Jae-Min Kim1, Hee-Ju Kang1, Kyung-Yeol Bae1, Sung-Wan Kim1, Il-Seon Shin1, Hye-Ran Kim2, Myung-Geun Shin3, Jin-Sang Yoon4. 1. Department of Psychiatry, Chonnam National University Medical School, Gwangju, Korea. 2. Brain Korea 21 Project, Center for Biomedical Human Resources, Chonnam National University Medical School, Gwangju, Korea. 3. Department of Laboratory Medicine, Chonnam National University Medical School, Gwangju, Korea. 4. Department of Psychiatry, Chonnam National University Medical School, Gwangju, Korea. Electronic address: jsyoon@chonnam.ac.kr.
Abstract
OBJECTIVES: Brain-derived neurotrophic factor (BDNF) has been considered a risk factor for suicidal behavior in adult populations. BDNF secretion is influenced by epigenetic (DNA promoter methylation) and genetic (val66met polymorphism) profiles. We investigated the independent and interactive effects of BDNF methylation status and val66met polymorphisms on late-life suicidal ideation. METHODS: In total, 732 Korean community residents aged 65+ years were evaluated; of 639 without suicidal ideation, 579 (90.6%) were followed up 2 years later. The prevalence and incidence of suicidal ideation were ascertained using the Geriatric Mental State Schedule. Sociodemographic and clinical covariates included age, sex, education, depressive symptoms, cognitive function, and disability. The independent effects of BDNF methylation status on the prevalence and incidence of suicidal ideation were investigated using multivariate logistic regression models. The two-way interactions of BDNF methylation status and val66met polymorphism on suicidal ideation were assessed using the same models. RESULTS: Higher BDNF methylation status was significantly associated with both prevalence and incidence of suicidal ideation, independent of potential covariates. No significant methylation-genotype interaction was found. CONCLUSIONS: The BDNF hypothesis and the epigenetic origin of the suicidal behavior were supported, even in old age. BDNF promoter methylation status may be useful as a biological marker for suicidality in late life.
OBJECTIVES:Brain-derived neurotrophic factor (BDNF) has been considered a risk factor for suicidal behavior in adult populations. BDNF secretion is influenced by epigenetic (DNA promoter methylation) and genetic (val66met polymorphism) profiles. We investigated the independent and interactive effects of BDNF methylation status and val66met polymorphisms on late-life suicidal ideation. METHODS: In total, 732 Korean community residents aged 65+ years were evaluated; of 639 without suicidal ideation, 579 (90.6%) were followed up 2 years later. The prevalence and incidence of suicidal ideation were ascertained using the Geriatric Mental State Schedule. Sociodemographic and clinical covariates included age, sex, education, depressive symptoms, cognitive function, and disability. The independent effects of BDNF methylation status on the prevalence and incidence of suicidal ideation were investigated using multivariate logistic regression models. The two-way interactions of BDNF methylation status and val66met polymorphism on suicidal ideation were assessed using the same models. RESULTS: Higher BDNF methylation status was significantly associated with both prevalence and incidence of suicidal ideation, independent of potential covariates. No significant methylation-genotype interaction was found. CONCLUSIONS: The BDNF hypothesis and the epigenetic origin of the suicidal behavior were supported, even in old age. BDNF promoter methylation status may be useful as a biological marker for suicidality in late life.
Authors: Ming Ai; Jun Wang; Jianmei Chen; Wo Wang; Xiaoming Xu; Yao Gan; Xuemei Li; Xinyuan Gou; Jun Cao; Zhen Lv; Xiaorong Chen; Hengguang Wang; Qing Ma; Li Kuang Journal: Pharmgenomics Pers Med Date: 2019-07-02
Authors: Dominik A Moser; Ariane Paoloni-Giacobino; Ludwig Stenz; Wafae Adouan; Aurélia Manini; Francesca Suardi; Maria I Cordero; Marylene Vital; Ana Sancho Rossignol; Sandra Rusconi-Serpa; François Ansermet; Alexandre G Dayer; Daniel S Schechter Journal: PLoS One Date: 2015-12-09 Impact factor: 3.240