Dr. Youngjin Lee (李永鎮博士)

Postdoctoral Fellow (Johns Hopkins University)
PhD (University of Alabama at Birmingham)
M.S. Pharm. & B. Pharm. (Sungkyunkwan University)

Associate Professor, Department of Neuroscience

Office: 1A-205, 2/F, Block 1, To Yuen Building
Phone: +852 3442-4313
Fax: +852 3442-0549
Email: younglee@cityu.edu.hk
Web: Personal Homepage, CityU Scholars
Dr. Youngjin Lee

Dr Youngjin Lee received his Bachelor’s and Master’s degree from the School of Pharmacy at the Sungkyunkwan University in Korea. After working a few years as a clinical pharmacist, he moved to United States for studying neuroscience at the University of Alabama at Birmingham Medical Center, and he began to do research on glial biology in the central nervous system (CNS) under the guidance of Dr Michael Brenner. After completion of his PhD thesis in 2007, he joined Jeffrey Rothstein’s lab in the school of medicine at the Johns Hopkins University for postdoctoral training in 2009, and he has investigated the role of glia in Amyotrophic Lateral Sclerosis pathogenesis before joining the Department of Biomedical Sciences at the City University of Hong Kong in 2015. During graduate- and postdoctoral- training, he significantly contributed to understanding the properties and role of glia, including astroglia and oligodendroglia, in health and disease. He was a recipient of the Research Fellowship Award from the Health Fellowship Foundation in Korea (1996), and the W. Barry Wood, Jr. Research Award at the Johns Hopkins University in USA (2013). Dr Lee also was a principal investigator on Development Grant from Muscular Dystrophy Association (2011–2014).

Research Interests

Neurons have historically been thought as the only major cell to play a key role in CNS health and disease. However, glial cells, including astroglia and oligodendroglia, comprise 80–90% of CNS cell numbers and volume. Accumulating evidence over recent decades suggests that glia are both a physically supporting and an active cell type controlling CNS development, maintenance, and disease response through its interaction with the neuron. Among neuron-glia interactions, energy metabolic coupling is particularly important in maintaining CNS health. The CNS consumes significantly high amounts of energy per second, and disrupted energy metabolism is one of the key factors that directly causes axonal degeneration and neuronal death in several neurodevelopmental-and-neurodegenerative-diseases, including Cerebral Palsy and Ataxia.

Dr Lee’s Lab focuses on developing new tools, particularly mouse models and viral delivery systems to comprehensively understand glia-neuron energy metabolic coupling in neurological diseases. Critical CNS energy substrates are glucose and monocarboxylates such as lactate and ketone bodies. Particularly, glia-neuron metabolic coupling via monocarboxylate transporters (MCTs) may be an essential element for proper CNS development, including myelin formation, axon and synapse maturation, and neuronal circuitry development as well as for the maintenance of axonal and neuronal integrity during neuropathogenesis. Therefore, the study of MCTs during neurodevelopment and neuropathogenesis will provide novel therapeutic targets for those diseases, and also facilitate the development and application of inhibitors or activators specific to MCTs to prevent disease progression.

Position Available

We are looking for PhD students and research assistants with great enthusiasm in exploring neuroscience and neurological diseases through the use of diverse in vivo and in vitro models. Interested candidates please send a cover letter together with a full C.V. to Dr Lee.


