报告题目：Pathogenesis and Early Diagnosis of Neurodegenerative Disease
报告人：叶克强教授（深圳理工大学）
报告地点：36365线路检测中心入口生命科学楼408室
报告时间：2023年9月4日下午2：30-4：00
主办单位：36365线路检测中心入口
报告人简介：
叶克强博士，现任深圳理工大学教授，曾任美国埃默里大学终身教授，博士生导师，国家特聘专家。叶克强教授是世界公认的小分子化合物治疗研发的领军科学家之一，是研发小分子化合物治疗神经退行性疾病领域的国际权威。主持美国国立卫生研究院、国防部科学基金和美国癌症协会/基金会等基金资助，总研究经费超过3000万美元。共发表论文258篇，包括Nature、Cell和Nature Medicine等国际顶级期刊，总影响因子超过2974分，H因子74，被引次数共计19700次。申请美国及世界发明专利24项，其中获批15项。曾荣获多项国际科学奖项，包括美国杰出青年科学基金（Distinguished Young Scientist Award, The Sontag Foundation）、癌症学会研究学者奖（American Cancer Society Scholar）等奖励。
报告内容：
Aging is the key risk factor for neurodegenerative diseases. Accumulating evidence suggests that C/EBPb/AEP signaling drives both Alzheimer’s disease (AD) and Parkinson’s disease (PD) onset and progression. C/EBPb acts as a major transcription factor for AEP (asparagine endopeptidase, also called legumain), and neuronal C/EBPb transgenic mice display gene dose-dependent short lifespan. Deletion of AEP from Thy1-C/EBPb Tg mice extends the lifespan. AEP levels are escalated in the brain in an age-dependent manner, cleaving APP, Tau and -Synuclein (a-Syn) at N585, N368 and N103, respectively, and triggering Abeta amyloids and Tau aggregation and a-Syn inclusions. Knockout of AEP substantially ameliorates AD and PD pathologies in their mouse models, restoring the behavioral functions. Thus, AEP proteolytic cleavage acts upstream of senile plaques and NFT and Lewy body pathologies, laying foundation for the early diagnosis of these devastating diseases. Quantitative SIMOA (single molecule array) methods have been developed for determining serum APP N585, C586 and Tau N368 levels. Early diagnosis of these neurodegenerative diseases will allow us to therapeutically treat or cure these devastating diseases in the future.
