Evidence map›Paper›PMID 40563832›Full record

ArticleBrain sciences2025

Cortical and Striatal Functional Connectivity in Juvenile-Onset Huntington's Disease.

Amy Barry, Peg C Nopoulos

Abstract read
In one paragraph

Article in Brain sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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

What it found

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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

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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

1 citing paper in PubMed.

  1. 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

2 authors.

Amy BarryInterdisciplinary Graduate Program in Neuroscience, University of Iowa, Iowa City, IA 52242, USA.
Peg C NopoulosDepartment of Psychiatry, Carver College of Medicine, University of Iowa, Iowa City, IA 52242, USA.ORCID 0000-0001-8810-1903

Funding

Growth and Development of the Striatum in Huntington's DiseaseR01NS055903 · NINDS · UNIVERSITY OF IOWA · PI PEGGY C NOPOULOS · 2009 to 2026
$5.0M
University of Iowa - Research 3T MRI Connectome UpgradeS10OD025025 · OD · UNIVERSITY OF IOWA · PI MAGNOTTA, VINCENT A · 2018 to 2018
$1.9M
CHDI Foundation 071108NIH HHS 1R01NS055903-09NIH HHS S10 OD025025NIH, Office of the Director (Institute code is OD) 1S10OD025025-01NINDS NIH HHS R01 NS055903
6 · The paper itself

Abstract

backgroundHuntington's disease (HD) is a neurodegenerative disorder caused by a CAG repeat expansion in the HTT gene, with a rare juvenile-onset form (JoHD) marked by early, rigid motor symptoms. This study examined cortical and subcortical resting-state connectivity in JoHD, hypothesizing preserved cortical networks but altered striatal connectivity, in line with early subcortical atrophy despite relatively spared cortical volume.

methodsParticipants included children and young adults with clinician-confirmed Juvenile-Onset Huntington's Disease (JoHD;

resultsJoHD participants showed reduced connectivity within the left somatomotor network and striatal circuits, despite largely typical cortical network connectivity. Striatal connectivity was associated with disease burden and cognitive ability, while left somatomotor connectivity was unrelated to clinical outcomes.

conclusionsThese findings support the hypothesis of antagonistic pleiotropy in JoHD, where early neural advantages-such as relatively preserved or possibly enhanced cortical function-may contribute to later striatal vulnerability and degeneration. The observed left-lateralized somatomotor hypoconnectivity aligns with prior volumetric and gene expression research, highlighting the role of excitotoxic glutamatergic input and the selective vulnerability of high-functioning circuits in disease progression.

Indexed as

antagonistic pleiotropyjuvenile-onset Huntington’s diseaseresting-state functional connectivitysomatomotor networkstriatal hypoconnectivity

Identifiers

PMID40563832
PMCPMC12191134

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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.