孙安阳：

1966年10月生，教授、博士生导师。1996年在原上海医科大学获博士学位，导师杨藻宸教授。1996年－1999年在原上海医科大学医学神经生物学国家重点实验室工作，任副教授。1999年7月－12月在德国亚琛应用科技大学从事自由基的研究；2000年3月－2005年6月在美国肯塔基大学和哈佛医学院从事阿尔茨海默病的基础研究。回国前任哈佛医学院Instructor。2005年7月加盟复旦大学神经生物学研究所。主要应用多种遗传性小鼠模型、细胞培养和AD患者脑组织等材料，从整体、细胞和分子不同层次开展阿尔茨海默病的神经生物学基础研究。


近期论著

1. Pastorino L* , Sun AY *, Lu PJ* , Zhou XZ, Balasˇtík M, Finn G, Wulf GM , Lim J, Li SH, Li X, Xia W, Nicholson L, Lu KP. The prolyl isomerase Pin1 regulates amyloid precursor protein processing and Ab production. Nature 2006, 440:538-534. *共同第一作者.
2. Bing G, Nguyen XV, Liu M, William R. Markesbery WR, Sun AY. Biophysical and biochemical characterization of the intrinsic fluorescence from neurofibrillary tangles. Neurobiology of Aging 2006, 27: 823-830.
3. Liou Y*, Sun AY*, Ryo A, Zhou XZ, Yu ZX, Huang H., Uchida T., Bronson R., Bing G., Li X., Hunter T., Lu KP. Role of the prolyl isomerase Pin1 in protecting against age-dependent neurodegeneration. Nature 2003; 424: 556-561. *共同第一作者.
4. Sun AY, Liu M, Nguyen XV, Bing G. p38 MAP kinase is activated at the early stage in Alzheimer’s Disease Brain. Experimental Neurology 2003; 183 (2): 394-405. Also see the commentary on this work (Exp Neurol 2003; 183: 263-268).
5. Sun AY, Koelsch G, Tang J, Bing G. Localization of bb-secretase memapsin 2 in the brain of Alzheimer's patients and normal aged controls. Experimental Neurology. 2002; 175(1): 10-22.

Dr. Sun received his Ph.D. degree in Pharmacology from Shanghai Medical University in 1996.  He completed his postdoctoral training and had been promoted as an instructor in Harvard Medical School in 2004.   In 2005, Dr. Sun joined the Institute of Neurobiology, Fudan University as the head of Unit of Neurodegenerative Diseases and holds a joint appointment from the State Key Laboratory of Medical Neurobiology in 2007.  Currently, Dr. Sun’s research interests include exploring pathological events at early stages of Alzheimer's disease (AD) towards understanding its pathogenesis. For this purpose, a couple of AD-related bigenic mouse models generated from selected transgenic and knockout mice, as well as post-mortem human brain tissues with increasing Braak stages, are employed as the materials. The on-going or future projects include 1) identifying early cascades before the appearance of AD pathological hallmarks (amyloid plaques and neurofibrillary tangles) that eventually lead to neuron or/and brain dysfunction; 2) seeking potential interventions that will delay the developments of AD pathology; 3) examining synaptic changes and its modulation under brain disease conditions, in particular changes in synapse subtypes, synaptic strength and plasticity.