Evidence map›Paper›PMID 31491822›Full record

ArticleNeuroImage. Clinical2019

Cortical neurodevelopment in pre-manifest Huntington's disease.

Katharina M Kubera, Mike M Schmitgen, Dusan Hirjak, Robert Christian Wolf, Michael Orth

Open access · goldAbstract read
In one paragraph

Article in NeuroImage. Clinical, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
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  6. Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. The Neurodevelopmental Hypothesis of Huntington's Disease.Journal of Huntington's disease · 2020
    Review
  12. Review
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.

Katharina M KuberaCenter for Psychosocial Medicine, Department of General Psychiatry, Heidelberg University, Germany.
Mike M SchmitgenCenter for Psychosocial Medicine, Department of General Psychiatry, Heidelberg University, Germany.
Dusan HirjakDepartment of Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Robert Christian WolfCenter for Psychosocial Medicine, Department of General Psychiatry, Heidelberg University, Germany. Electronic address: christian.wolf@med.uni-heidelberg.de.
Michael OrthDepartment of Neurology, Ulm University, Germany. Electronic address: michael.orth@uni-ulm.de.
Heidelberg University · DEUniversität Ulm · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe expression of the HTT CAG repeat expansion mutation causes neurodegeneration in Huntington's disease (HD).

objectivesIn light of the - mainly in-vitro - evidence suggesting an additional role of huntingtin in neurodevelopment we used 3T MRI to test the hypothesis that in CAG-expanded individuals without clinical signs of HD (preHD) there is evidence for neurodevelopmental abnormalities.

methodsWe specifically investigated the complexity of cortical folding, a measure of cortical neurodevelopment, employing a novel method to quantify local fractal dimension (FD) measures that uses spherical harmonic reconstructions.

resultsThe complexity of cortical folding differed at a group level between preHD (n = 57) and healthy volunteers (n = 57) in areas of the motor and visual system as well as temporal cortical areas. However, there was no association between the complexity of cortical folding and the loss in putamen volume that was clearly evident in preHD.

conclusionsOur results suggest that HTT CAG repeat length may have an influence on cortical folding without evidence that this leads to developmental pathology or was clinically meaningful. This suggests that the HTT CAG-repeat expansion mutation may influence the processes governing cortical neurodevelopment; however, that influence seems independent of the events that lead to neurodegeneration.

Indexed as

Prodromal SymptomsAdultCerebral CortexCorpus StriatumFemaleHumansHuntingtin ProteinHuntington DiseaseMagnetic Resonance ImagingMaleMiddle AgedTrinucleotide Repeat ExpansionYoung AdultHTT protein, humanHuntingtin ProteinCAT12CortexHuntingtonMRINeurodevelopmentStriatum

Identifiers

PMID31491822
PMCPMC6627026
OpenAlexW2954505665

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.