耳聋是发病率最高的感官性缺陷性疾病，随着人类的平均寿命将进一步延长，特别今后若干年人口老龄化更加明显，老年性聋（presbycusis）受到了越来越多的关注。目前老年性聋相关基因鉴定进展较为缓慢，对于老年性聋的分子机制也所知甚少，构建老年性聋的动物模型对解决以上问题尤为重要。我们计划模拟NAT2、GSTT1及GSTM1与老年性聋相关的突变，构建基因敲除\敲入小鼠，利用构建的动物模型对这些基因在老年性聋发生中的作用进行探讨，包括检测基因突变小鼠听力水平，检测基因突变小鼠耳蜗ROS水平，利用形态学，组织化学和分子生物学等技术对突变小鼠进行深入研究。研究结果将对老年性聋的预防和诊治具有重要的意义。

Deafness is a kind sensory disease with high morbidity ratio. With the prolongation of average age in human, especially the condition that population aging will become more serious in the future years, presbycusis is attracting more attention for scientific research. The identification of genes related to presbycusis progress slowly, and the molecular mechanisms about presbycusis remain unrevealed. Animal models on presbycusis are urgently needed for solving these problems. In our research plan, we will mimic NAT2, GSTT1 and GSTM1 gene mutations in human and construct gene knock out/in mouse models. These mouse models will be used to reveal gene functions,including hearing ability and cochlear ROS levels. In addition, we will use other methods, including histochemistry, morphology, molecular biology technology, to explore the mechanisms of causing presbycusis in these mutant mice. Our research will contribute to the prevention and diagnosis to presbycusis disease.