Evidence map›Paper›PMID 28168210›Full record

ArticleAnnals of clinical and translational neurology2017

White matter predicts functional connectivity in premanifest Huntington's disease.

Peter McColgan, Sarah Gregory, Adeel Razi, Kiran K Seunarine, Fatma Gargouri, Alexandra Durr, Raymund A C Roos, Blair R Leavitt, Rachael I Scahill, Chris A Clark and 26 more

Open access · goldAbstract read
In one paragraph

Article in Annals of clinical and translational neurology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed, 2 pooled it
1.7field-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

21 citing papers in PubMed, 2 syntheses or guidelines pooled it, 43 citations in OpenAlex.

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  3. Observational
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  17. Diffusion imaging in Huntington's disease: comprehensive review.Journal of neurology, neurosurgery, and psychiatry · 2020
    Review
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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

36 authors at 7 institutions in 5 countries.

Peter McColganDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
Sarah GregoryWellcome Trust Centre for Neuroimaging UCL Institute of Neurology London WC1N 3BG United Kingdom.
Adeel RaziWellcome Trust Centre for Neuroimaging UCL Institute of Neurology London WC1N 3BG United Kingdom; Department of Electronic Engineering NED University of Engineering and Technology Karachi Pakistan.
Kiran K SeunarineDevelopmental Imaging and Biophysics Section UCL Institute of Child Health London WC1N 1EH United Kingdom.
Fatma GargouriAPHP Department of Genetics Groupe Hospitalier Pitié-Salpêtrière and ICM (Brain and Spine Institute) INSERM U1127 CNRS UMR 7225 Sorbonne Universités - UPMC Université Paris VI UMR_S 1127 Paris France.
Alexandra DurrAPHP Department of Genetics Groupe Hospitalier Pitié-Salpêtrière and ICM (Brain and Spine Institute) INSERM U1127 CNRS UMR 7225 Sorbonne Universités - UPMC Université Paris VI UMR_S 1127 Paris France.
Raymund A C RoosDepartment of Neurology Leiden University Medical Centre Leiden 2300RC The Netherlands.
Blair R LeavittDepartment of Medical Genetics Centre for Molecular Medicine and Therapeutics University of British Columbia 950 West 28th Avenue Vancouver BC V5Z 4H4 Canada.
Rachael I ScahillDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
Chris A ClarkDevelopmental Imaging and Biophysics Section UCL Institute of Child Health London WC1N 1EH United Kingdom.
Sarah J TabriziDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom; National Hospital for Neurology and Neurosurgery Queen Square London WC1N 3BG United Kingdom.
Geraint ReesWellcome Trust Centre for Neuroimaging UCL Institute of Neurology London WC1N 3BG United Kingdom.
Track On‐HD Investigators
A ColemanDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
J DecolongonDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
M FanDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
T PetkauDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
C JauffretDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
D JustoDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
S LehericyDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
K NigaudDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
R ValabrègueDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
A ChoonderbeekDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
E P T HartDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
D J Hensman MossDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
H CrawfordDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
E JohnsonDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
M PapoutsiDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
C BernaDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
R ReilmannDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
N WeberDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
J StoutDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
I LabuschagneDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
B LandwehrmeyerDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
M OrthDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
H JohnsonDepartment of Neurodegenerative Disease UCL Institute of Neurology London WC1N 3BG United Kingdom.
University College London · GBCentre National de la Recherche Scientifique · FRWellcome Centre for Human Neuroimaging · GBLeiden University Medical Center · NLNational Hospital for Neurology and Neurosurgery · GBNED University of Engineering and Technology · PKUniversity of British Columbia · CA

Funding

Medical Research Council MR/L012936/1Wellcome Trust 200181/Z/15/Z
6 · The paper itself

Abstract

objectivesThe distribution of pathology in neurodegenerative disease can be predicted by the organizational characteristics of white matter in healthy brains. However, we have very little evidence for the impact these pathological changes have on brain function. Understanding any such link between structure and function is critical for understanding how underlying brain pathology influences the progressive behavioral changes associated with neurodegeneration. Here, we demonstrate such a link between structure and function in individuals with premanifest Huntington's.

methodsUsing diffusion tractography and resting state functional magnetic resonance imaging to characterize white matter organization and functional connectivity, we investigate whether characteristic patterns of white matter organization in the healthy human brain shape the changes in functional coupling between brain regions in premanifest Huntington's disease.

resultsWe find changes in functional connectivity in premanifest Huntington's disease that link directly to underlying patterns of white matter organization in healthy brains. Specifically, brain areas with strong structural connectivity show decreases in functional connectivity in premanifest Huntington's disease relative to controls, while regions with weak structural connectivity show increases in functional connectivity. Furthermore, we identify a pattern of dissociation in the strongest functional connections between anterior and posterior brain regions such that anterior functional connectivity increases in strength in premanifest Huntington's disease, while posterior functional connectivity decreases.

interpretationOur findings demonstrate that organizational principles of white matter underlie changes in functional connectivity in premanifest Huntington's disease. Furthermore, we demonstrate functional antero-posterior dissociation that is in keeping with the caudo-rostral gradient of striatal pathology in HD.

Identifiers

PMID28168210
PMCPMC5288460
OpenAlexW2577189914

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.