Evidence map›Paper›PMID 22922585›Full record

SynthesisNeuro-degenerative diseases2013

Consistent neurodegeneration and its association with clinical progression in Huntington's disease: a coordinate-based meta-analysis.

Imis Dogan, Simon B Eickhoff, Jörg B Schulz, N Jon Shah, Angela R Laird, Peter T Fox, Kathrin Reetz

Abstract readMeta-Analysis
In one paragraph

Synthesis in Neuro-degenerative diseases, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed, 3 pooled it
2.9field-weighted citation impact, top 9% 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

41 citing papers in PubMed, 3 syntheses or guidelines pooled it, 74 citations in OpenAlex.

  1. Systemic Symptoms in Huntington's Disease: A Comprehensive Review.Movement disorders clinical practice · 2024
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  10. Review
  11. Autonomic dysfunction in Huntington's disease: AJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 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

7 authors at 5 institutions in 2 countries.

Imis Dogan *Department of Neurology, RWTH Aachen University, Aachen.
Simon B Eickhoff *Institute of Neuroscience and Medicine, Research Center Jülich GmbH, Jülich.
Jörg B SchulzDepartment of Neurology, RWTH Aachen University, Aachen.
N Jon ShahDepartment of Neurology, RWTH Aachen University, Aachen.
Angela R LairdResearch Imaging Center, University of Texas Health Science Center San Antonio, San Antonio, Tex. , USA.
Peter T FoxResearch Imaging Center, University of Texas Health Science Center San Antonio, San Antonio, Tex. , USA.
Kathrin ReetzDepartment of Neurology, RWTH Aachen University, Aachen.
Forschungszentrum Jülich · DEImaging Center · USJülich Aachen Research Alliance · DERWTH Aachen University · DEThe University of Texas Health Science Center at San Antonio · US

Funding

Meta-anaylsis in human brain mappingR01MH074457 · NIMH · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI FOX, PETER THORNTON · 2006 to 2024
$10.5M
NIMH NIH HHS R01 MH074457NIMH NIH HHS R01-MH074457-01A1
6 · The paper itself

Abstract

backgroundThe neuropathological hallmark of Huntington's disease (HD) is progressive striatal loss starting several years prior to clinical onset. In the past decade, whole-brain magnetic resonance imaging (MRI) studies have provided accumulating evidence for widely distributed cortical and subcortical atrophy in the early course of the disease.

objectiveIn order to synthesize current morphometric MRI findings and to investigate the impact of clinical and genetic features on structural changes, we performed a coordinate-based meta-analysis of voxel-based morphometry (VBM) studies in HD.

methodsTwenty HD samples derived from 17 studies were integrated in the analysis comparing a total of 685 HD mutation carriers [345 presymptomatic (pre-HD) and 340 symptomatic (symp-HD) subjects] and 507 controls. Convergent findings across studies were delineated using the anatomical likelihood estimation approach. Effects of genetic and clinical parameters on the likelihood of observing VBM findings were calculated by means of correlation analyses.

resultsPre-HD studies featured convergent evidence for neurodegeneration in the basal ganglia, amygdala, thalamus, insula and occipital regions. In symp-HD, cerebral atrophy was more pronounced and spread to cortical regions (i.e., inferior frontal, premotor, sensorimotor, midcingulate, frontoparietal and temporoparietal cortices). Higher cytosine-adenosine-guanosine repeats were associated with striatal degeneration, while parameters of disease progression and motor impairment additionally correlated with cortical atrophy, especially in sensorimotor areas.

conclusionThis first quantitative meta-analysis in HD demonstrates the extent of striatal atrophy and further consistent extrastriatal degeneration before clinical conversion. Sensorimotor areas seem to be core regions affected in symp-HD and, along with widespread cortical atrophy, may account for the clinical heterogeneity in HD.

Indexed as

AtrophyBrainDisease ProgressionFemaleHumansHuntington DiseaseLikelihood FunctionsMagnetic Resonance ImagingMaleNerve Degeneration

Identifiers

PMID22922585
PMCPMC4801478
OpenAlexW2076362842

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.