Evidence map›Paper›PMID 26500502›Full record

ArticleFrontiers in cellular neuroscience2015

First evidence for glial pathology in late life minor depression: S100B is increased in males with minor depression.

Maryna Polyakova, Christian Sander, Katrin Arelin, Leonie Lampe, Tobias Luck, Melanie Luppa, Jürgen Kratzsch, Karl-Titus Hoffmann, Steffi Riedel-Heller, Arno Villringer and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

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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

12 authors at 2 institutions in 1 country.

Maryna PolyakovaDepartment of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; University Clinic for Psychiatry and Psychotherapy, Leipzig University Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.
Christian SanderUniversity Clinic for Psychiatry and Psychotherapy, Leipzig University Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.
Katrin ArelinDepartment of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.
Leonie LampeDepartment of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.
Tobias LuckLIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Institute of Social Medicine, Occupational Health and Public Health (ISAP), Leipzig University Leipzig, Germany.
Melanie LuppaLIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Institute of Social Medicine, Occupational Health and Public Health (ISAP), Leipzig University Leipzig, Germany.
Jürgen KratzschLIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Institute of Laboratory Medicine, Clinical Chemistry and Molecular Diagnostics, Leipzig University Leipzig, Germany.
Karl-Titus HoffmannDepartment of Neuroradiology, Leipzig University Leipzig, Germany.
Steffi Riedel-HellerLIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Institute of Social Medicine, Occupational Health and Public Health (ISAP), Leipzig University Leipzig, Germany.
Arno VillringerDepartment of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Clinic for Cognitive Neurology, University of Leipzig Leipzig, Germany.
Peter SchoenknechtUniversity Clinic for Psychiatry and Psychotherapy, Leipzig University Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany.
Matthias L SchroeterDepartment of Neurology, Max Planck Institute for Human Cognitive and Brain Sciences Leipzig, Germany ; LIFE-Leipzig Rsearch Center for Civilization Diseases, Leipzig University Leipzig, Germany ; Clinic for Cognitive Neurology, University of Leipzig Leipzig, Germany.
Leipzig University · DEMax Planck Institute for Human Cognitive and Brain Sciences · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Minor depression is diagnosed when a patient suffers from 2 to 4 depressive symptoms for at least 2 weeks. Though minor depression is a widespread phenomenon, its pathophysiology has hardly been studied. To get a first insight into the pathophysiological mechanisms underlying this disorder we assessed serum levels of biomarkers for plasticity, glial and neuronal function: brain-derived neurotrophic factor (BDNF), S100B and neuron specific enolase (NSE). 27 subjects with minor depressive episode and 82 healthy subjects over 60 years of age were selected from the database of the Leipzig population-based study of civilization diseases (LIFE). Serum levels of BDNF, S100B and NSE were compared between groups, and correlated with age, body-mass index (BMI), and degree of white matter hyperintensities (score on Fazekas scale). S100B was significantly increased in males with minor depression in comparison to healthy males, whereas other biomarkers did not differ between groups (p = 0.10-0.66). NSE correlated with Fazekas score in patients with minor depression (rs = 0.436, p = 0.048) and in the whole sample (rs = 0.252, p = 0.019). S100B correlated with BMI (rs = 0.246, p = 0.031) and with age in healthy subjects (rs = 0.345, p = 0.002). Increased S100B in males with minor depression, without alterations in BDNF and NSE, supports the glial hypothesis of depression. Correlation between white matter hyperintensities and NSE underscores the vascular hypothesis of late life depression.

Indexed as

BDNFbiomarkerglialate life depressionminor depressionNSES100Bwhite matter hyperintensities

Identifiers

PMID26500502
PMCPMC4598479
OpenAlexW2264632913

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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.