Evidence map›Paper›PMID 37674553›Full record

ArticleFrontiers in psychiatry2023

Evidence for increased DNA damage repair in the postmortem brain of the high stress-response group of schizophrenia.

Risa Shishido, Yasuto Kunii, Mizuki Hino, Ryuta Izumi, Atsuko Nagaoka, Hideki Hayashi, Akiyoshi Kakita, Hiroaki Tomita, Hirooki Yabe

Open access · goldAbstract read
In one paragraph

Article in Frontiers in psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 38% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Novel Techniques for Mapping DNA Damage and Repair in the Brain.International journal of molecular sciences · 2024
    Review
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 3 institutions in 1 country.

Risa ShishidoDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Yasuto KuniiDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Mizuki HinoDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Ryuta IzumiDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Atsuko NagaokaDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Hideki HayashiDepartment of Pathology, Brain Research Institute, Niigata University, Niigata, Japan.
Akiyoshi KakitaDepartment of Pathology, Brain Research Institute, Niigata University, Niigata, Japan.
Hiroaki TomitaDepartment of Disaster Psychiatry, International Research Institute of Disaster Science, Tohoku University, Sendai, Japan.
Hirooki YabeDepartment of Neuropsychiatry, School of Medicine, Fukushima Medical University, Fukushima, Japan.
Fukushima Medical University · JPNiigata University · JPTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Schizophrenia (SZ) is a disorder diagnosed by specific symptoms and duration and is highly heterogeneous, clinically and pathologically. Although there are an increasing number of studies on the association between genetic and environmental factors in the development of SZ, the actual distribution of the population with different levels of influence of these factors has not yet been fully elucidated. In this study, we focused on stress as an environmental factor and stratified SZ based on the expression levels of stress-responsive molecules in the postmortem prefrontal cortex. Methods: We selected the following stress-responsive molecules: interleukin (IL) -1β, IL-6, IL-10, tumor necrosis factor-α, interferon-γ, glucocorticoid receptor, brain-derived neurotrophic factor, synaptophysin, S100 calcium-binding protein B, superoxide dismutase, postsynaptic density protein 95, synuclein, apolipoprotein A1 (ApoA1), ApoA2, and solute carrier family 6 member 4. We performed RNA sequencing in the prefrontal gray matter of 25 SZ cases and 21 healthy controls and conducted a hierarchical cluster analysis of SZ based on the gene expression levels of stress-responsive molecules, which yielded two clusters. After assessing the validity of the clusters, they were designated as the high stress-response SZ group and the low stress-response SZ group, respectively. Ingenuity Pathway Analysis of differentially expressed genes (DEGs) between clusters was performed, and Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining was conducted on four cases each in the high and low stress-response SZ groups to validate DNA damage. Results: We found higher prevalence of family history of SZ in the low stress-response SZ group (0/3 vs. 5/4, Conclusion: Our results suggest that there are subgroups of SZ with different degrees of stress impact. Furthermore, the pathophysiology of these subgroups may be associated with DNA damage repair. These results provide new insights into the interactions and heterogeneity between genetic and environmental factors.

Indexed as

DNA double-strand breakDNA double-strand break repair by homologous recombinationenvironmental factorheterogeneitypostmortem brainRNA-Seqschizophreniastress

Identifiers

PMID37674553
PMCPMC10478254
OpenAlexW4386070413

What OpenQuestion holds

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LicenceCC BY
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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.