Qiang Zhou
  • Qiang Zhou

  • Principal Investigator, Co-director of DDC, Professor
  • Tel:+86-755-2603-2459
  • Email:zhouqiang@pkusz.edu.cn
  • Web:http://web.pkusz.edu.cn/zhouq/
  • Education & Experience
    2014 – present        Professor, PKUSZ
    2009 – 2013            Scientist, Department of Neuroscience, Genentech, Inc./Roche
    2004 - 2009             Assistant professor, Department of Neurology, Mount Sinai School of Medicine
    2003 - 2004             Associate specialist, Department of Molecular and Cell Biology, University of California, Berkeley
    2001 - 2003             Post-doctoral fellow, Department of Molecular and Cell Biology, University of California, Berkeley
    1998-2000               Post-doctoral fellow, Department of Cellular and Molecular Pharmacology, University of California, San Francisco
    1993 – 1998             Ph. D., Department of Neurobiology and behavior, State University of New York Stony Brook
    1991 – 1993             M.Sc, Department of physiology, School of Medicine, University of Pittsburgh                               
    1985 – 1990             B.Sc, Tsinghua University
  • Awards & Honors
    1999 - 2000            NIH institutional traineeship at UCSF
    2001 - 2004            National research service award (Activity-dependent Plasticity of retinotectal synapses)               
    2006 - 2009            New scholar award (Ellison Medical Foundation)
    2013                       Top poster award, Society of Biological Psychiatry
    1994 - present        Member, Society for Neuroscience
    Journal of neurological disorders
    International journal of neurological research
    SM Journal of Depression Research and Treatment
    Journal of Systems and Integrative Neuroscience 
  • Research Fields
    The primary focus of my lab is to understand the cellular and molecular mechanisms underlying the diseases of the nervous systems, such as Alzheimer’s disease and psychiatric disorders. We approach this problem at the levels of synapse, neural network and behavior, using a combination of electrophysiology, fluorescence imaging, animal behavioral testing and molecular approaches. With a better understanding of the pathophysiology of these diseases, we aim to identify novel therapeutic targets in treating these diseases. One under-explored area is the use of traditional Chinese herbal medicine to treat nervous system diseases. Through our studies, we will investigate the therapeutic potentials of Chinese herbs, with collaboration with colleagues in the chemistry group.
  • Selected Publications
    1.  Hanson JE, Pare JF, Deng L, Smith Y, Zhou Q. Altered GluN2B NMDA receptor function and synaptic plasticity during early pathology in the PS2APP mouse model of Alzheimer's disease. Neurobiol Dis.74:254-62, 2015.
    2.  Hanson JE, Meilandt WJ, Gogineni A, Reynen P, Herrington J, Weimer RM, Scearce-Levie K, Zhou Q. Chronic GluN2B antagonism disrupts behavior in wild-type mice without protecting against synapse loss or memory impairment in Alzheimer's disease mouse models. J Neurosci. 34(24):8277-88, 2014.
    3.  Zhou Q. GluN2B-NMDA receptors in Alzheimer's disease: beyond synapse loss and cell death. Neural Regen Res.9(21):1878-9, 2014.
    4.  Zhou Q and Sheng M. NMDA receptors in nervous system diseases. Neuropharmacology 74:69-75, 2013.
    5.  Paoletti P, Bellone C, Zhou Q. NMDA receptor subunit diversity: impact on receptor properties, synaptic plasticity and disease. Nat Rev Neurosci. 14:383-400, 2013.
    6.  Hanson JE, Deng L, Hackos DH, Lo SC, Lauffer BE, Steiner P, Zhou Q. Histone deacetylase 2 cell autonomously suppresses excitatory and enhances inhibitory synaptic function in CA1 pyramidal neurons. J Neurosci. 33:5924-9, 2013.
    7.  Hanson JE, Weber M, Meilandt WJ, Wu T, Luu T, Deng L, Shamloo M, Sheng M, Scearce-Levie K, Zhou Q. GluN2B Antagonism Affects Interneurons and Leads to Immediate and Persistent Changes in Synaptic Plasticity, Oscillations, and Behavior. Neuropsychopharmacology. 38:1221-33, 2013.
    8.  Yang Y, Wang XB, Zhou Q. Perisynaptic GluR2-lacking AMPA receptors control the reversibility of synaptic and spines modifications. Proc. Natl. Acad. USA. 107: 11999-2004, 2010.
    9.  Yang Y and Zhou Q. Spine modifications associated with long-term potentiation. Neuroscientist. 15: 464-76, 2009.
    10.  Yang Y, Wang X, Frerking M and Zhou Q. Delivery of AMPA receptors to perisynaptic sites precedes the full expression of long-term potentiation. Proc. Natl. Acad. USA. 105: 11388-11393, 2008.
    11.  Wang X, Yang Y and Zhou Q. Independent expression of synaptic and morphological plasticity associated with long-term depression. J. Neurosci. 27:12419-29, 2007.
    12.  Zhou Q, Homma, K and Poo, M-m. Shrinkage of dendritic spines associated with long-term depression of hippocampal synapses. Neuron. 44:749-757, 2004.
    13.  Zhou Q, Tao HW and Poo M-m. Reversal and stabilization of synaptic modifications in a developing visual system. Science. 300, 1953-1957, 2003.
    14.  Zhou Q, Xiao MY and Nicoll RA. Contribution of cytoskeleton to the internalization of AMPA receptors. Proc. Natl. Acad. USA. 98: 1261-1266, 2001.