Evidence map›Paper›PMID 38199813›Full record

ArticleJournal of neurology, neurosurgery, and psychiatry2024

Rates of cortical thinning in Alzheimer's disease signature regions associate with vascular burden but not with β-amyloid status in cognitively normal adults at age 70.

Sarah E Keuss, William Coath, David M Cash, Josephine Barnes, Jennifer M Nicholas, Christopher A Lane, Thomas D Parker, Ashvini Keshavan, Sarah M Buchanan, Aaron Z Wagen and 15 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neurology, neurosurgery, and psychiatry, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. 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

25 authors.

Sarah E KeussDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0002-7403-281X
William CoathDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
David M CashDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Josephine BarnesDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Jennifer M NicholasDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Christopher A LaneDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Thomas D ParkerDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0001-7679-4220
Ashvini KeshavanDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Sarah M BuchananDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Aaron Z WagenDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Mathew StoreyDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Matthew HarrisDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Kirsty LuDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0002-8416-2183
Sarah-Naomi JamesMRC Unit for Lifelong Health and Ageing at UCL, University College London, London, UK.
Rebecca StreetDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Ian B MaloneDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Carole H SudreDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
David L ThomasDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.ORCID 0000-0003-1491-1641
John C DicksonInstitute of Nuclear Medicine, University College London Hospitals NHS Foundation Trust, London, UK.
Frederik BarkhofDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Heidi Murray-SmithDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Andrew WongMRC Unit for Lifelong Health and Ageing at UCL, University College London, London, UK.
Marcus RichardsMRC Unit for Lifelong Health and Ageing at UCL, University College London, London, UK.
Nick C FoxDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK.
Jonathan M SchottDementia Research Centre, UCL Queen Square Institute of Neurology, University College London, London, UK j.schott@ucl.ac.uk.ORCID 0000-0003-2059-024X

Funding

British Heart Foundation PG/17/90/33415Medical Research Council MC_UU_00019/1Medical Research Council MC_UU_00019/3Medical Research Council MC_UU_12019/1Medical Research Council MC_UU_12019/3Wellcome TrustWellcome Trust 200109/Z/15/Z
6 · The paper itself

Abstract

backgroundConsistent patterns of reduced cortical thickness have been identified in early Alzheimer's disease (AD). However, the pathological factors that influence rates of cortical thinning within these AD signature regions remain unclear.

methodsParticipants were from the Insight 46 substudy of the MRC National Survey of Health and Development (NSHD; 1946 British birth cohort), a prospective longitudinal cohort study. Linear regression was used to examine associations of baseline cerebral β-amyloid (Aβ) deposition, measured using florbetapir positron emission tomography, and baseline white matter hyperintensity volume (WMHV) on MRI, a marker of cerebral small vessel disease, with subsequent longitudinal changes in AD signature cortical thickness quantified from baseline and repeat MRI (mean [SD] interval 2.4 [0.2] years).

resultsIn a population-based sample of 337 cognitively normal older white adults (mean [SD] age at baseline 70.5 [0.6] years; 48.1% female), higher global WMHV at baseline related to faster subsequent rates of cortical thinning in both AD signature regions (~0.15%/year faster per 10 mL additional WMHV), whereas baseline Aβ status did not. Among Aβ positive participants (n=56), there was some evidence that greater global Aβ standardised uptake value ratio at baseline related to faster cortical thinning in the AD signature Mayo region, but this did not reach statistical significance (p=0.08).

conclusionsCortical thinning within AD signature regions may develop via cerebrovascular pathways. Perhaps reflecting the age of the cohort and relatively low prevalence of Aβ-positivity, robust Aβ-related differences were not detected. Longitudinal follow-up incorporating additional biomarkers will allow assessment of how these relationships evolve closer to expected dementia onset.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesCerebral Cortical ThinningMagnetic Resonance ImagingPositron-Emission TomographyWhite MatterAgedAniline CompoundsCerebral CortexCerebral Small Vessel DiseasesEthylene GlycolsFemaleHumansLongitudinal StudiesMaleProspective StudiesAmyloid beta-PeptidesAniline CompoundsEthylene GlycolsflorbetapirALZHEIMER'S DISEASEAMYLOIDCEREBROVASCULAR DISEASE

Identifiers

PMID38199813
PMCPMC11287522

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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.