Evidence map›Paper›PMID 32128927›Full record

ArticleJournal of neuroimaging : official journal of the American Society of Neuroimaging2020

White and Gray Matter Abnormalities in Manifest Huntington's Disease: Cross-Sectional and Longitudinal Analysis.

Wafaa Sweidan, Fen Bao, Navid-Seraji Bozorgzad, Edwin George

Open access · bronzeAbstract read
In one paragraph

Article in Journal of neuroimaging : official journal of the American Society of Neuroimaging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 21% 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

11 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Pain in Huntington's disease and its potential mechanisms.Frontiers in aging neuroscience · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Diffusion imaging in Huntington's disease: comprehensive review.Journal of neurology, neurosurgery, and psychiatry · 2020
    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

4 authors at 2 institutions in 1 country.

Wafaa SweidanDepartment of Psychiatry, Wayne State University, Detroit, MI.ORCID 0000-0003-0207-9747
Fen BaoDepartment of Neurology, Wayne State University, Detroit, MI.
Navid-Seraji BozorgzadDepartment of Neurology, University of Michigan, Ann Arbor, MI.
Edwin GeorgeDepartment of Neurology, Wayne State University, Detroit, MI.
Wayne State University · USUniversity of Michigan · US

Funding

Michigan Alzheimer's Disease Core CenterP30AG053760 · NIA · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI LIEBERMAN, ANDREW P · 2016 to 2020
$10.1M
NIA NIH HHS P30 AG053760
6 · The paper itself

Abstract

background and purposeEarly white matter (WM) changes and cortical atrophy in Huntington's disease (HD) are often evident before disease onset and extend through the brain during manifest stages. The trajectory of these brain abnormalities in symptomatic stages remains relatively unexplored. The aim of this study is to investigate how the pattern of WM and gray matter (GM) alterations progress over time.

methodsWe investigated alterations in brain WM, cortical thickness, and subcortical structures using diffusion and structural magnetic resonance imaging, in manifest HD patients (n = 13) compared to age-matched healthy controls (n = 11). Imaging and clinical data for the HD group were collected at follow-up (7 months) to explore possible longitudinal changes.

resultsCross-sectional analyses identified significant posterior cortical thinning (P < .05) and symmetric fractional anisotropy (FA) reduction (P < .01) in brain WM of HD group compared to HC. These changes were strongly correlated with impairment in motor symptoms and processing speed. Subcortical atrophy was significant in caudate, putamen, globus pallidus, and thalamus (P < .001). Regions of interest analysis revealed a significant reduction in FA of the corpus callosum (CC) (-2.19%, P < .05) upon follow-up, whereas no significant cortical thinning and subcortical atrophy was found.

conclusionsThis study showed broad GM and WM abnormalities in manifest HD patients. Reductions in FA and cortical thinning correlated significantly with the disturbances of motor and cognitive processing that describe HD. Follow-up assessment showed that the CC is compromised in the absence of detectable GM changes or motor decline, suggesting it plays an important role in disease progression.

Indexed as

AdultAgedAnisotropyAtrophyBrainCross-Sectional StudiesDisease ProgressionFemaleGray MatterHumansHuntington DiseaseMagnetic Resonance ImagingMaleMiddle AgedWhite Matterclinical markerscortical thinningHuntington's diseasewhite matter

Identifiers

PMID32128927
PMCPMC7489289
OpenAlexW3009301587

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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.