Evidence map›Paper›PMID 19409230›Full record

ReviewNeuroscience2009

Magnetic resonance imaging of Huntington's disease: preparing for clinical trials.

S Klöppel, S M Henley, N Z Hobbs, R C Wolf, J Kassubek, S J Tabrizi, R S J Frackowiak

Abstract readReview
In one paragraph

Review in Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

39 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Diffusion imaging in Huntington's disease: comprehensive review.Journal of neurology, neurosurgery, and psychiatry · 2020
    Review
  11. Review
  12. Article
  13. Article
  14. Study of plasma-derived miRNAs mimic differences in Huntington's disease brain.Movement disorders : official journal of the Movement Disorder Society · 2015
    Article
  15. Article
  16. Observational
  17. Longitudinal task-negative network analyses in preclinical Huntington's disease.European archives of psychiatry and clinical neuroscience · 2014
    Article
  18. Article
  19. Genetics of Huntington disease.AJNR. American journal of neuroradiology · 2014
    Article
  20. 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

7 authors.

S KlöppelDepartment of Psychiatry and Psychotherapy, Freiburg Brain Imaging, University Clinic Freiburg, Freiburg, Germany. stefan.kloeppel@uniklinik-freiburg.de
S M Henley
N Z Hobbs
R C Wolf
J Kassubek
S J Tabrizi
R S J Frackowiak

Funding

Wellcome TrustWellcome Trust 075,696 2/04/2
6 · The paper itself

Abstract

The known genetic mutation causing Huntington's disease (HD) makes this disease an important model to study links between gene and brain function. An autosomal dominant family history and the availability of a sensitive and specific genetic test allow pre-clinical diagnosis many years before the onset of any typical clinical signs. This review summarizes recent magnetic resonance imaging (MRI)-based findings in HD with a focus on the requirements if imaging is to be used in treatment trials. Despite its monogenetic cause, HD presents with a range of clinical manifestations, not explained by variation in the number of CAG repeats in the affected population. Neuroimaging studies have revealed a complex pattern of structural and functional changes affecting widespread cortical and subcortical regions far beyond the confines of the striatal degeneration that characterizes this disorder. Besides striatal dysfunction, functional imaging studies have reported a variable pattern of increased and decreased activation in cortical regions in both pre-clinical and clinically manifest HD-gene mutation carriers. Beyond regional brain activation changes, evidence from functional and diffusion-weighted MRI further suggests disrupted connectivity between corticocortical and corticostriatal areas. However, substantial inconsistencies with respect to structural and functional changes have been reported in a number of studies. Possible explanations include methodological factors and differences in study samples. There may also be biological explanations but these are poorly characterized and understood at present. Additional insights into this phenotypic variability derived from study of mouse models are presented to explore this phenomenon.

Indexed as

AnimalsBiomarkersClinical Trials as TopicHumansHuntington DiseaseMagnetic Resonance ImagingBiomarkers

Identifiers

PMID19409230
PMCPMC2771270

What OpenQuestion holds

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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.