  • Qiu G, Thakur A, Xu C, NG SP, Lee Y*, Wu CML*. Detection of glioma-derived exosomes with the biotinylated antibody-functionalized Titanium Nitride plasmonic biosensor. Advanced Functional Materials. 2018, 1806761 DOI: 10.1002/adfm.201806761
  • Thakur A, Qiu G, Siu-Pang NG, Wu CML, Lee Y*. Detection of membrane antigen of extracellular vesicles by surface plasmon resonance. Journal of Laboratory and Precision Medicine, 2017; 2: 98. DOI: 10.21037/jlpm.2017.12.08
  • Thakur A#, Qiu G#, NG S P, Guan J, Yue J, Lee Y *, Wu CML* Direct detection of two different tumor-derived extracellular vesicles by SAM-AuNIs LSPR biosensor, Biosensors and Bioelectronics, 2017 (On-line). DOI: 10.1016/j.bios.2017.03.036
  • Zhang PW , Haidet-Phillips AM , Pham JT, Lee Y, Huo Y, Tienari PJ, Maragakis NJ, Sattler R , Rothstein J D. Generation of GFAP::GFP astrocyte reporter lines from human adult fibroblast-derived iPS cells using zinc-finger nuclease technology. Glia. 21 AUG 2015 (on-line).
  • Morrison BM, Tsingalia A, Vidensky S, Lee Y, Jin L, Farah M.H, Lengacher S, Magistretti PJ, Pellerin L, Rothstein JD. 2015. Deficiency in Monocarboxylate Transporter 1 (MCT1) Delays Regeneration of Peripheral Nerves following Sciatic Nerve Crush. Experimental Neurology. 263:325-338.
  • Morrison BM, Lee Y, Rothstein JD. 2013. Oligodendroglia: metabolic supporters of axons. Trends Cell Biol. S0962-8924(13)00120-7.
  • Lee Y*, Morrison BM*, Li Y, Lengacher S, Farah MH, Hoffman PN, Liu Y, Tsingalia A, Jin L, Zhang PW, Pellerin L, Magistretti PJ, Rothstein JD. 2012. Oligodendroglia metabolically support axons and contribute to neurodegeneration. Nature (Article). 487(7408):443-8.
    Comment in Nature News and Views 2012, 487(7408):435-6 “Neuroscience: The wrap that feeds neurons” (Rinholm JE & Bergersen LH), Nat Rev Neurosci. 2012, 13(9):601“Glia: Oligodendrocyte transporters feed axons” (Jones R), Dis Model Mech. 2012, 5(6):711-2 “Lactate-starved neurons in ALS” (Martinez BA), and Mov Disord. 2012, 27(11):1357 “Oligodendroglial dysfunction associated with lactate transport deficiency contributes to neurodegeneration” (Ozawa T).This article also was evaluated post-publication by Faculty of 1000 Members and given a rating of ‘Exceptional’.
  • Lee Y, Messing A, Su M, Brenner M. 2008. GFAP promoter elements required for region-specific and astrocyte-specific expression. Glia. 56(5):481-93.
  • Lee Y, Su M, Messing A, Brenner M. 2006. Astrocyte heterogeneity revealed by expression of a GFAP-LacZ transgene. Glia (Cover Article). 53(7): 677-87.
  • Su M, Hu H, Lee Y, d’Azzo A, Messing A, Brenner M. 2004. Expression specificity of GFAP transgenes. Neurochem Res. 29(11): 2075-93.
  • Lee YJ, Nam SW, Seo DW, Ahn SH, Ko YK, Sung DS, Han JW, Hong SY, Lee HW. 1997. Changes of nitric oxide synthase activity and free methylarginines contents in regenerating rat liver after partial hepatectomy. Archives of Pharmacal Research. 20(3): 239-246.
  • Nam SW, Lee YJ, Ko YK, Chang MS, Choi WS, Kim KB, Woo TW, Han JW, Hong SY, Lee HW.1996. Skin Irritation Study of the Syndella gel, Topical Drug Containing Deproteinised Dialysate of Calf’s Blood and Micronomicin Sulfate in Rabbits. J. Applied Pharmacol. 4:415-418.
  • Nam TK, Han JW, Nam SW, Seo DW, Lee YJ, Ko YK, Lee HW.1996. Vasoactive Intestinal Peptide (VIP)-induced Enzyme Secretion in Rat Pancreatic Tissue is not associated with Activation of Nitric Oxide Synthase (NOS) and Increase in Cyclic GMP Level. Archives of Pharmacal Research. 19(3): 201-206.
  • Seo DW, Nam SW, Nam TK, Lee YJ, Ko YK, Lee HW. 1995. Effect of Cholecystokinin-pancreozymin on the Nitric Oxide Synthase Activity and Cyclic GMP Level in Rat Pancreatic Tissue. 1995. Archives of Pharmacal Research. 18(6): 434-439.