![]() ![]() Molecular Therapy Nucleic Acids 4, e242, 2015 May 12. Shyam R, Ren Y, Lee J, Braunstein KE, Mao H-Q and Wong PC: Intraventricular delivery of siRNAs nanoparticles to the central nervous system. “BACE1 is the major b-secretase for generation of Ab peptides by neurons.” Nature Neuroscience 4: 233, 2001.Ĭhiang P-M, Ling J, Jeong YH, Price DL, Aja S and Wong PC: Deletion of TDP-43 down-regulates Tbc1d1, a gene linked to obesity, and alters body fat metabolism. “The brain's susceptibility to amyloid plaques.” Science 293:1434, 2001.Ĭai H, Wang Y, McCarthy D, Wen H, Borchelt DR, Price DL and Wong PC. “Mutant SOD1 causes motor neuron disease independent of copper chaperone-mediated copper loading.” Nature Neuroscience 5:301, 2002. Subramaniam JR, Lyons WE, Liu J, Bartinakas TB, Rothstein J, Price DL, Cleveland DW, Gitlin JD and Wong PC. “Genetically Engineered Mouse Models of Neurodegenerative Diseases.” Nature Neuroscience 5:633, 2002 Wong PC, Cai H, Borchelt DR and Price DL. “Nicastrin is required for assembly of presenilin/g-secretase complexes to mediate Notch Signaling, and for processing and trafficking of b-APP in mammals.” J. “Aph-1a is the principal mammalian Aph-1 isoform present in g-secretase complexes during embryonic development.” J. “Loss of ALS2 function is insufficient to trigger motor neuron degeneration in knockout mice, but predisposes neurons to oxidative stress.” J. Neuroscience 25:11693–11709, 2005.Ĭai H, Lin X, Xie C, Laird FM, Lai C, Wen H, Chiang HC, Shim H, Farah M, Hoke A, Price DL, and Wong PC. “BACE1, a Major Determinant of Selective Vulnerability of the Brain to Amyloid-b Amyloidogenesis is Essential for Cognitive, Emotional and Synaptic Functions.” J. Laird FM, Cai H, Savonenko AV, Farah MH, He K, Melnikova T, Wen H, Chiang HC, Xu G, Koliatsos VE, Borchelt DR, Price DL, Lee H-K and Wong PC. Hu X, Hicks CW, He W, Wong PC, Macklin WB, Trapp BD & Yan R “Bace1 modulates myelination in the central and peripheral nervous system.” Nature Neuroscience, online November 12, 2006. “Modeling an anti-amyloid combination therapy for Alzheimer’s Disease.” Science Translational Medicine 2:1-11, 2010 PROFESSOR OF OPTHROMOLOGY AT JOHN HOPKINS HOPITAL SKINWong’s lab is working on the role of Alzheimer’s b-secretase, BACE1 and APP signaling in learning and memory the role of Alzheimer’s g-secretase, including its function as a tumor suppressor in the skin and the molecular mechanism of motor neuron disease linked to mutations in dynactin p150glued, SOD1, ALS4 and ALS2 with a focus on alterations in axonal transport.Ĭhow VW, Savonenko AV, Melnikova T, Kim H, Price DL, Li T and Wong PC. Wong’s work has been recognized with the 2004 Zenith Fellow’s Award from the Alzheimer’s Association.read moreĭr. Wong is a member of the New York Academy of Sciences and the Society of Neuroscience and is a member of the editorial board for Neuro-Signals. Wong joined the Johns Hopkins faculty in 1994.ĭr. He completed a postdoctoral fellowship in cellular and molecular biology at the Johns Hopkins University School of Medicine in the Department of Biological Chemistry. in biochemistry and molecular biology from the University of Western Ontario in Canada. He received his undergraduate degree in biochemistry and his Ph.D. The mouse models are instrumental for study of disease mechanisms as well as for design and testing of therapeutic strategies for AD and ALS. Wong’s team takes a molecular/cellular approach, including transgenic, gene targeting and RNAi strategies in mice, to develop models that facilitate their understanding of pathogenesis of Alzheimer’s and ALS as well as the identification and validation of novel targets for mechanism-based therapeutics. His research focuses on understanding the molecular mechanisms of neurodegenerative disorders, such as Alzheimer''s disease and amyotrophic lateral sclerosis (ALS).ĭr. Philip Wong is a professor of pathology at the Johns Hopkins University School of Medicine. ![]()
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