Evidence map›Paper›PMID 33615219›Full record

ArticleBrain communications2021

Visuomotor integration deficits are common to familial and sporadic preclinical Alzheimer's disease.

Kirsty Lu, Jennifer M Nicholas, Philip S J Weston, Julie C Stout, Alison M O'Regan, Sarah-Naomi James, Sarah M Buchanan, Christopher A Lane, Thomas D Parker, Sarah E Keuss and 12 more

Open access · goldAbstract read
In one paragraph

Article in Brain communications, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
1.1field-weighted citation impact, top 27% 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

8 citing papers in PubMed, 10 citations in OpenAlex.

  1. Article
  2. Review
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  8. Dissociable effects ofNature aging · 2021
    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

22 authors at 5 institutions in 2 countries.

Kirsty LuDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0002-8416-2183
Jennifer M NicholasDepartment of Medical Statistics, London School of Hygiene and Tropical Medicine, London, WC1E 7HT, UK.
Philip S J WestonDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Julie C StoutTurner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Melbourne, Victoria, Australia.ORCID 0000-0001-9637-8590
Alison M O'ReganTurner Institute for Brain and Mental Health, School of Psychological Sciences, Monash University, Melbourne, Victoria, Australia.
Sarah-Naomi JamesMRC Unit for Lifelong Health and Ageing at UCL, London, WC1E 7HB, UK.
Sarah M BuchananDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Christopher A LaneDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Thomas D ParkerDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Sarah E KeussDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Ashvini KeshavanDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Heidi Murray-SmithDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
David M CashDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0001-7833-616X
Carole H SudreMRC Unit for Lifelong Health and Ageing at UCL, London, WC1E 7HB, UK.
Ian B MaloneDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
William CoathDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Andrew WongMRC Unit for Lifelong Health and Ageing at UCL, London, WC1E 7HB, UK.
Marcus RichardsMRC Unit for Lifelong Health and Ageing at UCL, London, WC1E 7HB, UK.
Susie M D HenleyDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Nick C FoxDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
Jonathan M SchottDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.ORCID 0000-0003-1422-4358
Sebastian J CrutchDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, WC1N 3BG, UK.
UK Dementia Research Institute · GBMRC Unit for Lifelong Health and Ageing · GBMonash University · AUKing's College London · GBUniversity of London · GB

Funding

British Heart Foundation PG/17/90/33415Medical Research Council MC_UU_00019/3Medical Research Council MC_UU_12019/3Medical Research Council MR/M003108/1Wellcome Trust
6 · The paper itself

Abstract

We investigated whether subtle visuomotor deficits were detectable in familial and sporadic preclinical Alzheimer's disease. A circle-tracing task-with direct and indirect visual feedback, and dual-task subtraction-was completed by 31 individuals at 50% risk of familial Alzheimer's disease (19 presymptomatic mutation carriers; 12 non-carriers) and 390 cognitively normal older adults (members of the British 1946 Birth Cohort, all born during the same week; age range at assessment = 69-71 years), who also underwent β-amyloid-PET/MRI to derive amyloid status (positive/negative), whole-brain volume and white matter hyperintensity volume. We compared preclinical Alzheimer's groups against controls cross-sectionally (mutation carriers versus non-carriers; amyloid-positive versus amyloid-negative) on speed and accuracy of circle-tracing and subtraction. Mutation carriers (mean 7 years before expected onset) and amyloid-positive older adults traced disproportionately less accurately than controls when visual feedback was indirect, and were slower at dual-task subtraction. In the older adults, the same pattern of associations was found when considering amyloid burden as a continuous variable (Standardized Uptake Value Ratio). The effect of amyloid was independent of white matter hyperintensity and brain volumes, which themselves were associated with different aspects of performance: greater white matter hyperintensity volume was also associated with disproportionately poorer tracing accuracy when visual feedback was indirect, whereas larger brain volume was associated with faster tracing and faster subtraction. Mutation carriers also showed evidence of poorer tracing accuracy when visual feedback was direct. This study provides the first evidence of visuomotor integration deficits common to familial and sporadic preclinical Alzheimer's disease, which may precede the onset of clinical symptoms by several years.

Indexed as

Alzheimer’s diseaseamyloid imagingattentionbiomarkersneurodegenerationproprioception

Identifiers

PMID33615219
PMCPMC7882207
OpenAlexW3114097522

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.