Evidence map›Paper›PMID 30201713›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

The brain's hemodynamic response function rapidly changes under acute psychosocial stress in association with genetic and endocrine stress response markers.

Immanuel G Elbau, Benedikt Brücklmeier, Manfred Uhr, Janine Arloth, Darina Czamara, Victor I Spoormaker, Michael Czisch, Klaas Enno Stephan, Elisabeth B Binder, Philipp G Sämann

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 61 citations in OpenAlex.

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  2. HRNeurophotonics · 2026
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  15. Neurovascular coupling: motive unknown.Trends in neurosciences · 2022
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 3 institutions in 4 countries.

Immanuel G ElbauDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Benedikt BrücklmeierMax Planck Institute of Psychiatry, D-80804 Munich, Germany.
Manfred UhrMax Planck Institute of Psychiatry, D-80804 Munich, Germany.
Janine ArlothDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Darina CzamaraDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Victor I SpoormakerDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Michael CzischMax Planck Institute of Psychiatry, D-80804 Munich, Germany.
Klaas Enno StephanTranslational Neuromodeling Unit, Institute for Biomedical Engineering, University of Zurich and Swiss Federal Institute of Technology Zurich, 8032 Zurich, Switzerland.
Elisabeth B BinderDepartment of Translational Research in Psychiatry, Max Planck Institute of Psychiatry, D-80804 Munich, Germany.
Philipp G SämannMax Planck Institute of Psychiatry, D-80804 Munich, Germany; saemann@psych.mpg.de.ORCID 0000-0001-8523-3628
Max Planck Institute of Psychiatry · DEEmory University · USWellcome Centre for Human Neuroimaging · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ample evidence links dysregulation of the stress response to the risk for psychiatric disorders. However, we lack an integrated understanding of mechanisms that are adaptive during the acute stress response but potentially pathogenic when dysregulated. One mechanistic link emerging from rodent studies is the interaction between stress effectors and neurovascular coupling, a process that adjusts cerebral blood flow according to local metabolic demands. Here, using task-related fMRI, we show that acute psychosocial stress rapidly impacts the peak latency of the hemodynamic response function (HRF-PL) in temporal, insular, and prefrontal regions in two independent cohorts of healthy humans. These latency effects occurred in the absence of amplitude effects and were moderated by regulatory genetic variants of

Indexed as

BrainCerebrovascular CirculationEndocrine CellsGenetic VariationHemodynamicsHumansMagnetic Resonance ImagingNeurovascular CouplingStress, Psychologicalfunctional MRIhemodynamic responseneurovascular couplingpsychosocial stressstress

Identifiers

PMID30201713
PMCPMC6205450
OpenAlexW2891454663

What OpenQuestion holds

Textmetadata
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.