Evidence map›Paper›PMID 41528030›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2026

Discovery of disrupted sustained attention and altered functional connectivity in far-from-onset Huntington's disease gene-expanded young adults.

Christelle Langley, Michela Leocadi, Nicola Z Hobbs, Mena Farag, Michael J Murphy, Kate Fayer, Rachael I Scahill, James B Rowe, Trevor W Robbins, Sarah J Tabrizi and 1 more

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Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2026. 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

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

1 citing paper in PubMed.

  1. Article
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

11 authors.

Christelle LangleyDepartment of Psychiatry, University of Cambridge, Cambridge, UK.ORCID https://orcid.org/0000-0001-5061-2820
Michela LeocadiHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Nicola Z HobbsHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Mena FaragHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Michael J MurphyHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Kate FayerHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Rachael I ScahillHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
James B RoweDepartment of Clinical Neurosciences, University of Cambridge, Cambridge, UK.
Trevor W RobbinsBehavioural and Clinical Neuroscience Institute, University of Cambridge, Cambridge, UK.
Sarah J TabriziHuntington's Disease Centre, Department of Neurodegenerative Disease, UCL Queen Square Institute of Neurology, University College London, London, UK.
Barbara J SahakianDepartment of Psychiatry, University of Cambridge, Cambridge, UK.ORCID https://orcid.org/0000-0001-7352-1745

Funding

Wellcome TrustWellcome Trust 220258Wellcome Trust 223082/Z/21/Z
6 · The paper itself

Abstract

backgroundCognitive impairments are a hallmark of Huntington's disease (HD).

methodsSeventy-one participants (43 HD gene-expanded [HDGE], 28 healthy controls) from the HD-Young Adult Study at two timepoints ≈ 4.7 years apart, completed the Cambridge Neuropsychological Test Automated Battery Rapid Visual Information Processing task and underwent resting-state functional magnetic resonance imaging. We focused on predefined regions of interest that are involved in sustained attention.

resultsHDGE individuals showed significantly poorer sustained attention than controls (p DISCUSSION: These findings demonstrate early and persistent attention deficits in HDGE, linked to altered FC in attention-related circuits. This supports the presence of early cognitive dysfunction in HD and highlights potential compensatory and pathological changes in brain networks prior to the onset of clinical motor symptoms. HIGHLIGHTS: We detail the discovery of early sustained attention deficits in Huntington's disease (HD) gene-expanded (HDGE) young adults. These sustained attention deficits do not measurably decline over a 4.7-year period. Altered functional connectivity was observed in attention-related brain networks. Alterations in regions include occipital, opercular, lentiform, and frontal areas. Findings support attention as an early cognitive biomarker in HDGE young adults.

Indexed as

AttentionBrainHuntington DiseaseAdultBrain MappingFemaleHumansMagnetic Resonance ImagingMaleNeural PathwaysNeuropsychological TestsYoung AdultHuntington's diseaseresting‐state fMRIsustained attention

Identifiers

PMID41528030
PMCPMC12797252

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Registered trials

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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.