Evidence map›Paper›PMID 35875796›Full record

ArticleFrontiers in aging neuroscience2022

Cerebrospinal Fluid Cortisol and Dehydroepiandrosterone Sulfate, Alzheimer's Disease Pathology, and Cognitive Decline.

Sami Ouanes, Christopher Clark, Jonas Richiardi, Bénédicte Maréchal, Piotr Lewczuk, Johannes Kornhuber, Clemens Kirschbaum, Julius Popp

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.3field-weighted citation impact, top 6% 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

21 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
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  4. Stress, stress systems, and Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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  9. An Update of Salivary Biomarkers for the Diagnosis of Alzheimer's Disease.International journal of molecular sciences · 2025
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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

8 authors at 5 institutions in 3 countries.

Sami OuanesService of Old Age Psychiatry, Department of Psychiatry, Lausanne University Hospital, Lausanne, Switzerland.
Christopher ClarkCentre for Gerontopsychiatric Medicine, Geriatric Psychiatry, University Hospital of Psychiatry Zürich, Zurich, Switzerland.
Jonas RichiardiDepartment of Radiology, Lausanne University Hospital, Lausanne, Switzerland.
Bénédicte MaréchalDepartment of Radiology, Lausanne University Hospital, Lausanne, Switzerland.
Piotr LewczukDepartment of Psychiatry and Psychotherapy, University Hospital, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
Johannes KornhuberDepartment of Psychiatry and Psychotherapy, University Hospital, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
Clemens KirschbaumChair of Biopsychology, Technische Universität Dresden, Andreas-Schubert-Bau, Dresden, Germany.
Julius PoppService of Old Age Psychiatry, Department of Psychiatry, Lausanne University Hospital, Lausanne, Switzerland.
Friedrich-Alexander-Universität Erlangen-Nürnberg · DEUniversity Hospital of Zurich · CHUniversity of Lausanne · CHHamad Medical Corporation · QATU Dresden · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Introduction: Elevated cortisol levels have been reported in Alzheimer's disease (AD) and may accelerate the development of brain pathology and cognitive decline. Dehydroepiandrosterone sulfate (DHEAS) has anti-glucocorticoid effects and it may be involved in the AD pathophysiology. Objectives: To investigate associations of cerebrospinal fluid (CSF) cortisol and DHEAS levels with (1) cognitive performance at baseline; (2) CSF biomarkers of amyloid pathology (as assessed by CSF Aβ levels), neuronal injury (as assessed by CSF tau), and tau hyperphosphorylation (as assessed by CSF p-tau); (3) regional brain volumes; and (4) clinical disease progression. Materials and Methods: Individuals between 49 and 88 years ( Results: Higher CSF cortisol was associated with poorer global cognitive performance and higher disease severity at baseline. Cortisol and cortisol/DHEAS ratio were positively associated with tau and p-tau CSF levels, and negatively associated with the amygdala and insula volumes at baseline. Higher CSF cortisol predicted more pronounced cognitive decline and clinical disease progression over 36 months. Higher CSF DHEAS predicted more pronounced disease progression over 36 months. Conclusion: Increased cortisol in the CNS is associated with tau pathology and neurodegeneration, and with decreased insula and amygdala volume. Both CSF cortisol and DHEAS levels predict faster clinical disease progression. These results have implications for the identification of patients at risk of rapid decline as well as for the development of interventions targeting both neurodegeneration and clinical manifestations of AD.

Indexed as

Alzheimer’s diseasecerebrospinal fluidcognitive declinecortisolDHEASneurodegeneration

Identifiers

PMID35875796
PMCPMC9301040
OpenAlexW4284893007

What OpenQuestion holds

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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.