李传洲

专业方向：神经退行性疾病机理

个人简介：2007年武汉大学生科院获学士学位；2012年武汉大学获得细胞生物学博士学位；2013-2018年澳大利亚昆士兰脑研究所从事博士后研究。2018年4月入职太阳成集团tyc122cc医学遗传系，研究方向为阿尔茨海默病（AD）致病机理。具体包括：1）AD中微管结合蛋白Tau和酪氨酸激酶Fyn的相互调控机理；2）Tau蛋白在胞体树突中形成NFTs的机制；3）AD风险因子Pyk2对神经功能及学习记忆的影响。近年来发表唯一第一作者 J Azheimers Dis; 唯一第一作者EMBO J封面文章；唯一第一作者Nat. Rev. Drug. Discov封面文章；一作顶级眼科杂志Invest. Ophthalmol. Vis. Sci. 以及Acta Neuropathol. Commun.、Nat. Rev. Neurol.、BBA、BBRC等。

联系方式： chuanzhouli@hust.edu.cn

联系地址：太阳成集团tyc122cc2号楼1220室

Li, C., Pandit, R., Li, L., Liu, H., Götz, J.(2019) Self-aggregates of Pyk2 induce ER stress-mediated neurodegeneration. (in preparation)

Li, C. and J. Götz, Pyk2 is a Novel Tau Tyrosine Kinase that is Regulated by the Tyrosine Kinase Fyn. J Alzheimers Dis, 2018. 64(1): p. 205-221. （受Fyn调控的新型Tau酪氨酸激酶Pyk2；唯一第一作者；杂志网页推荐文章；影响因子3.92）

Polanco, J.C., Li, C. Durisic, N. Sullivan, R. Götz, J. et al., Exosomes taken up by neurons hijack the endosomal pathway to spread to interconnected neurons. Acta Neuropathol Commun, 2018. 6(1): p. 10.（影响因子5.414）

Polanco, J.C., Li, C., Bodea L.G., Marmol, R.M., Meunier, F., and Götz, J. (2017) Amyloid-beta and tau complexity - towards improved biomarkers and targeted therapies. Nat Rev Neurol, 2018. 14(1): p. 22-39.（β淀粉样蛋白和tau的多态性—更好生物标志物和靶向治疗；影响因子20.2）

Li, C. and J. Gotz (2017). "Somatodendritic accumulation of Tau in Alzheimer's disease is promoted by Fyn-mediated local protein translation." EMBO Journal 36(21): 3120-3138.（阿尔兹海默症中Fyn 介导的局部蛋白质合成促进了Tau在胞体树突的聚集；唯一第一作者；影响因子9.792；权威学术论坛Alzforum 对此发表长篇评论；入选杂志封面）

Li, C. and J. Gotz (2017). "Tau-based therapies in neurodegeneration: opportunities and challenges." Nat Rev Drug Discov 16(12): 863-883.（以Tau为基础的神经退行性疾病的多元化靶向治疗；唯一第一作者；影响因子57 ）

Xia, D., Li, C., and Götz, J. (2015). "Pseudophosphorylation of Tau at distinct epitopes or the presence of the P301L mutation targets the microtubule-associated protein Tau to dendritic spines." Biochim. Biophys. Acta. 1852(5): 913-924.（影响因子5.725）

Li, C., Wang, L., and Zheng, L. (2012). "Endoplasmic reticulum stress in retinal vascular degeneration: protective role of resveratrol." Invest. Ophthalmol. Vis. Sci. 53(6): 3241-3249. (眼科研究型杂志中排名第一; 影响因子3.427）

Li, C., Wang, L., Huang, K., and Zheng, L. (2012). "Inhibition of poly(ADP-ribose) polymerase inhibits ischemia/reperfusion induced neurodegeneration in retina via suppression of endoplasmic reticulum stress." Biochem. Biophys. Res. Commun. 423(2):276-281.（影响因子：2.5559）

Wang, L., Li, C., Guo, H., Kern, T.S., Huang, K., and Zheng, L. (2011). Curcumin inhibits neuronal and vascular degeneration in retina after ischemia and reperfusion injury. PLoS ONE 6(8):e23194.（影响因子：2.766）

Sullivan, M.A., Li, J., Li, C., Vilaplana, F., Stapleton, D., Gray-Weale, A.A., Bowen, S., Zheng, L., and Gilbert ,R.G. (2011). Molecular structural differences between type-2-diabetic and healthy glycogen. Biomacromolecules 12(6):1983-1986.（影响因子：5.246）

Gong, H., Zhang, X., Cheng, B., Sun, Y., Li, C., Li, T., Zheng, L., and Huang, K. (2013). "Bisphenol a Accelerates Toxic Amyloid Formation of Human Islet Amyloid Polypeptide: A Possible Link between Bisphenol a Exposure and Type 2 Diabetes." PLoS One 8, no. 1:e54198.（影响因子：2.766）

Cheng, B., Liu, X., Gong, H., Huang, L., Chen, H., Zhang, X., Li, C., Yang, M., Ma, B., Jiao, L., Zheng, L. and Huang, K. (2011). Coffee Components Inhibit Amyloid Formation of Human Islet Amyloid Polypeptide in Vitro: Possible Link between Coffee Consumption and Diabetes Mellitus. J. Agric. Food Chem. 59(24):13147-13155.（影响因子：3.154）

         Zhang, X., Cheng, B., Gong, H., Li, C., Chen, H., Zheng, L., and Huang, K. (2011). Porcine is let amyloid polypeptide fragments are refractory to amyloid formation. FEBS Lett 585(1):71-77.（影响因子：2.999）