阿尔茨海默病（AD）是以学习记忆障碍为特征的神经退行性疾病，严重危害老年人群身心健康，但机制不明。近年来，神经环路异常在AD学习记忆障碍中的研究得到国内外学者的关注。我们最近报道内嗅皮层II区锥体神经元-海马CA1区PV神经元（ECIIPN-CA1PV）环路异常在AD学习记忆障碍中起重要作用，但其具体分子机制不明。本项目将综合运用生物信息学、分子生物学、电生理、分子成像及行为学检测等手段，明确我们通过二代测序发现的在内嗅皮层异常升高的长链非编码RNA mSYT-AS在ECIIPN-CA1PV环路功能障碍中的机理并探索其在AD脑内升高的分子机制，同时评估特异性调控mSYT-AS在AD早期防治中的意义，为AD早期防治提供新的分子靶标。

Alzheimer's disease is a neurodegenerative disease characterized by the deficits of learning and memory and seriously damages mental and physical health of elderly people. However, the underlying mechanisms are still missing. Recently, the role of neural circuit dysfunction in the learning and memory loss in AD has been gained extensively attention. .We recently reported that a novel neural circuit from the pyramidal neurons in the layer II of entorhinal cortex to the CA1 palvalbulmin neurons in the hippocampus plays an important role in the Alzheimer’s memory deficits. While the underlying mechanisms are not clear. Here, we we will explore the detailed roles and mechanisms of mSYT-AS, a novel lncRNA that was found by our RNA sequence results and increased in the entorhinal cortex, in the dysfunction of ECIIPN-CA1PV circuit of AD and evaluate the significance of lncRNA manipulation in the early prevention of AD by using bioinformatics, molecular biological, electrophysiological, molecular imaging and behavioral approach。