General

Fude Huang, Ph.D, Principal Investigator and Lab head

Shanghai Advanced Research Institute and Sino-Dansish Research and Education Center

University of Chinese Academy of Sciences, Chinese Academy of Sciences

Email: huangfd@sari.ac.cn 

Telephone: 021-20350962
Address: 

Bldg 6, Rm 504

#99 Haike Road Zhangjiang High-Tech Park, Pudong District, Shanghai, China
Postcode: 201210

Research Areas

1 Molecular and cellular mechanisms of neural diseases, including Alzheimer's disease and stroke

2 Drug screening and development for treating neural diseases


Education

2002.9-2005.12, Ph.D, Vanderbilt University. Nashiville, USA

1999.9-2002.8, Neuroscience program, University of Utah, Utah, USA

1994.9-1997.8, MSc, Shanghai Brain Research Institute, CAS, Shanghai, China.

1987.9-1992.7, M.D., Hengyang Medical College, Hunan, China.


Publications

Publications  “ * ” corresponding author

1.     An automated rapid iterative negative geotaxis assay for analyzing adult climbing behavior in a Drosophila model of neurodegeneration. JoVE, in press

2.    Xia Y, Meng S, Lim NK, Wang WA and Huang FD* (2017) An efficient and reliable assay for investigating the effects of hypoxia/anoxia on Drosophila. Neuroscience Bulletin. In press.

3.    Zhang X, Wang WA, Zhang L, He Y, Liu HY, Jiang LX, Jiao CP, Peng J, Zhou YD and Huang FD* (2017) Down regulation of RBO-PI4KIIIα facilitates Aβ42 secretion and ameliorates neural deficits in Drosophila. J. Neurosci. doi: 10.1523/JNEUROSCI.3567-16.2017

4.    Wang Q, Liu Z, Ji S, Liu Q, Lv J, Ma Y, Xu Y, Wu H, Huang FD* and Xiang M* (2017) Efr3a Insufficiency Attenuates the Degeneration of Spiral Ganglion Neurons after Hair Cell Loss. Front. Mol. Neurosci. 10:86. doi: 10.3389/fnmol.2017.00086

5.    Qian, Q, Liu, Q, Zhou, D, Pan, H, Liu, Z, He, F, Ji, S, Wang, D, Bao, W, Liu, X, Liu, Z, Zhang, H, Zhang, X, Zhang, L, Wang, M, Xu, Y, Huang, FD*, Luo, B, Sun B* (2017) Brain-specific ablation of Efr3a promotes adult hippocampal neurogenesis via the brain-derived neurotrophic factor pathway. FASEB J. Feb 13. doi: 10.1096/fj.201601207R

6.    Shen YJ, Xia YL, Men SQ, Lim NK, Wang WA*, Huang, FD*. (2017) SH2B1 is involved in the accumulation of Aβ42 in Alzheimer’s disease model. J Alz Dis.55 (2): 835-847.

7.    Tong Y, Li G, Deng Y, Shi C, Huang FD, Fang G (2016) Inhibition of primary cultured hepatic stellate cells activation by phenylarsine oxide in vitro. J Prac Hepatol. 19(4):413-416.

8.    Shen YJ, Wang WA, Huang FD, Chen J, Liu HY, Xia LY, Han M and Zhang L. (2016) The use of MMSE and MoCA in patients with acute ischemic stroke in clinical. Int J Neurosci. 126(5): 442-447.

9.    Han M, Huang JK, Liu HY, Wang WA, Sun XJ and Huang FD*. (2015) Neither insufficiency nor overexpression of sac1 affects the accumulation of Aβ42 in Drosophila expressing Aβ42. Eur Rev Med Pharmacol Sci, 19(9): 1700-1705.

10. Liu HY, Han M, Li QY, Zhang X, Wang WA and Huang FD*. (2015). Automated rapid iterative negative geotaxis assay and its use in a genetic screening for modifiers of Aβ42-induced locomotor decline in Drosophila. Neuroscience Bulletin. 31(5): 541-549.

11. Han M, Ma PL, Ye CY, Zhang BZ, Zhang HY, Sun, XJ and Huang FD*. (2015). The toxicity of beta amyloid peptide depends on its length in transgenic Drosophila model of Alzheimer’s disease. China Journal of Gerontology, 35:1315-1317. in Chinese

12. Lin JY, Wang WA, Zhang X, Zhao XL and Huang FD*. (2014). Intraneuronal accumulation of Aβ42 induced age-dependent slowdown of neural transmission. Neuroscience Bulletin, 30(2): 185-190

13. Huang FD*. (2014). The gradual understanding of the role of beta amyloid in Alzheimer’s disease. Chinese Bulletin of Life Sciences, 26(1): 9-12. In Chinese

14. Huang JK, Ma PL, Zhao XL, Ji SY, Tan JX, Sun XJ* and Huang FD*. (2013). Age-dependent alterations in the presynaptic active zone in a Drosophila model of Alzheimer’s disease. Neurobiol. Dis., 51:161-167

15. Bao GS, Wang WA, Wang TZ, Huang JK, Liu ZG, Huang FD*. (2011). Overexpression of human MRP1 in neurons causes resistance to antiepileptic drugs in Drosophila. J. Neurogen., 25: 201-206

16. Yu Y, Xu C, Pan X, Ren H, Wang W, Meng X, Huang FD, Chen N*. (2010). Identification and functional analysis of novel mutations of the CLCNKB gene in Chinese patients with classic Bartter syndrome. Clin. Genet., 77: 155–162

17. Zhao X, Wang WA, Tan JX, Huang JK, Zhang X, Zhang BZ, Wang YH, YangCheng HY, Zhu HL, Sun XJ and Huang FD* (2010). Expression of β-amyloid induced age-dependent presynaptic and axonal changes in Drosophila. J. Neurosci., 30(4):1512-22.

