Evidence map›Paper›PMID 31769621›Full record

ArticleNeuropsychopharmacology reports2020

Structural variation in the glycogen synthase kinase 3β and brain-derived neurotrophic factor genes in Japanese patients with bipolar disorders.

Yosuke Suga, Keiichiro Yoshimoto, Shusuke Numata, Shinji Shimodera, Shogo Takamura, Naoto Kamimura, Ken Sawada, Hiromitsu Kazui, Tetsuro Ohmori, Shigeru Morinobu

Open access · goldAbstract read
In one paragraph

Article in Neuropsychopharmacology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 37% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. Article
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 5 institutions in 2 countries.

Yosuke SugaDepartment of Neuropsychiatry, Kochi Medical School, Kochi University, Nankoku, Japan.
Keiichiro YoshimotoWatarigawa Hostipal, Shimanto, Japan.
Shusuke NumataDepartment of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
Shinji ShimoderaGinza Shimodera Clinic, Tokyo, Japan.
Shogo TakamuraWatarigawa Hostipal, Shimanto, Japan.
Naoto KamimuraDepartment of Neuropsychiatry, Kochi Medical School, Kochi University, Nankoku, Japan.
Ken SawadaDepartment of Neuropsychiatry, Kochi Medical School, Kochi University, Nankoku, Japan.
Hiromitsu KazuiDepartment of Neuropsychiatry, Kochi Medical School, Kochi University, Nankoku, Japan.
Tetsuro OhmoriDepartment of Psychiatry, Course of Integrated Brain Sciences, Medical Informatics, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima, Japan.
Shigeru MorinobuDepartment of Neuropsychiatry, Kochi Medical School, Kochi University, Nankoku, Japan.ORCID 0000-0002-7496-7519
Kochi Medical School Hospital · JPTokushima University · JPWorld Water Watch · USCHI Health · USMinamiaoyama Eye Clinic · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLithium is the first-line drug for the treatment of bipolar disorders (BDs); however, not all patients responded. Glycogen synthase kinase (GSK) 3β and brain-derived neurotrophic factor (BDNF) play a role in the therapeutic action of lithium. Since structural variations were reported in these genes, it is possible that these genomic variations may be involved in the therapeutic responses to lithium.

methodFifty patients with BDs and 50 healthy subjects (mean age 55.0 ± 15.0 years; M/F 19/31) participated. We examined structural variation of the GSK3β and BDNF genes by real-time PCR. We examined the influence of structural variation of these genes on the therapeutic responses to lithium and the occurrence of antidepressant-emergent affective switch (AEAS). The efficacy of lithium was assessed using the Alda scale, and AEAS was evaluated using Young Mania Rating Scale.

resultsAlthough we examined structural variations within intron II and VII of the GSK3

conclusionThe amplification of the BDNF gene influenced neither the therapeutic responses to lithium nor the occurrence of AEAS.

Indexed as

AdultAgedAntimanic AgentsBipolar DisorderBrain-Derived Neurotrophic FactorCytoskeletal ProteinsFemaleHumansJapanLithium CompoundsMaleMiddle AgedNuclear ProteinsPharmacogenomic TestingAntimanic AgentsBDNF protein, humanBrain-Derived Neurotrophic FactorCytoskeletal ProteinsLithium CompoundsNIN protein, humanNuclear Proteinsbipolar disorderbrain-derived neurotrophic factorcopy number variationglycogen synthase kinase 3®lithium

Identifiers

PMID31769621
PMCPMC7292225
OpenAlexW2991199072

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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.