Evidence map›Paper›PMID 28119691›Full record

ArticleFrontiers in immunology2016

Microglial CD206 Gene Has Potential as a State Marker of Bipolar Disorder.

Masahiro Ohgidani, Takahiro A Kato, Yoshinori Haraguchi, Toshio Matsushima, Yoshito Mizoguchi, Toru Murakawa-Hirachi, Noriaki Sagata, Akira Monji, Shigenobu Kanba

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 46 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

9 authors at 2 institutions in 1 country.

Masahiro OhgidaniDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University , Fukuoka , Japan.
Takahiro A KatoDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan; Innovation Center for Medical Redox Navigation, Kyushu University, Fukuoka, Japan.
Yoshinori HaraguchiDepartment of Psychiatry, Graduate School of Medical Sciences, Saga University , Saga , Japan.
Toshio MatsushimaDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University , Fukuoka , Japan.
Yoshito MizoguchiDepartment of Psychiatry, Graduate School of Medical Sciences, Saga University , Saga , Japan.
Toru Murakawa-HirachiDepartment of Psychiatry, Graduate School of Medical Sciences, Saga University , Saga , Japan.
Noriaki SagataDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University , Fukuoka , Japan.
Akira MonjiDepartment of Psychiatry, Graduate School of Medical Sciences, Saga University , Saga , Japan.
Shigenobu KanbaDepartment of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University , Fukuoka , Japan.
Kyushu University · JPSaga University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathophysiology of bipolar disorder, especially the underlying mechanisms of the bipolarity between manic and depressive states, has yet to be clarified. Microglia, immune cells in the brain, play important roles in the process of brain inflammation, and recent positron emission tomography studies have indicated microglial overactivation in the brain of patients with bipolar disorder. We have recently developed a technique to induced microglia-like (iMG) cells from peripheral blood (monocytes). We introduce a novel translational approach focusing on bipolar disorder using this iMG technique. We hypothesize that immunological conditional changes in microglia may contribute to the shift between manic and depressive states, and thus we herein analyzed gene profiling patterns of iMG cells from three patients with rapid cycling bipolar disorder during both manic and depressive states, respectively. We revealed that the gene profiling patterns are different between manic and depressive states. The profiling pattern of case 1 showed that M1 microglia is dominant in the manic state compared to the depressive state. However, the patterns of cases 2 and 3 were not consistent with the pattern of case 1. CD206, a mannose receptor known as a typical M2 marker, was significantly downregulated in the manic state among all three patients. This is the first report to indicate the importance of shifting microglial M1/M2 characteristics, especially the CD206 gene expression pattern between depressive and manic states. Further translational studies are needed to dig up the microglial roles in the underlying biological mechanisms of bipolar disorder.

Indexed as

bipolar disorderCD206induced microglia-like (iMG) cellsM1/M2 polarizationmicrogliarapid cyclingstate markertranslational research

Identifiers

PMID28119691
PMCPMC5220016
OpenAlexW2585717798

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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.