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Psychiatry Clin Neurosci. 2018 Apr;72(4):245-254. doi: 10.1111/pcn.12645. Epub 2018 Mar 11.

DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder.

Author information

1
Department of Neuropsychiatry, Faculty of Life Sciences, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
2
Support Center for Women Health Care Professionals and Researchers, Tokyo Women's Medical University, Tokyo, Japan.
3
Department of Molecular Brain Science, Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.
4
Department of Neuropsychiatry, The University of Tokyo, Tokyo, Japan.
5
Department of Psychiatry, Fujita Health University School of Medicine, Aichi, Japan.
6
Department of Psychiatry, Shonan Kamakura General Hospital, Kamakura, Japan.
7
Laboratory of Health Education, Graduate School of Education, The University of Tokyo, Tokyo, Japan.
8
Laboratory for Molecular Dynamics of Mental Disorders, RIKEN Brain Science Institute, Saitama, Japan.
9
PRESTO, Japan Science and Technology Agency, Tokyo, Japan.

Abstract

AIM:

Schizophrenia (SZ) and bipolar disorder (BD) have been known to share genetic and environmental risk factors, and complex gene-environmental interactions may contribute to their pathophysiology. In contrast to high genetic overlap between SZ and BD, as revealed by genome-wide association studies, the extent of epigenetic overlap remains largely unknown. In the present study, we explored whether SZ and BD share epigenetic risk factors in the same manner as they share genetic components.

METHODS:

We performed DNA methylation analyses of the CpG sites in the top five candidate regions (FAM63B, ARHGAP26, CTAGE11P, TBC1D22A, and intergenic region [IR] on chromosome 16) reported in a previous methylome-wide association study (MWAS) of SZ, using whole blood samples from subjects with BD and controls.

RESULTS:

Among the five candidate regions, the CpG sites in FAM63B and IR on chromosome 16 were significantly hypomethylated in the samples from subjects with BD as well as those from subjects with SZ. On the other hand, the CpG sites in TBC1D22A were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ.

CONCLUSION:

Hypomethylation of FAM63B and IR on chromosome 16 could be common epigenetic risk factors for SZ and BD. Further comprehensive epigenetic studies for BD, such as MWAS, will uncover the extent of similarity and uniqueness of epigenetic alterations.

KEYWORDS:

FAM63B; DNA methylation; MWAS; bipolar disorder; schizophrenia

PMID:
29430824
DOI:
10.1111/pcn.12645
[Indexed for MEDLINE]
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