Evidence map›Paper›PMID 26629536›Full record

ArticleEBioMedicine2015

Compensation in Preclinical Huntington's Disease: Evidence From the Track-On HD Study.

Stefan Klöppel, Sarah Gregory, Elisa Scheller, Lora Minkova, Adeel Razi, Alexandra Durr, Raymund A C Roos, Blair R Leavitt, Marina Papoutsi, G Bernhard Landwehrmeyer and 11 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in EBioMedicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 77 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
77citing papers in PubMed, 1 pooled it
7.5field-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

77 citing papers in PubMed, 1 synthesis or guideline pooled it, 141 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Neural Mechanisms of Object Location Memory in Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  8. Article
  9. Article
  10. Review
  11. Brain Age as a New Measure of Disease Stratification in Huntington's Disease.Movement disorders : official journal of the Movement Disorder Society · 2025
    Article
  12. Article
  13. Article
  14. Optimizing Screening for Intrastriatal Interventions in Huntington's Disease Using Predictive Models.Movement disorders : official journal of the Movement Disorder Society · 2024
    Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Temporal dynamics predict symptom onset and cognitive decline in familial frontotemporal dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023
    Article

17 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

21 authors at 12 institutions in 8 countries.

Stefan KlöppelAlbert-Ludwigs-University Freiburg, University Medical Center, Division Freiburg Brain Imaging, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, University Medical Center, Department of Psychiatry and Psychotherapy, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, University Medical Center, Department of Neurology, Freiburg, Germany.
Sarah GregoryWellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, UK.
Elisa SchellerAlbert-Ludwigs-University Freiburg, University Medical Center, Division Freiburg Brain Imaging, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, University Medical Center, Department of Psychiatry and Psychotherapy, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, Department of Psychology, Laboratory for Biological and Personality Psychology, Freiburg, Germany.
Lora MinkovaAlbert-Ludwigs-University Freiburg, University Medical Center, Division Freiburg Brain Imaging, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, University Medical Center, Department of Psychiatry and Psychotherapy, Freiburg, Germany ; Albert-Ludwigs-University Freiburg, Department of Psychology, Laboratory for Biological and Personality Psychology, Freiburg, Germany.
Adeel RaziWellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, UK ; Department of Electronic Engineering, N.E.D University of Engineering & Technology, Karachi, Pakistan.
Alexandra DurrAPHP Department of Genetics, Groupe Hospitalier Pitié-Salpêtrière, UPMC Université Paris VI UMR_S1127, Paris France ; Institut du Cerveau et de la Moelle, INSERM U1127, CNRS UMR7225, UPMC Université Paris VI UMR_S1127, Paris France.
Raymund A C RoosLeiden University Medical Center, Department of Neurology, Leiden, The Netherlands.
Blair R LeavittCentre for Molecular Medicine and Therapeutics, Department of Medical Genetics, University of British Columbia, Canada.
Marina PapoutsiDepartment of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, UK.
G Bernhard LandwehrmeyerDepartment of Neurology, Ulm University, Ulm, Germany.
Ralf ReilmannGeorge-Huntington-Institute, Muenster, Germany ; University of Tuebingen, Department of Neurodegenerative Diseases and Hertie-Institute for Clinical Brain Research, Tuebingen, Germany.
Beth BorowskyCHDI Management/CHDI Foundation, Princeton, NJ, USA.
Hans JohnsonDepartment of Electrical and Computer Engineering, University of Iowa, Iowa City, IA, USA.
James A MillsDepartment of Psychiatry, Carver College of Medicine, University of Iowa, Iowa City, IA, USA.
Gail OwenDepartment of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, UK.
Julie StoutSchool of Psychological Sciences and Institute of Clinical and Cognitive Neuroscience, Monash University, Melbourne, Australia.
Rachael I ScahillDepartment of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, UK.
Jeffrey D LongDepartment of Psychiatry, Carver College of Medicine, University of Iowa, Iowa City, IA, USA ; Department of Biostatistics, College of Public Health, University of Iowa, Iowa City, IA, USA.
Geraint ReesWellcome Trust Centre for Neuroimaging, Institute of Neurology, University College London, London, UK ; Institute of Cognitive Neuroscience, University College London, London, UK.
Sarah J TabriziDepartment of Neurodegenerative Disease, UCL Institute of Neurology, University College London, London, UK.
Track-On investigators
University College London · GBUniversity of Freiburg · DEUniversity of Iowa · USWellcome Centre for Human Neuroimaging · GBCentre National de la Recherche Scientifique · FRCHDI Foundation · USHertie Institute for Clinical Brain Research · DELeiden University Medical Center · NLMonash University · AUNED University of Engineering and Technology · PKUniversität Ulm · DEUniversity of British Columbia · CA

Funding

Medical Research Council MR/L012936/1Medical Research Council MR/L02053X/1Wellcome Trust 091593Wellcome Trust 100227
6 · The paper itself

Abstract

backgroundCognitive and motor task performance in premanifest Huntington's disease (HD) gene-carriers is often within normal ranges prior to clinical diagnosis, despite loss of brain volume in regions involved in these tasks. This indicates ongoing compensation, with the brain maintaining function in the presence of neuronal loss. However, thus far, compensatory processes in HD have not been modeled explicitly. Using a new model, which incorporates individual variability related to structural change and behavior, we sought to identify functional correlates of compensation in premanifest-HD gene-carriers.

methodsWe investigated the modulatory effects of regional brain atrophy, indexed by structural measures of disease load, on the relationship between performance and brain activity (or connectivity) using task-based and resting-state functional MRI.

findingsConsistent with compensation, as atrophy increased performance-related activity increased in the right parietal cortex during a working memory task. Similarly, increased functional coupling between the right dorsolateral prefrontal cortex and a left hemisphere network in the resting-state predicted better cognitive performance as atrophy increased. Such patterns were not detectable for the left hemisphere or for motor tasks.

interpretationOur findings provide evidence for active compensatory processes in premanifest-HD for cognitive demands and suggest a higher vulnerability of the left hemisphere to the effects of regional atrophy.

Indexed as

AgedAged, 80 and overBrain MappingCase-Control StudiesConnectomeFemaleHeterozygoteHumansHuntingtin ProteinHuntington DiseaseImage Processing, Computer-AssistedMagnetic Resonance ImagingMaleMemory, Short-TermMutationNerve Tissue ProteinsHTT protein, humanHuntingtin ProteinNerve Tissue ProteinsCognitiveHuntington's diseaseMotorMRINeural compensationPreclinical

Identifiers

PMID26629536
PMCPMC4634199
OpenAlexW1179800764

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.