Lung For-Wey, Fan Pao-Luo, Chen Nathan C, Shu Bih-Ching
Department of Psychiatry, Military Kaohsiung General Hospital, No. 2 Chung Cheng 1st Rd, Kaohsiung, Taiwan.
Psychiatr Genet. 2005 Mar;15(1):31-5. doi: 10.1097/00041444-200503000-00006.
Telomere shortening and increased MAOA gene activity both occur with aging. We undertook to develop a predictive model of telomere shortening and to investigate the possible association between MAOA gene promoter polymorphisms and telomere length as influenced by age and gender.
A stratified random household sample was selected from a community in southern Taiwan. Of 1231 subjects attending our health-screening program, 441 agreed to have additional venous blood withdrawn for DNA extraction and genetic study. Exactly 433 subjects completed the questionnaires and genetic analysis. Their telomere lengths were distributed (6.4-11.63 kb).
The rate of shortening per year was 69 base pairs, and the gender difference in length was not statistically significant (F = 0.091, P = 0.763). The lognormal distribution of telomere lengths was linear. The polynomial regression analysis showed Ln (telomere length) = -2.57-0.007 x age - 0.34 MAOA (adjusted R-square = 0.60). The gender effect on telomere length was not statistically significant (P = 0.52). No interaction effects were found between age, gender and MAOA gene polymorphisms. The high-activity allele of the MAOA promoter polymorphisms were negatively associated with telomere length (P = 0.013). Structural equation modeling confirmed the null model structure. The present data suggest that high-activity MAOA promoter gene polymorphisms, as in aging, are a risk factor for telomeric shortening.
Central nervous system serotonergic activity correlates with human aggressive behavior and depression in many studies, and the MAOA promoter gene may also serve as a clinical marker in the treatment of cardiovascular disease. The predictive model and table of telomere length presented in this study will provide a quick reference for future studies.
端粒缩短和单胺氧化酶A（MAOA）基因活性增加均与衰老有关。我们致力于建立一个端粒缩短的预测模型，并研究MAOA基因启动子多态性与受年龄和性别影响的端粒长度之间可能存在的关联。
从台湾南部的一个社区中选取分层随机家庭样本。在参加我们健康筛查项目的1231名受试者中，441人同意额外抽取静脉血用于DNA提取和基因研究。恰好433名受试者完成了问卷调查和基因分析。他们的端粒长度分布在（6.4 - 11.63 kb）之间。
每年的缩短速率为69个碱基对，长度的性别差异无统计学意义（F = 0.091，P = 0.763）。端粒长度的对数正态分布呈线性。多项式回归分析显示，ln（端粒长度）= -2.57 - 0.007×年龄 - 0.34×MAOA（调整后的决定系数 = 0.60）。性别对端粒长度的影响无统计学意义（P = 0.52）。未发现年龄、性别与MAOA基因多态性之间存在交互作用。MAOA启动子多态性的高活性等位基因与端粒长度呈负相关（P = 0.013）。结构方程模型证实了无效模型结构。目前的数据表明，MAOA启动子基因多态性的高活性，与衰老一样，是端粒缩短的一个危险因素。
在许多研究中，中枢神经系统血清素能活性与人类攻击行为和抑郁症相关，MAOA启动子基因也可能作为心血管疾病治疗的临床标志物。本研究中呈现的端粒长度预测模型和表格将为未来的研究提供快速参考。
