Evidence map›Paper›PMID 40174930›Full record

ArticleJournal of psychiatry & neuroscience : JPN

Genome-wide DNA methylation profiling of blood samples from patients with major depressive disorder: correlation with symptom heterogeneity.

Yukiko Nagao, Mao Fujimoto, Ying Tian, Shinichi Kameyama, Kotaro Hattori, Shinsuke Hidese, Hiroshi Kunugi, Yae Kanai, Eri Arai

Abstract read
In one paragraph

Article in Journal of psychiatry & neuroscience : JPN. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Review
  2. Article
  3. 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.

Yukiko Nagao *From the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Mao Fujimoto *From the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Ying TianFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Shinichi KameyamaFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Kotaro HattoriFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Shinsuke HideseFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Hiroshi KunugiFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori).
Yae KanaiFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori) ykanai@keio.jp earai@keio.jp.
Eri AraiFrom the Department of Pathology, Keio University School of Medicine (Nagao, Fujimoto, Tian, Kameyama, Kanai, Arai); the Department of Mental Disorder Research, National Institute of Neuroscience, National Center for Neurology and Psychiatry (Hattori, Hidese, Kunugi); the Department of Bioresources, Medical Genome Center, National Center for Neurology and Psychiatry, Tokyo, Japan (Hattori) ykanai@keio.jp earai@keio.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAlterations in DNA, such as DNA methylation, may be key molecular events involved in the development of major depressive disorder (MDD). We sought to clarify correlations between DNA methylation profiles and symptom heterogeneity among patients with MDD.

methodsWe conducted a genome-wide DNA methylation analysis of blood samples from patients with MDD and controls, using the Infinium MethylationEPIC BeadChip.

resultsWe analyzed 283 blood samples, including 141 from an initial cohort (69 patients with MDD, 72 controls) and 142 from a second validation cohort (67 patients with MDD, 75 controls). After adjustment for age, sex, and blood cell heterogeneity, DNA methylation status at 2699 CpG sites tended to differ between patients with MDD and controls in both the initial and second cohorts. Hierarchical clustering of patients based on DNA methylation status at these 2699 CpG sites revealed a significant correlation with scores for GRID-Hamilton Depression Rating Scale (GRID-HAMD) items (depressed mood, guilt, early insomnia, middle insomnia, work and activities, psychic anxiety, loss of appetite, general somatic symptoms, and total score), suggesting the feasibility of severity diagnostics based on blood DNA methylation testing. Pathway over-representation analysis revealed that genes whose DNA methylation status was correlated with epigenetic clustering were accumulated in molecular pathways involved in various cellular functions, especially nerve development. For LIMITATIONS: Although we performed marker exploration using 2 cohorts including 283 participants, the heterogeneity of the molecular mechanisms operating in MDD might necessitate a larger cohort for establishment of criteria with sufficient diagnostic impact.

conclusionThese findings indicate that the DNA methylation status of specific genes may correlate with the severity of MDD symptoms, and that genome-wide DNA methylation analysis of blood samples would be useful for clarifying the DNA methylation profiles related to symptom heterogeneity.

Indexed as

DNA MethylationMajor Depressive DisorderAdultCohort StudiesCpG IslandsFemaleGenome-Wide Association StudyHumansMaleMiddle Aged

Identifiers

PMID40174930
PMCPMC11975397

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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.