Published on Sept. 1, 2015 in J Affect Disord volume 183DP - 2015 Sep 1TI - An association study of the m6A genes with major depressive disorder in Chinese Hanpopulation.PG - 279-86LID - S0165-0327(15)00325-0 [pii]LID - 10.1016/j.jad.2015.05.025 [doi]AB - BACKGROUND: Major depressive disorder (MDD) is a common, chronic and recurrentmental disease but the precise mechanism behind this disorder remains unknown. FTOis one of the N6-methyladenosine (m6A) modification genes and has recently beenfound to be associated with depression. N6-methyladenosine (m6A) is the mostabundant internal modification on RNA, which is highly enriched within the brain.There are five genes involved in m6A modification including FTO, but whether thesem6A modification genes could confer a risk of MDD is still unclear. This study aimedto investigate the genetic influence of the m6A modification genes on risk of MDD.METHODS: We genotyped 23 SNPs in 5 modification genes among 738 patients with MDDand 1098 controls. The UNPHASED program was applied to analyze the genotyping datafor allelic and genotypic association with MDD. RESULTS: Of the 23 SNPs selected,rs12936694 from the m6A demethylase gene ALKBH5 showed allelic association(χ(2)=11.19, p=0.0008, OR=1.491, 95%CI 1.179-1.887) and genotypic association(χ(2)=12.26, df=2, p=0.0022) with MDD. LIMITATIONS: Replication and functional studyare required to draw a firm conclusion. CONCLUSIONS: The ALKBH5 gene may play a rolein conferring risk of MDD in the Chinese population.CI - Copyright © 2015 Elsevier B.V. All rights reserved.FAU - Du, TingfuAU - Du TAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Rao, ShuquanAU - Rao SAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Wu, LinAU - Wu LAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Ye, NingAU - Ye NAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Liu, ZeyueAU - Liu ZAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Hu, HuilingAU - Hu HAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Xiu, JianboAU - Xiu JAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Shen, YanAU - Shen YAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China.FAU - Xu, QiAU - Xu QAD - National Laboratory of Medical Molecular Biology, Institute of Basic MedicalSciences and Neuroscience Center, Chinese Academy of Medical Sciences and PekingUnion Medical College, Tsinghua University, Beijing 100005, China. Electronicaddress: xuqi@pumc.edu.cn.LA - engPT - Journal ArticlePT - Research Support, Non-U.S. Gov&#39;tDEP - 20150521PL - NetherlandsTA - J Affect DisordJT - Journal of affective disordersJID - 7906073RN - 0 (Membrane Proteins)RN - 1867-73-8 (N6-methyladenosine (m6A))RN - EC 1.13.11.- (Dioxygenases)RN - EC 1.14.11.- (ALKBH5 protein, human)RN - EC 1.14.11.- (AlkB Homolog 5, RNA Demethylase)RN - K72T3FS567 (Adenosine)SB - IMMH - Adenosine/*analogs &amp; derivatives/geneticsMH - AdultMH - AlkB Homolog 5, RNA DemethylaseMH - AllelesMH - Asian Continental Ancestry Group/*geneticsMH - Case-Control StudiesMH - China/epidemiologyMH - Depressive Disorder, Major/*geneticsMH - Dioxygenases/*geneticsMH - FemaleMH - GenotypeMH - HumansMH - MaleMH - Membrane Proteins/*geneticsMH - Middle AgedMH - Polymorphism, Single NucleotideMH - Risk FactorsOTO - NOTNLMOT - ALKBH5OT - Major depressive disorderOT - RNA methylationOT - m6A modificationEDAT- 2015/06/06 06:00MHDA- 2016/01/13 06:00CRDT- 2015/06/06 06:00PHST- 2015/01/28 00:00 [received]PHST- 2015/04/17 00:00 [revised]PHST- 2015/05/11 00:00 [accepted]PHST- 2015/06/06 06:00 [entrez]PHST- 2015/06/06 06:00 [pubmed]PHST- 2016/01/13 06:00 [medline]AID - S0165-0327(15)00325-0 [pii]AID - 10.1016/j.jad.2015.05.025 [doi]PST - ppublishSO - J Affect Disord. 2015 Sep 1;183:279-86. doi: 10.1016/j.jad.2015.05.025. Epub 2015May 21.</pre></div></body></html>().

PubMed ID: 26047305

DOI: S0165-0327(15)00325-0


Abstract:

BACKGROUND: Major depressive disorder (MDD) is a common, chronic and recurrentmental disease but the precise mechanism behind this disorder remains unknown. FTOis one of the N6-methyladenosine (m6A) modification genes and has recently beenfound to be associated with depression. N6-methyladenosine (m6A) is the mostabundant internal modification on RNA, which is highly enriched within the brain.There are five genes involved in m6A modification including FTO, but whether thesem6A modification genes could confer a risk of MDD is still unclear. This study aimedto investigate the genetic influence of the m6A modification genes on risk of MDD.METHODS: We genotyped 23 SNPs in 5 modification genes among 738 patients with MDDand 1098 controls. The UNPHASED program was applied to analyze the genotyping datafor allelic and genotypic association with MDD. RESULTS: Of the 23 SNPs selected,rs12936694 from the m6A demethylase gene ALKBH5 showed allelic association(χ(2)=11.19, p=0.0008, OR=1.491, 95%CI 1.179-1.887) and genotypic association(χ(2)=12.26, df=2, p=0.0022) with MDD. LIMITATIONS: Replication and functional studyare required to draw a firm conclusion. CONCLUSIONS: The ALKBH5 gene may play a rolein conferring risk of MDD in the Chinese population.CI - Copyright © 2015 Elsevier B.V. All rights reserved.



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