Comprehensive DNA methylation analysis of peripheral blood cells derived from patients with first-episode schizophrenia
Abstract
Epidemiological studies have revealed that schizophrenia is highly heritable. However, genetic studies have not fully elucidated its etiology. Accumulating evidence suggests that epigenetic alterations may provide an additional explanation of its pathophysiology. We investigated the methylation profiles of DNA in peripheral blood cells from 18 patients with first-episode schizophrenia (FESZ) and from 15 normal controls. Schizophrenia patients were confined to those at the stage of first-episode psychosis. We analyzed the DNA methylation status of 27,578 CpG sites by means of the Illumina Infinium HumanMethylation27 BeadChip array. Differentially methylated CpG sites, which were particularly abundant within CpG islands, were enriched in genes related to the nuclear lumen, to transcription factor binding, and to nucleotide binding. We also observed differential methylation of the promoters of HTR1E and COMTD1, which are functionally related to genes found to be differentially methylated in schizophrenia patients in previous studies. Our results indicate the site-specific epigenetic alterations in patients with FESZ.
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EWAS studies have identified differential DNAm in HTR2A, HTR5A and HTR1E genes in those with psychosis.
“Further, EWAS studies have identified differential DNAm in HTR2A (Numata, Ye, Herman, & Lipska, 2014), HTR5A and HTR1E (Nishioka et al., 2013; Pidsley et al., 2014) genes in those with psychosis.”
From Can epigenetics shine a light on the biological pathways underlying major mental disorders? (2022) · cites this paper as Nishioka et al., 2013
EWAS studies comparing SCZ patients with controls have found hypomethylation of SLC6A3, COMTD1 and FAM63B.
“EWAS studies comparing SCZ patients with controls have found hypomethylation of SLC6A3, a dopamine transporter (Nishioka et al., 2013), COMTD1 and FAM63B, a gene linked to dopaminergic gene expression (Aberg et al., 2014).”
From Can epigenetics shine a light on the biological pathways underlying major mental disorders? (2022) · cites this paper as Nishioka et al., 2013
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References 42 · Cited by 101
- Authors
- Nishioka, M., Bundo, M., Koike, S., Takizawa, R., Kakiuchi, C., Araki, T., Kasai, K., & Iwamoto, K.
- Affiliations
- The University of Tokyo (JP)
- University of London (GB)
- Corresponding author
- Iwamoto, Kazuya
- ORCID
- Venue
- Journal of Human Genetics
- Published
- 2012-12-13
- Volume
- 58
- Issue
- 2
- Pages
- 91-97
- ISSN
- 1434-5161 (ISSN-L)
- 1435-232X
- OpenAlex
- W1993421515
- Cited by
- 101
- References
- 42
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 3 · 2023: 5 · 2022: 9 · 2021: 9 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 8 · 2016: 12 · 2015: 13 · 2014: 19 · 2013: 5
- FWCI
- 4.75
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Human Genetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Ministry of Education, Culture, Sports, Science and Technology
- University of Tokyo
- Japan Society for the Promotion of Science (24390279, 22659214, 23791310, 24591676, 23791309)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- schizophrenia, first-episode schizophrenia, DNA methylation, epigenetics, peripheral blood cells, CpG sites, differentially methylated regions, CpG islands, promoter methylation
- MeSH terms
- Adolescent, Adult, Female, Humans, Male, Schizophrenia, Cluster Analysis, Case-Control Studies, CpG Islands, DNA Methylation, Principal Component Analysis, Young Adult
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