Evidence map›Paper›PMID 26251601›Full record

ArticleNeuropsychiatric disease and treatment2015

Genetic association between G protein-coupled receptor kinase 6/β-arrestin 2 and dopamine supersensitivity psychosis in schizophrenia.

Yasunori Oda, Nobuhisa Kanahara, Hiroshi Kimura, Hiroyuki Watanabe, Kenji Hashimoto, Masaomi Iyo

Open access · goldAbstract read
In one paragraph

Article in Neuropsychiatric disease and treatment, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 28% 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

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 10 citations in OpenAlex.

  1. Pooled it
  2. Dopamine supersensitivity psychosis: a critical evaluation of diagnostic validators.Journal of neural transmission (Vienna, Austria : 1996) · 2026
    Review
  3. Article
  4. Article
  5. Burn injury induces elevated inflammatory traffic: the role of NF-κB.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Review
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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

6 authors at 2 institutions in 1 country.

Yasunori OdaDepartment of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan.
Nobuhisa KanaharaDivision of Medical Treatment and Rehabilitation, Chiba University Center for Forensic Mental Health, Chiba, Japan.
Hiroshi KimuraDepartment of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan.
Hiroyuki WatanabeDivision of Medical Treatment and Rehabilitation, Chiba University Center for Forensic Mental Health, Chiba, Japan.
Kenji HashimotoDivision of Clinical Neuroscience, Chiba University Center for Forensic Mental Health, Chiba, Japan.
Masaomi IyoDepartment of Psychiatry, Chiba University Graduate School of Medicine, Chiba, Japan.
Center for Forensic Mental Health, Chiba University · JPChiba University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

aimDopamine supersensitivity psychosis (DSP), clinically characterized by unstable and severe psychosis or tardive dyskinesia and often categorized as treatment-resistant schizophrenia, is promoted by long-term antipsychotic treatment. An upregulation of the dopamine D2 receptor caused by antipsychotic(s) is involved in the development of DSP. The present study explored the potential roles of G protein-coupled receptor kinase 6 (GRK6) and β-arrestin 2 (ARRB2) that are involved in the trafficking of DRD2 in patients with DSP.

methodsWe conducted a genetic association study of GRK6/ARRB2 between the patients with DSP episodes [DSP(+) group: N=108] and the patients without DSP(-) episodes [DSP(-) group: N=169] from the total group of patients (N=333). Based on the patients' treatment history, a DSP episode was defined as withdrawal psychosis, developed tolerance to antipsychotic effect, and tardive dyskinesia (the remaining 56 patients were excluded due to insufficient information).

resultsThe results revealed that none of the allelic or genotyping distributions of five single nucleotide polymorphisms (SNPs) of GRK6 and three SNPs of ARRB2 showed any significant difference between the DSP(+) and DSP(-) groups.

conclusionThe results suggest that the SNP analyses of these two molecules fail to classify patients into the potential clinical subtype of DSP(+) or DSP(-) group. However, since GRK6 and ARRB2 are surely involved in dopamine D2 receptor metabolism, further studies based on prospective observations of the onset of DSP under specific antipsychotic treatments are needed.

Indexed as

antipsychoticdopamine D2 receptortardive dyskinesiatreatment-resistant

Identifiers

PMID26251601
PMCPMC4524575
OpenAlexW2120014078

What OpenQuestion holds

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LicenceCC BY-NC
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.