TY - JOUR
T1 - DNA methylation analyses of the candidate genes identified by a methylome-wide association study revealed common epigenetic alterations in schizophrenia and bipolar disorder
AU - Sugawara, Hiroko
AU - Murata, Yui
AU - Ikegame, Tempei
AU - Sawamura, Rie
AU - Shimanaga, Shota
AU - Takeoka, Yusuke
AU - Saito, Takeo
AU - Ikeda, Masashi
AU - Yoshikawa, Akane
AU - Nishimura, Fumichika
AU - Kawamura, Yoshiya
AU - Kakiuchi, Chihiro
AU - Sasaki, Tsukasa
AU - Iwata, Nakao
AU - Hashimoto, Mamoru
AU - Kasai, Kiyoto
AU - Kato, Tadafumi
AU - Bundo, Miki
AU - Iwamoto, Kazuya
N1 - Publisher Copyright:
© 2018 The Authors. Psychiatry and Clinical Neurosciences published by John Wiley & Sons Australia, Ltd on behalf of Japanese Society of Psychiatry and Neurology
PY - 2018/4
Y1 - 2018/4
N2 - 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.
AB - 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.
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U2 - 10.1111/pcn.12645
DO - 10.1111/pcn.12645
M3 - Article
C2 - 29430824
AN - SCOPUS:85045102806
SN - 1323-1316
VL - 72
SP - 245
EP - 254
JO - Psychiatry and clinical neurosciences
JF - Psychiatry and clinical neurosciences
IS - 4
ER -