ResearchNeurodegenerative disorders, including Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis (ALS), are among the most common challenging diseases that affect the population with extreme medical and financial burdens. Unfortunately, there are no treatments that slow or prevent disease development and progression. Most central pathological feature of the neurodegenerative diseases is neuroimmunological responses. To understand the neuroinflammatory mechanisms and molecular pathways in the progression of neurodegenerative disease, we will selectively manipulate specific glia cells in the central nervous system and the immunol cells in the peripheral system via transgenic disease mouse model and genome editing tools, combining electrophysiological, molecular/cellular biological and behavioral approaches.
2004-2009 Shanghai Jiao Tong University, Pharmacology, B.S.
2009-2014 Zhejiang University, Pharmaceutical Sciences, Ph.D.
2015-2017 Zhejiang University, Postdoctoral Fellow
2017-2021 University of California, San Diego, Postdoctoral Fellow
2021-present The Brain Cognition and Brain Disease Institute of Shenzhen Institutes of Advanced Technology, Associate Investigator
- B Feng, A Freitas, L Gorodetski, R Tian, YR Lee, J Wang, A Grewal, and Y Zou*. Planar cell polarity signaling regulates adult synapse maintenance and is a direct target of amyloid-βassociated synapse degeneration. Science Advances 2021; 7 : eabh2307
- Y Ban, T Yu, B Feng, C Lorenz, X Wang, C Baker, and Y Zou*. Prickle promotes the formation and maintenance of glutamatergic synapses by stabilizing the intercellular planar cell polarity complex. Science Advances
- Y Wan#, B Feng#, Y You#, J Yu, C Xu, H Dai, B Trapp, P Shi, Z Chen*, W Hu*. Microglial Displacement of GABAergic Synapses Is a Protective Event during Complex Febrile Seizures.Cell Reports 2020 33 (5), 108346 (#Equal Contribution)
- Y Tang#, B Feng#, Y Wang, H Sun, Y You, J Yu, B Chen, C Xu, Y Ruan, S Cui, G Hu, T Hou, and Z Chen* Structure‐based discovery of caspase‐1 inhibitor with therapeutic potential for febrile seizures and later enhanced epileptogenic susceptibility. British Journal of Pharmacology 177:3519–3534 (#Equal Contribution)
- K Onishi, R Tian, B Feng, Y Liu, J Wang, Y Li, Y Zou*. LRRK2 mediates axon development by regulating Frizzled3 phosphorylation and growth cone-growth cone communication. Proceedings of the National Academy of Sciences 117 (30) 18037-18048.
- D Wu#, B Feng#, Y Dai#, X Wu, B Chen, C Xu, Y Tang, K Wang, S Zhang, S Wang, B Luo, and Z Chen*. Intergenerational Transmission of Enhanced Seizure Susceptibility after Febrile Seizures. EBioMedicine.2017 Mar;17:206-215 (#Equal Contribution)
- B Chen#, B Feng#, Y Tang, Y You, Y Wang, W Hou, W Hu and Z Chen*. Blocking GluN2B subunits reverses the enhanced seizure susceptibility after prolonged febrile seizures with a wide therapeutic time-window. Experimental Neurology. 2016 May 27; 283:29-38 (#Equal Contribution)
- B Feng,Z Chen*. Generation of Febrile Seizures and Subsequent Epileptogenesis. Neuroscience Bulletin. 2016 Oct; 32(5):481-492. (Review)
- B Feng,Y Tang, B Chen, C Xu, Y Wang, Y Dai, D Wu, J Zhu, S Wang, Y Zhou, L Shi, W Hu, X Zhang, and Z Chen*. Transient increase of interleukin-1β after prolonged febrile seizures promotes adult epileptogenesis through long-lasting upregulating endocannabinoid signaling. Scientific Reports. 2016 Feb 23;6:21931.