ATAD3A调控线粒体动力学在OSAS大鼠认知障碍中的机制研究

阻塞性睡眠呼吸暂停综合征与认知障碍密切相关，但具体的发生机制尚不明确，突触可塑性的变化影响着认知功能，突触可塑性与能量代谢相关，线粒体在能量代谢的调控中起着关键作用。本课题组前期研究发现，OSAS大鼠出现认知功能障碍，海马神经元线粒体分裂与融合蛋白发生变化。而ATAD3A在线粒体动力学中起着至关重要的作用。那么ATAD3A是否可通过调控线粒体动力学，从而影响OSAS大鼠认知功能的形成？本项目拟构建ATAD3A病毒，观察OSAS大鼠行为学，用膜片钳监测脑片电生理变化，分子生物技术检测神经细胞相关分子的表达，观察干预前后ATAD3A的功能变化，比较OSAS患者和健康人血液及脑脊液中相关分子的表达，从分子机制的角度揭示OSAS认知障碍形成的机制，期望为治疗提供新的药物靶标。

Obstructive sleep apnea syndrome（OSAS） is closely related to the Cognitive dysfunction, but its specific mechanism is not clear. Synaptic.plasticity can affect cognitive function, while synaptic plasticity is related to energy metabolism. Mitochondria plays a key role in the regulation of energy metabolism. Our previous study found that OSAS rats presented cognitive dysfunction, mitochondrial division and fusion protein changes in hippocampal neurons.While ATAD3A plays an important role in mitochondrial dynamics. So can ATAD3A affect the formation of cognitive function in OSAS rats by regulating mitochondrial dynamics? The project intends to construct ATAD3A virus to observe animal behavior, monitor the electrophysiological changes of brain slices with patch clamp, and detect the expression of hippocampus related proteins by molecules biology techniques. At last, it will reveal the formation mechanism of cognitive dysfunction after OSAS from the perspective of molecular signaling pathway, and provide a new target for its treatment.