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| First Name: | Fu-De | | Last Name: | Huang | | Title: | Principal Investigator | | Advanced Degrees: | Ph.D | | Affiliation: | Shanghai Advanced Research Institute, Chinese Academy of Sciences | | Department: | SARI Center for Stem Cell and NanoMedicine | | Street Address 1: | 99 Hai Ke Road | | City: | Shanghai | | Zip/Postal Code: | 201210 | Country/Territory: | China | | Phone: | 86-21-20350962 | | Fax: | 86-21-20350980 | | Email Address: |  |
Disclosure:
(view policy)
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Member reports no financial or other potential conflicts of interest. [Last Modified: 29 January 2013]
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View all comments by Fu-De Huang
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Aging Process, Alzheimer Disease, Tauopathies, Neuromuscular Disorders (ALS, etc.)
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A-beta PP/A-beta, Animal Models, Neurobiology, Neurotransmission, Molecular and Cell biology, Genetics, Neuropathology, Electrophysiology, Tau/Cytoskeleton
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Dr. Fu-De Huang received his bachelor degree in medicine from Heng Yang Medical College in 1992, M.S. in neurobiology from Shanghai Brain Research Institute, CAS in 1997, and M.S in physiology from National University of Singapore in 2000, and Ph.D degree in Biological Sciences from Vanderbilt University in 2006. He was as an associate investigator of the Laboratory of Neural Plasticity in ION during 2006-2007, and was appointed as Unit Head and Principal Investigator of the Unit of Neurodegenerative Diseases in 2008. His current research focuses on the cellular and molecular mechanisms in neurodegenerative diseases, using Drosophila and mouse as model systems. |
1. Zhao XL, Wang WA., Tan JX, Huang JK, Zhang X, Zhang BZ, Wang YH, YangCheng HY, Zhu HL, Sun XJ, Huang FD.* (2010). Expression of β-Amyloid Induced Age-Dependent Presynaptic and Axonal Changes in Drosophila. J. Neurosci. 30(4):1512-1522.
2. 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.
3. Tai SK, Huang FD, Moochhala S, and Khanna, S* (2006). Hippocampal theta state in relation to formalin nociception. Pain, 121 (1-2):29-42.
4. 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.
5. 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. |
What are the nature and progression of functional and structrual changes of neurons or synapses in neurodegeneration? |
1 Impaired balance of mitochondrial fission and fusion in Alzheimer's disease. Wang X, Su B, Lee HG, Li X, Perry G, Smith MA, Zhu X. J Neurosci. 2009 Jul 15;29(28):9090-103.
2 Dendritic Function of Tau Mediates Amyloid-beta Toxicity in Alzheimer's Disease Mouse Models.
Ittner LM, Ke YD, Delerue F, Bi M, Gladbach A, van Eersel J, Wölfing H, Chieng BC, Christie MJ, Napier IA, Eckert A, Staufenbiel M, Hardeman E, Götz J. Cell. 2010 Aug 6;142(3):387-397. Epub 2010 Jul 22.
3 ABAD directly links Abeta to mitochondrial toxicity in Alzheimer's disease. Lustbader JW, Cirilli M, Lin C, Xu HW, Takuma K, Wang N, Caspersen C, Chen X, Pollak S, Chaney M, Trinchese F, Liu S, Gunn-Moore F, Lue LF, Walker DG, Kuppusamy P, Zewier ZL, Arancio O, Stern D, Yan SS, Wu H. Science. 2004 Apr 16;304(5669):448-52.
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generate non-human primate AD model and investigate the following question.
What are the nature and progression of functional and structrual changes of neurons or synapses in neurodegeneration? |
beta amyloid (Abeta) plays a central role in AD, intracellular and plasma membrane accumulation of oligomeric Abeta during aging disrupts mitochondria function, and relatively speicifcally binds to hydrophilic structral and signaling molecules, thereby dirsupt neuronal or synaptic function.
Lipidic abnormalities should be major component of the pathological changes in AD. |
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