Evidence map›Paper›PMID 26298692›Full record

ArticlePsychoneuroendocrinology2015

Does white matter structure or hippocampal volume mediate associations between cortisol and cognitive ageing?

Simon R Cox, Sarah E MacPherson, Karen J Ferguson, Natalie A Royle, Susana Muñoz Maniega, Maria Del C Valdés Hernández, Mark E Bastin, Alasdair M J MacLullich, Joanna M Wardlaw, Ian J Deary

Open access · hybridAbstract read
In one paragraph

Article in Psychoneuroendocrinology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Remission is insufficient: predictors and mechanistic models of recurrence in late-life depression.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  7. Promoting Successful Cognitive Aging: A Ten-Year Update.Journal of Alzheimer's disease : JAD · 2021
    Review
  8. Article
  9. Disruption of Neural Homeostasis as a Model of Relapse and Recurrence in Late-Life Depression.The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry · 2019
    Review
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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

10 authors at 1 institution in 1 country.

Simon R CoxCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Department of Psychology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK. Electronic address: simon.cox@ed.ac.uk.
Sarah E MacPhersonCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Department of Psychology, University of Edinburgh, UK.
Karen J FergusonCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Edinburgh Delirium Research Group, Geriatric Medicine, University of Edinburgh, UK.
Natalie A RoyleCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK; Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK.
Susana Muñoz ManiegaCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK; Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK.
Maria Del C Valdés HernándezCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK; Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK.
Mark E BastinCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK; Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK.
Alasdair M J MacLullichCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Edinburgh Delirium Research Group, Geriatric Medicine, University of Edinburgh, UK.
Joanna M WardlawCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Brain Research Imaging Centre, Neuroimaging Sciences, University of Edinburgh, UK; Scottish Imaging Network, A Platform for Scientific Excellence (SINAPSE) Collaboration, Edinburgh, UK.
Ian J DearyCentre for Cognitive Ageing and Cognitive Epidemiology, University of Edinburgh, UK; Department of Psychology, University of Edinburgh, UK.
University of Edinburgh · GB

Funding

Biotechnology and Biological Sciences Research CouncilMedical Research Council G0700704Medical Research Council G0701120Medical Research Council G1001245Medical Research Council MR/K026992/1
6 · The paper itself

Abstract

Elevated glucocorticoid (GC) levels putatively damage specific brain regions, which in turn may accelerate cognitive ageing. However, many studies are cross-sectional or have relatively short follow-up periods, making it difficult to relate GCs directly to changes in cognitive ability with increasing age. Moreover, studies combining endocrine, MRI and cognitive variables are scarce, measurement methods vary considerably, and formal tests of the underlying causal hypothesis (cortisol→brain→cognition) are absent. In this study, 90 men, aged 73 years, provided measures of fluid intelligence, processing speed and memory, diurnal and reactive salivary cortisol and two measures of white matter (WM) structure (WM hyperintensity volume from structural MRI and mean diffusivity averaged across 12 major tracts from diffusion tensor MRI), hippocampal volume, and also cognitive ability at age 11. We tested whether negative relationships between cognitive ageing differences (over more than 60 years) and salivary cortisol were significantly mediated by WM and hippocampal volume. Significant associations between reactive cortisol at 73 and cognitive ageing differences between 11 and 73 (r=-.28 to -.36, p<.05) were partially mediated by both WM structural measures, but not hippocampal volume. Cortisol-WM relationships were modest, as was the degree to which WM structure attenuated cortisol-cognition associations (<15%). These data support the hypothesis that GCs contribute to cognitive ageing differences from childhood to the early 70s, partly via brain WM structure.

Indexed as

AgedAgingCognitionCross-Sectional StudiesDiffusion Tensor ImagingHippocampusHumansHydrocortisoneMaleNeuropsychological TestsOrgan SizeSalivaWhite MatterHydrocortisoneAgeingCognitive changeCortisolHippocampusWhite matter

Identifiers

PMID26298692
PMCPMC4642652
OpenAlexW1905023764

What OpenQuestion holds

Textmetadata
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.