骨干人才
申 勇
申勇，1958年4月生于中国北京。中国教育部长江学者奖励计划讲座教授。1983年南京大学获人体及动物生理学专业理学学士学位；1986年中国科学院上海生理研究所获生理学专业理学硕士学位；1989年美国纽约州立大学获心理生物学及神经科学专业心理学博士学位；先后在荷兰皇家科学院Rudolf Magnus药物研究所(Rudolf Magnus奖金)学习并在美国国立卫生研究院 (NIH)精神卫生研究所(NIMH)以及美国霍普金斯大学(John Hopkins University)联合分子神经生物学及疾病计划从事博士后研究。 1993年申勇受邀加入美国亚培实验室(Abbott Labs)神经科学部任神经免疫探索研究小组 (Neuroimmunology Exploratory Group)组长及资深分子神经药理学家，参与制定和发展治疗阿尔兹海默病药物研发项目的规划；1997年任职于亚利桑那州的太阳城医学健康研究所(Sun Health Research Institute) L.J.罗伯特阿尔茨海默病研究中心 (L.J.Roberts Center for Alzheimer’s Disease) 冠名主任和教授（终身教授）及资深科学家并兼任亚利桑那州立大学分子细胞生物学教授；2000年起转任哈德起转任哈德曼分子及细胞神经生物学实验室冠名主任，教授（终身教授）及资深科学家及分子生物学教授。申勇教授和他的团队成功培养出老年人及痴呆病人脑中的小胶质细胞、神经元及神经干细胞。申勇教授及团队并且是世界上第一个发现老年痴呆病人脑组织、脑脊液及血液中b-分泌酶（BACE1）活性的实验室，为制药工业研制BACE1抑制剂药物提供了有效的监测指标以及为早期诊断及临床实验。2014年回国任中国科学技术大学教授。申勇教授获得多项奖项及荣誉称号包括：中国教育部颁发的“长江学者奖励计划特聘讲座教授”。最近获得中国阿尔兹海默病研究颁发的“科学人物奖 (Scientific Figure)”, 2016年起任中国科学技术部重大研究专项“脑小血管病发病机制及诊断关键技术”首席科学家和中国国家自然基金委员会“器官衰老和退行性变化”重大研究计划专家组组长。最近申勇教授又遴选为中国科学院学术委员会暨生命与健康专业委员会委员。申勇教授在神经科学及神经病学方面的国际知名学术期刊发表百余篇有关神经递质新受体的分子克隆和药理学鉴定，神经退变性疾病的分子机制及病理，神经免疫等方面的文章 。
主要研究方向及内容
1.衰老和老年痴呆病以及脑小血管病的分子机制研究包括新基因的发现；
2.建立神经退行性疾病（老年痴呆病、巴金森病以及脑小血管病）的动物模型；
3.神经退行性疾病治疗靶点的分子病理学鉴定以及药物发现；
4.神经退行性疾病的早期诊断及关键技术。
代表性论文
阿尔兹海默病与b-分泌酶：
Shen Y, Wang H, Sun Q, Yao H, Keegan AP, Mullan M, Wilson J, Lista S, Leyhe T, Laske C, Rujescu D, Wallin A, Blennow K, Li R, and Hampel H. (2017). Increased plasma β-site APP-cleaving enzyme 1 (BACE1) activity in subjects with mild cognitive impairment and patients with Alzheimer’s disease. Biological Psychiatry, 2017 Mar 27. pii: S0006
Cheng X, He P, Yao H, Dong Q, Li R, Shen Y (2014). Occludin deficiency with BACE1 elevation in cerebral amyloid angiopathy. Neurology. 82(19): 1707-1715.
Cheng X, He P, Lee T, Yao H, Li R and Shen Y (2014). High activities of BACE1 in brains with mild cognitive impairment. American Journal of Pathology, 184(1): 141-147.
Wang H, Li R and Shen Y (2013). secretase (BACE1): Its Biology as a Therapeutic Target in Diseases. Trends in Pharmacological Sciences. Apr;34(4):215-25. doi: 10.1016/j.tips.2013.01.008. Epub 2013 Feb 27. PMID: 23452816.
Walker KR, Kang EL, Whalen MJ, Shen Y and Tesco G. (2012). Depletion of GGA1 and GGA3 mediates post-injury elevation of BACE1. Journal of Neuroscience. 32(30): 10423-37.
Zhong, Z., Ewers, M., Teipel, S., Büger, K., Wallin, A., Blennow, K., Hampel, H., and Shen Y.(2007). High Levels of β-Secretase (BACE1) in Cerebrospinal Fluid as a Predictor of Risk in Mild Cognitive Impairment, the early stage of Alzheimer’s Disease, JAMA Psychiatry (Archives of General Psychiatry), 64(6):718-2.