18. Huang FD, Woodruff E, Mohrmann R, and Broadie K* (2006). Rolling Blackout is required for synaptic vesicle exocytosis in Drosophila. J. Neurosci., 26(9):2369-79        

19. Tai SK, Huang FD, Moochhala S, and Khanna, S* (2006). Hippocampal theta state in relation to formalin nociception. Pain, 121 (1-2):29-42.

20. Huang FD, Matthies HJ, Speese SD, Smith MA, and Broadie K.* (2004). Rolling blackout, a newly identified PIP2-DAG pathway lipase required for Drosophila phototransduction. Nat. Neurosci., 7, 1070-1078.

21. Huang FD, Chen J, Lin M, Keating MT, Sanguinetti MC*. (2001). Long-QT syndrome-associated missense mutations in the pore helix of the HERG potassium channel. Circulation, 104, 1071-1075.

22. Chen YC*, Huang FD, Chen NH, Shou JY, Wu L. (1998). Neuronal activity of monkey dorso-lateral premotor cortex during tasks of figure recognition guided motor sequence vs memorized spatial motor sequence. Sheng Li Xue Bao, 50(2): 121-131. in Chinese

Papers
   
Patents

1 Huang FD. (2014), Patent number: ZL 2014 2 0128803.0

2 Huang et al. (2015), Patent number: ZL 2012 1 0234165.6

3 Huang et al. (2015), Patent application number: PCT/CN2015/078058

4 Huang et al. (2015), Patent application number: PCT/CN2015/078070

5 Huang et al. (2016), Patent application number: PCT/CN2016/080907


Research Interests

In order to reveal novel therapeutic targets and develop new drugs for treating Alzheimer’s disease (AD), we study the cellular and molecular mechanisms underlying neural injury in cultured cell, Drosophila and mouse models of AD, with the combination of electrophysiology, morphology, genetics, molecular biology, biochemistry and behavior techniques. 


AD is characterized by progressive loss of learning and memory, accumulation of amyloid plaques and neurofibrillar tangles in the brain, but currently without any preventive or disease-modifying drug or intervention. Abnormal metabolism of beta amyloid (Aβ) plays a causal and central role in the pathogenesis of AD, which is supported by many lines of evidences, especially the genotype-phenotype relationship in familiar AD patients. Aβ accumulates both extra- and intracellularly in AD brains. Since clinical trials on the inhibition of Aβ production by β- and γ-secretase inhibitors, and the clearance of extracellular amyloid plaques have repetitively failed, we are testing whether reducing intracellular accumulation of Aβ42 by facilitating its cellular release is an alternative strategy for treating AD. 


By expressing Aβ42 in the Drosophila giant fiber (GF) pathway, we developed a neural circuit AD model exhibiting age-dependent neuronal accumulation of Aβ42 and associated synaptic transmission failure, which is evident and easy to record,providing a convenient platform for testing the role of candidate genes in neuronal accumulation of Aβ and associated synaptic deficits, and for performing genetic screening for modifiers of the those neural deficits. Using this model, we found an important role of RBO and PI4KIIIα in neuronal accumulation of Aβ42 and AD pathogenesis. Moreover, to gain a closer insight into the neurodegeneration in AD patients, we test our findings on mouse models of AD.


Conferences

Oral presentations:

 

1.      “The SDC Beijing, Shanghai, Aarhus collaboration on models of neurodegeneration” at Aarhus, Denmark, Key note lecture, 2016 (Invited talk)

2.      “4th Australia-China Biomedical Research Conference” at Hangzhou (China) 2013 (Invited talk)

3.      “SDC Life Sciences-Neuroscience and cognition", the first Research and education workshop in Beijing 2012 (Invited talk).

4.      2009 ION-NPAS-HKUST-NIMH Joint meeting-Symposium on Frontiers in Neuroscience 2009 (China)

5.      China/UK workshop on model organisms for neurodegenerative disease at Beijing (China) 2008 (invited talk).

6.      8th Biennial Meeting of the Asia-Pacific Society for Neurochemistry at Shanghai (China) 2008 (Invited talk).

7.      Neurobiology of Drosophila at Cold Spring Harbor Laboratory (USA) in 2005.

8.      International Annual Neuroscience Meeting at New Orleans (USA) in 2003.

 

Poster presentations:

1.      Gordan Research Conference for Neurobiology of Brain Disorders at Girona (Spain) in 2016.

2.      Gordan Research Conference for Molecular and Cellular Neurobiology at HUST (HK, China) in 2014 (invited poster).

3.      Gordan Research Conference for Molecular and Cellular Neurobiology at HUST (HK, China) in 2012 (invited poster).

4.      Neurobiology of Drosophila at Cold Spring Harbor Laboratory (USA) in 2009.

5.      Gordan Research Conference for Neurobiology of Brain Disorders at Oxford (UK) in 2008.

6.      International Annual Neuroscience Meeting at Orlando (USA) in 2002.

7.      Neurobiology of Drosophila at Cold Spring Harbor Laboratory (USA) in 2001.

8.      International Annual Neuroscience Meeting at Miami (USA) in 1999.

 

 


Collaboration

We are not only extensively collaborating with many domestic labs and pharmaceutic companies, but also with 

some international labs, such as two labs in Aarhus University in Denmark. 

Students

已指导学生

马平丽  02  19179  

张潇  01  19179  

张建夫  02  63228  

蒋理想  02  63228  

现指导学生

孙名皓  02  63228  

张起超  02  19179  

张丽瑶  02  19179  

沐舒静   02  63228