神经科学研究所学术报告[11月6日10:00]

发布者:系统管理员发布时间:2014-11-04浏览次数:446


神经科学研究所学术报告[11月6日10:00]

报告题目:Autophagy: a new target in AD research

报告人: 柳扬 博士,德国Saarland大学                                

报告时间: 2014年11月6日(周 四)上午10:00

报告地点: 苏州大学神经科学研究所会议室

报告人简介:

  柳扬博士1999年毕业于北京协和大学(八年制),获医学博士学位。1999-2001年在浙江大学第一附属医院担任内科医生。2001-2002年在德国海德堡大学(University of Heidelberg)曼海姆医院(Mannheim Hospital)神经科进行博士后研究。2002-2005年在德国G?ttingen 大学(University of G?ttingen)神经科进行博士后研究。2005年至今在德国萨尔大学(University of the Saarland)神经科担任学科带头人(终身职位)。

  柳扬博士主要研究方向是神经炎症在AD发病中的分子作用机制。尤其是小胶质细胞在AD发病中的重要作用以及小胶质细胞中IKKβ在Aβ形成和降解中的分子作用机理。曾在Brain、Journal of Immunology等著名期刊发表多篇论文,被国际同行多次引用,在该领域内具有重要贡献。

                                                                                                         神经科学研究所

                                                                                                              2014-11-6

Topic: Autophagy: a new target in AD research

Reporter: Dr. Yang Liu, Saarland University, Germany

Time: Nov 6, 2014, 10:00 AM

Location: Meeting Room, Institute of Neuroscience, Soochow University

Introduction of reporter:

Dr. Yang Liu graduated from Peking Union Medical College (8-year class) in 1999. After the practice as a neurologist in the First Affiliated Hospital of Zhejiang University for 2 years, he started his research career as a post-doctoral fellow in University of Heidelberg and University of G?ttingen, Germany. In 2005, he got a life-long position as a group leader in Department of Neurology, University of Saarland, Germany. His interest is to investigate the pathogenic role of microglia in neurodegenerative diseases, especially Alzheimer's disease. He has published a serial of papers on the pathogenic effects of microglial activation in Alzheimer's disease mouse models, such as: (Dr. Liu is the corresponding author for all listed papers)

1: Liu Y, Liu X, Hao W, Decker Y, Schomburg R, Fül?p L, Pasparakis M, Menger MD, Fassbender K. IKKβ Deficiency in Myeloid Cells Ameliorates Alzheimer's Disease-Related Symptoms and Pathology. J Neurosci. 2014 Sep 24;34(39):12982-99.

2: Xie K, Liu Y, Hao W, Walter S, Penke B, Hartmann T, Schachner M, Fassbender K. Tenascin-C deficiency ameliorates Alzheimer's disease-related pathology in mice.

Neurobiol Aging. 2013 Oct;34(10):2389-98.

3: Liu S, Liu Y, Hao W, Wolf L, Kiliaan AJ, Penke B, Rübe CE, Walter J, Heneka MT, Hartmann T, Menger MD, Fassbender K. TLR2 is a primary receptor for Alzheimer's amyloid β peptide to trigger neuroinflammatory activation. J Immunol.

2012 Feb 1;188(3):1098-107.

4: Hao W, Liu Y, Liu S, Walter S, Grimm MO, Kiliaan AJ, Penke B, Hartmann T, Rübe CE, Menger MD, Fassbender K. Myeloid differentiation factor 88-deficient bone marrow cells improve Alzheimer's disease-related symptoms and pathology. Brain. 2011 Jan;134(Pt 1):278-92.

5: Liu Y, Walter S, Stagi M, Cherny D, Letiembre M, Schulz-Schaeffer W, Heine H,

Penke B, Neumann H, Fassbender K. LPS receptor (CD14): a receptor for phagocytosis of Alzheimer's amyloid peptide. Brain. 2005 Aug;128(Pt 8):1778-89.

(学部办公室)