Evidence map›Paper›PMID 29076559›Full record

ArticleMovement disorders : official journal of the Movement Disorder Society2017

Genetic influences on cognition in progressive supranuclear palsy.

Adam Gerstenecker, Erik D Roberson, Gerard D Schellenberg, David G Standaert, David R Shprecher, Benzi M Kluger, Irene Litvan

Open access · greenAbstract read
In one paragraph

Article in Movement disorders : official journal of the Movement Disorder Society, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.4field-weighted citation impact, top 35% 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

6 citing papers in PubMed, 10 citations in OpenAlex.

  1. Pathomechanisms of cognitive impairment in progressive supranuclear palsy.Journal of neural transmission (Vienna, Austria : 1996) · 2023
    Review
  2. Review
  3. Review
  4. Tau and MAPT genetics in tauopathies and synucleinopathies.Parkinsonism & related disorders · 2021
    Review
  5. Genetic Insights into Alzheimer's Disease.Annual review of pathology · 2021
    Review
  6. 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

7 authors at 6 institutions in 2 countries.

Adam GersteneckerDepartment of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID http://orcid.org/0000-0003-2696-5380
Erik D RobersonDepartment of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Gerard D SchellenbergDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA.
David G StandaertDepartment of Neurology, University of Alabama at Birmingham, Birmingham, Alabama, USA.ORCID http://orcid.org/0000-0003-2921-8348
David R ShprecherBanner Sun Health Research Institute, Sun City, Arizona, USA.ORCID http://orcid.org/0000-0002-4217-0097
Benzi M KlugerDepartment of Neurology, University of Colorado, Aurora, Colorado, USA.
Irene LitvanDepartment of Neurosciences, Parkinson and Movement Disorders Center, University of California, San Diego, California, USA.
University of Alabama at Birmingham · USCivitan International · USUniversity of Arizona · USUniversity of California San Diego · USUniversity of Colorado Anschutz Medical Campus · USUniversity of Pennsylvania · US

Funding

VIRUS-INDUCED BRAIN PATHOLOGYP50AG005131 · NIA · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI BREWER, JAMES B · 1985 to 2018
$55.4M
UAB Neuroscience Core CenterP30NS047466 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2005 to 2019
$8.5M
Rehabilitation Research Resource to Enhance Clinical Trials (ReACT)P2CHD086851 · NICHD · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BAMMAN, MARCAS M · 2015 to 2019
$7.1M
TorsinA as a key link in receptor-mediated signalingP01NS087997 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI BREAKEFIELD, XANDRA OWENS, OZELIUS, LAURIE J. · 2015 to 2019
$6.4M
Training - The Frontotemporal Lobar Degeneration Clinical Research ConsortiumU54NS092089 · NINDS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI BOXER, ADAM L. · 2014 to 2018
$6.4M
CTE and Posttraumatic Neurodegeneration: Neuropathology and Ex Vivo ImagingU01NS086659 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI MCKEE, ANN C. · 2014 to 2017
$6.1M
Functional Change in Mild Cognitive ImpairmentR01AG021927 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI MARSON, DANIEL C · 2004 to 2014
$4.4M
T35 Short Term Research Training GrantT35HL007491 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SAVOIA, MARIA CHRISTINA · 1985 to 2015
$2.8M
Genetic and Environmental Risk Factors for PSPR01AG024040 · NIA · UNIVERSITY OF LOUISVILLE · PI LITVAN, IRENE · 2006 to 2010
$2.7M
UAB Research Education Program for Residents and Fellows in NeuroscienceR25NS079188 · NINDS · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI STANDAERT, DAVID G. · 2012 to 2022
$1.1M
NHLBI NIH HHS T35 HL007491NIA NIH HHS P50 AG005131NIA NIH HHS R01 AG021927NIA NIH HHS R01 AG024040NICHD NIH HHS P2C HD086851NINDS NIH HHS P01 NS087997NINDS NIH HHS P30 NS047466NINDS NIH HHS R25 NS079188NINDS NIH HHS U01 NS086659NINDS NIH HHS U54 NS092089
6 · The paper itself

Abstract

backgroundCognitive dysfunction is common in progressive supranuclear palsy, but the influence of genetics on cognition in this disorder has not been well studied. The objective of this study was to investigate the effect of genes previously identified as risk alleles, including microtubule-associated protein tau, myelin-associated oligodendrocyte basic protein, eukaryotic translation initiation factor 2-alpha kinase 3, and syntaxin 6, as well as apolipoprotein E, on cognitive function in progressive supranuclear palsy.

methodsThe sample was composed of 305 participants who met criteria for possible or probable progressive supranuclear palsy. Genetic information was determined by TaqMan genotyping assays. A neuropsychological battery was administered to all study participants. Measures included in the battery evaluated for general cognition, executive function, memory, attention, language, and visuospatial ability.

resultsCognition did not vary significantly between individuals homozygous or heterozygous for the microtubule-associated protein tau H1 haplotype. However, cognition varied significantly at the subhaplotype level, with carriers of the microtubule-associated protein tau rs242557/A allele, which marks the H1c subhaplotype, performing better than noncarriers on measures of general cognitive function, executive function, and attention. No associations were found for other genes.

conclusionsThe results of the current study indicate that variations in microtubule-associated protein tau influence cognition in progressive supranuclear palsy. Although the H1c-specific rs242557/A allele is a risk factor for progressive supranuclear palsy, carriers of this allele may exhibit better cognition than non-carriers in patients with the atypical parkinsonian syndrome. Further studies are needed. © 2017 International Parkinson and Movement Disorder Society.

Indexed as

AgedCognition DisordersCohort StudiesEukaryotic Initiation Factor-3FemaleGenetic Predisposition to DiseaseGenome-Wide Association StudyGenotypeHumansMaleMiddle AgedMutationMyelin ProteinsNeuropsychological TestsQa-SNARE ProteinsSupranuclear Palsy, ProgressiveEukaryotic Initiation Factor-3MOBP protein, humanMyelin ProteinsQa-SNARE ProteinsSTX6 protein, humantau ProteinscognitionGWASMAPTprogressive supranuclear palsy

Identifiers

PMID29076559
PMCPMC5818145
OpenAlexW2766798667

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.