Ewers M, Zhong Z, Bürger K, Wallin A, Blennow K, Teipel SJ, Shen Y, Hampel H. (2008). Increased CSF-BACE1 activity is associated with ApoE4 genotype in subjects with mild cognitive impairment (MCI) and Alzheimer's disease. Brain, 131(Pt 5): 1252-8.
Tesco G, Koh YH, Kang EL, Cameron AN, Das S, Sena-Esteves M, Hiltunen M, Yang SH, Zhong Z, Shen Y, Simpkins JW, Tanzi RE. (2007). Depletion of GGA3 stabilizes BACE and enhances β-secretase activity. Neuron. 54(5): 721-37.
Yang LB, Lindholm K, Yan R, Citron M, Xia W, Beach T, Sue L, Wong P, Price D, Li R, ShenY. (2003). Elevated β-secretase (BACE1) expression and enzymatic activity detected in sporadic Alzheimer disease. Nature Medicine, 9(1): 3-4.
Li R, Yang LB, Lindholm K, Yan R, Citron M, Beach T, Sue L, Subbagh M, Cai H, Wong P, Price D, Shen Y. (2004). Aβ load is correlated with elevated BACE activity in sporadic Alzheimer patients. Proc. Natl. Acad. Sci. USA, 101(10), 3632-3637.
Xia W., Yang T., Imelda M. Smith I. M., Shen Y., Walsh D. M. and Selkoe, D. J. (2009). A specific ELISA for measuring amyloid ?-protein oligomers in human plasma and the brains of Alzheimer patients. JAMA Neurology (Archives of Neurology), 66(2): 190-9.
阿尔兹海默病与神经免疫：
Li R., Lindholm K, Yang LB, Konishi Y, Hampel H, Zhang, D. Shen Y. (2004). TNF death receptor signaling cascade is required for amyloid-?-protein induced neuron death. Journal of Neuroscience, 28(7):1760-1771.
He P, Zhong Z, Lindholm K, Berning L, Lee W, Lemere C, Staufenbiel M, Li R and Shen Y. (2007). Deletion of TNF death receptor inhibits amyloid beta generation and prevents learning and memory deficits in Alzheimer’s mice. Journal of Cell Biology, 178(5): 829-841.(Highlighted by Nature Oct. 2007: Death receptor takes centrestage ; Hot story news by Science, 2007 : Death receptor and Alzheimer.
Jiang H, He P, Xie J, Staufenbiel M, Li R, Shen Y. (2014). Genetic deletion of TNFRII gene enhances the Alzheimer-like pathology in an APP transgenic mouse model via reduction of phosphorylated IκBα. Human Molecular Genetics. 23(18):4906-4918.
He P, Liu Q, Wu J and Shen Y (2011). Genetic Deletion of TNF Receptor Suppresses Excitatory Synaptic Transmission via Reducing AMPA Receptor Synaptic Localization in Cortical Neurons. FASEB Journal. 26(1): 334-45.
Cheng X, Shen Y and Li R (2014). Targeting TNF: A therapeutic strategy for Alzheimer’s disease. Drug Discovery Today, Jul 3. pii: S1359-6446(14)00271-2.
阿尔兹海默病与其他方面：
Konishi Y, Yang LB, He P, Lindholm K, Lu B, Li R and Shen Y (2014). Deficiency of GDNF receptor GFR？1 in Alzheimer Neurons Results In Neuronal Death. Journal of Neuroscience, 34(39):13127-38.
He P. and Shen Y. (2008).Interruption of β-catenin signaling reduces neurogenesis in Alzheimer’s disease’s brains. Journal of Neuroscience. (2009), 29(20): 6545-57.
Min S-W, Cho S-H, Zhou Y, Schroeder S, Haroutunian V, Seeley WW, Huang EJ, Shen Y, Masliah E, Mukherjee C, Meyers D, Cole PA, Ott M, Li Gan L (2010). Acetylation of tau inhibits Its degradation and contributes to tauopathy. Neuron, 67: 953-966.
He P，Staufenbiel M, Li R, Shen Y. (2014). Deficiency of patched 1-induced Gli1 signal transduction results in astrogenesis in Swedish mutated APP transgenic mice. Human Molecular Genetics. 23(24):6512-27.
Yu X, Du T, Song N, He Q, Shen Y, Jiang H, and Xie J (2013). Decreased iron levels in the temporal cortex in postmortem human brains with Parkinson’s disease. Neurology, 80(5): 492-495.