Evidence map›Paper›PMID 26859813›Full record

ArticleTranslational psychiatry2016

Genome-wide association analysis identifies genetic variations in subjects with myalgic encephalomyelitis/chronic fatigue syndrome.

K A Schlauch, S F Khaiboullina, K L De Meirleir, S Rawat, J Petereit, A A Rizvanov, N Blatt, T Mijatovic, D Kulick, A Palotás and 1 more

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed, 2 pooled it
7.2field-weighted citation impact, top 2% 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, 2 syntheses or guidelines pooled it, 77 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

11 authors at 3 institutions in 3 countries.

K A SchlauchDepartment of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, USA.
S F KhaiboullinaNevada Center for Biomedical Research, University of Nevada, Reno, NV, USA.
K L De MeirleirNevada Center for Biomedical Research, University of Nevada, Reno, NV, USA.
S RawatNevada Center for Biomedical Research, University of Nevada, Reno, NV, USA.
J PetereitDepartment of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, USA.
A A RizvanovInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russian Federation.
N BlattInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russian Federation.
T MijatovicR.E.D Laboratories, Zellik, Belgium.
D KulickMayo Clinic, Scottsdale, AZ, USA.
A PalotásInstitute of Fundamental Medicine and Biology, Kazan Federal University, Kazan, Russian Federation.
V C LombardiDepartment of Biochemistry and Molecular Biology, University of Nevada, Reno, NV, USA.
University of Nevada, Reno · USKazan Federal University · RUMayo Clinic in Arizona · US

Funding

Outreach/Diversity/Pipeline ProjectP20GM103440 · NIGMS · UNIVERSITY OF NEVADA RENO · PI Eduardo A Robleto · 2012 to 2026
$58.0M
New Strategies to Decipher the Pathophysiology of Chronic Fatigue SyndromeR01AI078234 · NIAID · NEVADA CENTER FOR BIOMEDICAL RESEARCH · PI LOMBARDI, VINCENT C · 2009 to 2013
$1.5M
NIAID NIH HHS R01 AI078234NIGMS NIH HHS P20 GM103440NIGMS NIH HHS P20GM103440
6 · The paper itself

Abstract

Myalgic encephalomyelitis, also known as chronic fatigue syndrome or ME/CFS, is a multifactorial and debilitating disease that has an impact on over 4 million people in the United States alone. The pathogenesis of ME/CFS remains largely unknown; however, a genetic predisposition has been suggested. In the present study, we used a DNA single-nucleotide polymorphism (SNP) chip representing over 906,600 known SNPs to analyze DNA from ME/CFS subjects and healthy controls. To the best of our knowledge, this study represents the most comprehensive genome-wide association study (GWAS) of an ME/CFS cohort conducted to date. Here 442 SNPs were identified as candidates for association with ME/CFS (adjusted P-value<0.05). Whereas the majority of these SNPs are represented in non-coding regions of the genome, 12 SNPs were identified in the coding region of their respective gene. Among these, two candidate SNPs resulted in missense substitutions, one in a pattern recognition receptor and the other in an uncharacterized coiled-coil domain-containing protein. We also identified five SNPs that cluster in the non-coding regions of T-cell receptor loci. Further examination of these polymorphisms may help identify contributing factors to the pathophysiology of ME/CFS, as well as categorize potential targets for medical intervention strategies.

Indexed as

Fatigue Syndrome, ChronicFemaleGenetic Predisposition to DiseaseGenetic VariationGenome-Wide Association StudyHumansMaleMiddle AgedPilot ProjectsPolymorphism, Single Nucleotide

Identifiers

PMID26859813
PMCPMC4872418
OpenAlexW2259714666

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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.