Authors
Na Cai, University of Oxford
Simon Chang, Chang Gung University
Yihan Li, University of Oxford
Qiban Li, BGI-Shenzhen
Jingchu Hu, BGI-Shenzhen
Jieqin Liang, BGI-Shenzhen
Li Song, BGI-Shenzhen
Warren Kretzschmar, University of Oxford
Xiangchao Gan, Max Planck Institute for Plant Breeding Research
Jerome Nicod, University of Oxford
Margarita Rivera, University of Granada, Institute of Psychiatry at King's College
Hong Deng, Mental Health Center of West China Hospital of Sichuan University
Bo Du, Hebei Mental Health Center
Keqing Li, Hebei Mental Health Center
Wenhu Sang, Hebei Mental Health Center
Jingfang Gao, Zhejiang Traditional Chinese Medical Hospital
Shugui Gao, Ningbo Kang Ning Hospital
Baowei Ha, Liaocheng No. 4 Hospital
Hung-Yao Ho, Chang Gung University
Chunmei Hu, No. 3 Hospital of Heilongjiang Province
Jian Hu, Harbin Medical University
Zhenfei Hu, BGI-Shenzhen
Guoping Huang, Sichuan Mental Health Center
Guoqing Jiang, Chongqing Mental Health Center
Tao Jiang, BGI-Shenzhen
Wei Jin, BGI-Shenzhen
Gongying Li, Mental Health Institute of Jining Medical College
Kan Li, Mental Hospital of Jiangxi Province
Yi Li, Wuhan Mental Health Center
Yingrui Li, BGI-Shenzhen
Youhui Li, No. 1 Hospital of Zhengzhou University
Yu-Ting Lin, Chang Gung University
Lanfen Liu, Shandong Mental Health Center
Tiebang Liu, Kangning Hospital
Ying Liu, The First Hospital of China Medical University
Yuan Liu, BGI-Shenzhen
Yao Lu, BGI-Shenzhen
Luxian Lv, Psychiatric Hospital of Henan Province
Huaqing Meng, No. 1 Hospital of Chongqing Medical University
Puyi Qian, BGI-Shenzhen
Hong Sang, Changchun Mental Hospital
Jianhua Shen, Tianjin Anding Hospital
Jianguo Shi, Xian Mental Health Center
Jing Sun, Brain Hospital of Nanjing Medical University
Ming Tao, Second Affiliated Hospital of Zhejiang Chinese Medical University
Gang Wang, Beijing Anding Hospital of Capital University of Medical Sciences
Guangbiao Wang, BGI-Shenzhen
Jian Wang, BGI-Shenzhen
Linmao Wang, BGI-Shenzhen
Xueyi Wang, First Hospital of Hebei Medical University
Xumei Wang, ShengJing Hospital of China Medical University
Huanming Yang, BGI-Shenzhen
Lijun Yang, Jilin Brain Hospital
Ye Yin, BGI-Shenzhen
Jinbei Zhang, No. 3 Hospital of Sun Yat-sen University
Kerang Zhang, No. 1 Hospital of Shanxi Medical University
Ning Sun, No. 1 Hospital of Shanxi Medical University
Wei Zhang, Daqing No. 3 Hospital of Heilongjiang Province
Xiuqing Zhang, BGI-Shenzhen
Zhen Zhang, No. 4 Hospital of Jiangsu University
Hui Zhong, Anhui Mental Health Center
Gerome Breen, Institute of Psychiatry at King’s College
Jun Wang, BGI-Shenzhen
Jonathan Marchini, University of Oxford
Yiping Chen, University of Oxford
Qi Xu, Chinese Academy of Medical Sciences and Peking Union Medical College
Xun Xu, BGI-Shenzhen
Richard Mott, University of Oxford
Guo-Jen Huang, Chang Gung University
Kenneth S. Kendler, Virginia Commonwealth UniversityFollow
Jonathan Flint, University of Oxford, East China Normal University
Original Publication Date
2015
Journal/Book/Conference Title
Current Biology
DOI of Original Publication
10.1016/j.cub.2015.03.008
Date of Submission
December 2015
Abstract
Adversity, particularly in early life, can cause illness. Clues to the responsible mechanisms may lie with the discovery of molecular signatures of stress, some of which include alterations to an individual’s somatic genome. Here, using genome sequences from 11,670 women, we observed a highly significant association between a stress-related disease, major depression, and the amount of mtDNA (p = 9.00 × 10−42, odds ratio 1.33 [95% confidence interval [CI] = 1.29–1.37]) and telomere length (p = 2.84 × 10−14, odds ratio 0.85 [95% CI = 0.81–0.89]). While both telomere length and mtDNA amount were associated with adverse life events, conditional regression analyses showed the molecular changes were contingent on the depressed state. We tested this hypothesis with experiments in mice, demonstrating that stress causes both molecular changes, which are partly reversible and can be elicited by the administration of corticosterone. Together, these results demonstrate that changes in the amount of mtDNA and telomere length are consequences of stress and entering a depressed state. These findings identify increased amounts of mtDNA as a molecular marker of MD and have important implications for understanding how stress causes the disease.
Rights
Copyright © 2015 The Authors This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/). This document was posted here by permission of the publisher. At the time of the deposit, it included all changes made during peer review, copy editing, and publishing. The U. S. National Library of Medicine is responsible for all links within the document and for incorporating any publisher-supplied amendments or retractions issued subsequently. The published journal article, guaranteed to be such by Elsevier, is available for free, on ScienceDirect, at: http://dx.doi.org/10.1016/j.cub.2015.03.008
Is Part Of
VCU Psychiatry Publications
Comments
Originally published at http://dx.doi.org/10.1016/j.cub.2015.03.008