PhD, Professor
studies the molecular basis of synapse development and plasticity, and pathological mechanisms underlying neurodegenerative disorders.
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Cognitive functions depend on the precise neural network formed by neurons in the brain. Neurons communicate through neurotransmission at the synapse, which comprises a presynaptic terminal that contains the active zone for neurotransmitter release, a postsynaptic apparatus that harbors a high density of receptors for relaying the signals to the target cell, and surrounding glial cells that modulate the efficacy of neurotransmission across the synapse. Synaptic dysfunction is associated with a number of neurodegenerative disorders, including Alzheimer’s disease and Parkinson disease. Therefore, the precise organization of synaptic proteins and the spatial and temporal coordination of synaptic signaling events are central research topics in neurobiology. We are interested to investigate
• the molecular basis of synapse development and plasticity in the central nervous system
• the pathophysiological mechanisms underlying neurodegeneration (e.g. Alzheimer’s disease).
• the biomarkers for the diagnosis and prognosis of Alzheimer’s disease and novel approaches for disease intervention.


Principal investigator at SIAT CAS since 2015
2010-2014, Research Assistant Professor, HKUST
2007-2010, Research Associate/Visiting Scholar, HKUST
2007, The Hong Kong University of Science and Technology, PhD.
2002, Sun Yat-Sen University, BSc in Biochemistry

Selected publications

1. Chen Y, Fu AKY, Ip NY. Research updates on the pathogenic mechanisms of Alzheimer's disease and therapeutic strategies. Pharmacology & Therapeutics. Invited.
2. Zhou XP*, Chen Y*, Mok KY, Zhao QH, Chen KL, Chen YW, Hardy J, Li Y, Fu AKY, Guo QH, Ip NY. Alzheimer’s Disease Neuroimaging Initiative. Proceedings of the National Academy of Sciences. 2018; 115(8):1697-1706. (equal contribution)
3. Chen Y#, Liang Z, Fei E, Chen Y, Zhou X, Fang W, Fu WY, Fu AK, Ip NY#. Axin Regulates Dendritic Spine Morphogenesis through Cdc42-Dependent Signaling. PLoS One. 2015,10(7): e0133115. (co-corresponding author)
4. Chen Y, Fu WY, Ip JPK, Ye T, Fu AKY, Chao MV, Ip NY. ARMS/Kidins220 is required for neurotrophin and ephrin receptor-dependent dendrite development. Journal of Neuroscience. 2012; 32:8263-9.
5. Chen Y, Fu AKY, Ip NY. Eph receptors at synapses: implications in neurodegenerative diseases. Cellular Signaling. 2012; 24:606-11.
6. Chen Y# and Fu WY#. EphB maintains dendritic spine morphology through focal adhesion kinase. Journal of Neuroscience. 2009; 29:13091-3.(co-corresponding author)
7. Fu WY*, Chen Y*, Sahin M, Zhao XS, Shi L, Bikoff JB, Lai KO, Yung WH, Fu AKY, Greenberg ME,Ip NY. Cdk5 regulates EphA4-mediated dendritic spine retraction through an ephexin1-dependent mechanism. Nature Neuroscience.2007;10:67-76. (equal contribution)
8. Luo S*, Chen Y*, Lai KO, Arevalo JC, Froehner SC, Adams ME, Chao MV, Ip NY. Alpha-Syntrophin regulates ARMS localization at the neuromuscular junction and enhances EphA4 signaling in an ARMS-dependent manner. Journal of Cell Biology. 2005;169:813-24. (equal contribution)