DNA methylation analyses of the candidate genes identified by a methylome‐wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder.
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| Title: | DNA methylation analyses of the candidate genes identified by a methylome‐wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder. |
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| Authors: | Sugawara, Hiroko, Murata, Yui, Ikegame, Tempei, Sawamura, Rie, Shimanaga, Shota, Takeoka, Yusuke, Saito, Takeo, Ikeda, Masashi, Yoshikawa, Akane, Nishimura, Fumichika, Kawamura, Yoshiya, Kakiuchi, Chihiro, Sasaki, Tsukasa, Iwata, Nakao, Hashimoto, Mamoru, Kasai, Kiyoto, Kato, Tadafumi, Bundo, Miki, Iwamoto, Kazuya |
| Source: | Psychiatry & Clinical Neurosciences. Apr2018, Vol. 72 Issue 4, p245-254. 10p. 1 Chart, 3 Graphs. |
| Subjects: | DNA methylation, Epigenetics, Genetics of schizophrenia, Genetics of bipolar disorder, Pathological physiology |
| 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 ( |
| Copyright of Psychiatry & Clinical Neurosciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 128973255 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: DNA methylation analyses of the candidate genes identified by a methylome‐wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Sugawara%2C+Hiroko%22">Sugawara, Hiroko</searchLink><br /><searchLink fieldCode="AR" term="%22Murata%2C+Yui%22">Murata, Yui</searchLink><br /><searchLink fieldCode="AR" term="%22Ikegame%2C+Tempei%22">Ikegame, Tempei</searchLink><br /><searchLink fieldCode="AR" term="%22Sawamura%2C+Rie%22">Sawamura, Rie</searchLink><br /><searchLink fieldCode="AR" term="%22Shimanaga%2C+Shota%22">Shimanaga, Shota</searchLink><br /><searchLink fieldCode="AR" term="%22Takeoka%2C+Yusuke%22">Takeoka, Yusuke</searchLink><br /><searchLink fieldCode="AR" term="%22Saito%2C+Takeo%22">Saito, Takeo</searchLink><br /><searchLink fieldCode="AR" term="%22Ikeda%2C+Masashi%22">Ikeda, Masashi</searchLink><br /><searchLink fieldCode="AR" term="%22Yoshikawa%2C+Akane%22">Yoshikawa, Akane</searchLink><br /><searchLink fieldCode="AR" term="%22Nishimura%2C+Fumichika%22">Nishimura, Fumichika</searchLink><br /><searchLink fieldCode="AR" term="%22Kawamura%2C+Yoshiya%22">Kawamura, Yoshiya</searchLink><br /><searchLink fieldCode="AR" term="%22Kakiuchi%2C+Chihiro%22">Kakiuchi, Chihiro</searchLink><br /><searchLink fieldCode="AR" term="%22Sasaki%2C+Tsukasa%22">Sasaki, Tsukasa</searchLink><br /><searchLink fieldCode="AR" term="%22Iwata%2C+Nakao%22">Iwata, Nakao</searchLink><br /><searchLink fieldCode="AR" term="%22Hashimoto%2C+Mamoru%22">Hashimoto, Mamoru</searchLink><br /><searchLink fieldCode="AR" term="%22Kasai%2C+Kiyoto%22">Kasai, Kiyoto</searchLink><br /><searchLink fieldCode="AR" term="%22Kato%2C+Tadafumi%22">Kato, Tadafumi</searchLink><br /><searchLink fieldCode="AR" term="%22Bundo%2C+Miki%22">Bundo, Miki</searchLink><br /><searchLink fieldCode="AR" term="%22Iwamoto%2C+Kazuya%22">Iwamoto, Kazuya</searchLink> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Psychiatry+%26+Clinical+Neurosciences%22">Psychiatry & Clinical Neurosciences</searchLink>. Apr2018, Vol. 72 Issue 4, p245-254. 10p. 1 Chart, 3 Graphs. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22DNA+methylation%22">DNA methylation</searchLink><br /><searchLink fieldCode="DE" term="%22Epigenetics%22">Epigenetics</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics+of+schizophrenia%22">Genetics of schizophrenia</searchLink><br /><searchLink fieldCode="DE" term="%22Genetics+of+bipolar+disorder%22">Genetics of bipolar disorder</searchLink><br /><searchLink fieldCode="DE" term="%22Pathological+physiology%22">Pathological physiology</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: 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 (<italic>FAM63B</italic>, <italic>ARHGAP26</italic>, <italic>CTAGE11P</italic>, <italic>TBC1D22A,</italic> 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 <italic>FAM63B</italic> 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 <italic>TBC1D22A</italic> were hypermethylated in the samples from subjects with BD, in contrast to hypomethylation in the samples from subjects with SZ. Conclusion: Hypomethylation of <italic>FAM63B</italic> 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. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Psychiatry & Clinical Neurosciences is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1111/pcn.12645 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 10 StartPage: 245 Subjects: – SubjectFull: DNA methylation Type: general – SubjectFull: Epigenetics Type: general – SubjectFull: Genetics of schizophrenia Type: general – SubjectFull: Genetics of bipolar disorder Type: general – SubjectFull: Pathological physiology Type: general Titles: – TitleFull: DNA methylation analyses of the candidate genes identified by a methylome‐wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Sugawara, Hiroko – PersonEntity: Name: NameFull: Murata, Yui – PersonEntity: Name: NameFull: Ikegame, Tempei – PersonEntity: Name: NameFull: Sawamura, Rie – PersonEntity: Name: NameFull: Shimanaga, Shota – PersonEntity: Name: NameFull: Takeoka, Yusuke – PersonEntity: Name: NameFull: Saito, Takeo – PersonEntity: Name: NameFull: Ikeda, Masashi – PersonEntity: Name: NameFull: Yoshikawa, Akane – PersonEntity: Name: NameFull: Nishimura, Fumichika – PersonEntity: Name: NameFull: Kawamura, Yoshiya – PersonEntity: Name: NameFull: Kakiuchi, Chihiro – PersonEntity: Name: NameFull: Sasaki, Tsukasa – PersonEntity: Name: NameFull: Iwata, Nakao – PersonEntity: Name: NameFull: Hashimoto, Mamoru – PersonEntity: Name: NameFull: Kasai, Kiyoto – PersonEntity: Name: NameFull: Kato, Tadafumi – PersonEntity: Name: NameFull: Bundo, Miki – PersonEntity: Name: NameFull: Iwamoto, Kazuya IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 04 Text: Apr2018 Type: published Y: 2018 Identifiers: – Type: issn-print Value: 13231316 Numbering: – Type: volume Value: 72 – Type: issue Value: 4 Titles: – TitleFull: Psychiatry & Clinical Neurosciences Type: main |
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