Evidence map›Paper›PMID 32732969›Full record

ArticleTranslational psychiatry2020

Neuroinflammatory alterations in trait anxiety: modulatory effects of minocycline.

Sinead Rooney, Anupam Sah, Michael S Unger, Maria Kharitonova, Simone B Sartori, Christoph Schwarzer, Ludwig Aigner, Helmut Kettenmann, Susanne A Wolf, Nicolas Singewald

Open access · goldAbstract read
In one paragraph

Article in Translational psychiatry, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
4.0field-weighted citation impact, top 5% 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

38 citing papers in PubMed, 70 citations in OpenAlex.

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  13. Minocycline AmelioratesBrain 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

10 authors at 4 institutions in 2 countries.

Sinead Rooney *Department of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Anupam Sah *Department of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Michael S UngerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria.
Maria KharitonovaDepartment of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Simone B SartoriDepartment of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria.
Christoph SchwarzerDepartment of Pharmacology, Medical University of Innsbruck, Innsbruck, Austria.
Ludwig AignerInstitute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria.
Helmut KettenmannDepartment of Cellular Neurosciences, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Susanne A WolfDepartment of Cellular Neurosciences, Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Nicolas SingewaldDepartment of Pharmacology and Toxicology, Institute of Pharmacy and Center for Molecular Biosciences Innsbruck (CMBI), University of Innsbruck, Innsbruck, Austria. Nicolas.Singewald@uibk.ac.at.ORCID http://orcid.org/0000-0002-0166-3370
Universität Innsbruck · ATMax Delbrück Center · DEParacelsus Medical University · ATInnsbruck Medical University · AT

Funding

Austrian Science Fund FWF I 3875
6 · The paper itself

Abstract

High trait anxiety is a substantial risk factor for developing anxiety disorders and depression. While neuroinflammation has been identified to contribute to stress-induced anxiety, little is known about potential dysregulation in the neuroinflammatory system of genetically determined pathological anxiety or high trait anxiety individuals. We report microglial alterations in various brain regions in a mouse model of high trait anxiety (HAB). In particular, the dentate gyrus (DG) of the hippocampus of HABs exhibited enhanced density and average cell area of Iba1+, and density of phagocytic (CD68+/Iba1+) microglia compared to normal anxiety (NAB) controls. Minocycline was used to assess the capacity of a putative microglia 'inhibitor' in modulating hyperanxiety behavior of HABs. Chronic oral minocycline indeed reduced HAB hyperanxiety, which was associated with significant decreases in Iba1+ and CD68+Iba1+ cell densities in the DG. Addressing causality, it was demonstrated that longer (10 days), but not shorter (5 days), periods of minocycline microinfusions locally into the DG of HAB reduced Iba-1+ cell density and attenuated hyperanxiety-related behavior, indicating that neuroinflammation in the DG is at least partially involved in the maintenance of pathological anxiety. The present data reveal evidence of disturbances in the microglial system of individuals with high trait anxiety. Minocycline attenuated HAB hyperanxiety, likely by modulation of microglial activity within the DG. Thus, the present data suggest that drugs with microglia-targeted anti-inflammatory properties could be promising as novel alternative or complimentary anxiolytic therapeutic approaches in specific subgroups of individuals genetically predisposed to hyperanxiety.

Indexed as

Anti-Anxiety AgentsMinocyclineAnimalsAnxietyAnxiety DisordersMiceMicrogliaAnti-Anxiety AgentsMinocycline

Identifiers

PMID32732969
PMCPMC7393101
OpenAlexW3045766713

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.