报告题目：淀粉样蛋白前体与阿尔茨海默症
报 告人：杨莉 教授（广州大学）
时 间：2018年6月7日（星期四） 上午 8:20
报告地点：文萃校区生命科学学院二楼学术报告厅
生命科学学院
2018年6月7日
附：报告人简介
杨莉，广州大学生命科学院教授
1985年在新疆师范大学获学士学位；分别于1991、1995年在华东师范大学获硕士和博士学位；1998-2010年间先后在南伊利诺大学医学院和贝勒医学院做博士后和助理研究员；2010-2017年间任华南师范大学教授,博导；2017年10月迄今：广州大学百人计划引进教授。
学术身份：中国心理学会生理心理分会委员；广东省脑发育与脑病防治学会常务理事；广东省神经科学会理事；广东省生物物理学会理事。
研究兴趣：1）神经退变性疾病的发病机理、神经环路以及早期生物标记物；2）社会行为及情感的神经生物学机制。在包括Neuron，PNAS，eLife，Cerebral Cortex，Journal of Neuroscience，Neurobiology of Aging在内的SCI刊物发表了30多篇研究论文。领衔翻译了John P.J. Pinel第九版《生物心理学》。
报告题目及摘要
APP and Alzheimer’s Disease
Alzheimer's disease (AD) is a neurodegenerative disorder characterized by progressive beta-amyloid (Aβ) deposition and cognitive decline. Genetic and biochemical studies have focused on the role of Aβ, a cleavage product of amyloid precursor protein (APP), in the pathogenesis of AD. In comparison, the physiological role of APP is still poorly understood. We have previously shown an impairment of hippocampal GABAergic short-term plasticity in APP knock-out (APP -/-) mice, but the precise mechanism underlying APP regulation of GABAergic synaptic activity has remained elusive. Using APP -/- and littermate controls, we show that APP physically interacts with KCC2, a neuron-specific K+-Cl- co-transporter, which is essential for Cl- homeostasis and fast GABAergic inhibition. APP deficiency results in significant reduction in levels of KCC2, leading to a depolarizing shift in the EGABA in hippocampal neurons. Moreover, restoration of normal KCC2 expression and function in APP-/- mice rescues the deficits. Furthermore, the in vivo Up-down state, a key feature of cortical synaptic integration associated with cognition and memory processing, demonstrates an enhanced excitation due to insufficient inhibition in the prefrontal cortex (PFC) of APP-/- compared to WT controls. While decreased excitation is observed in the PFC in mice overexpressing APP. These results elucidate novel molecular pathways in which APP regulates synaptic activities.