaluated on two days for patients (ON and OFF medication in a counterbalanced fashion) and a single session for controls. Investigators were blinded to genotype during data collection. Associations between genotype and medication responsiveness were analyzed using mixed model ANOVAs. A priori hypotheses were tested using GAITRite

resultsWe found that the DRD2 polymorphism, but neither COMT nor BDNF, was consistently associated with gait function and medication responsiveness in the patients. Specifically, Parkinson's disease patients with reduced striatal D2 expression (DRD2 T allele carriers) had worse gait dysfunction and showed greater dopamine responsiveness of gait function compared to patients who were homozygous for the G allele. There was no effect of any of the genetic polymorphisms on gait for controls. CONCLUSIONS AND RELEVANCE: The findings suggest that genetic subgrouping, in particular for DRD2, may be used to identify Parkinson's disease patient subgroups that are more dopamine responsive for gait function.

Indexed as

Gait Disorders, NeurologicPharmacognosyAgedAntiparkinson AgentsFemaleGenotypeHumansMaleMiddle AgedParkinson DiseasePolymorphism, Single NucleotideReceptors, Dopamine D2Antiparkinson AgentsDRD2 protein, humanReceptors, Dopamine D2Dopaminergic medication responsivenessDRD2GaitIndividual/subgroup differencesParkinson's disease

Identifiers

PMID29249680
PMCPMC5826846
OpenAlexW2773747603

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.