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Professor Min Li

Associate Dean of School of Chinese Medicine

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Professor Min Li

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About

Associate Dean of School of Chinese Medicine; Professor, Teaching and Research Division; Programme Director of Bachelor of Chinese Medicine & Bachelor of Science (Hons) in Biomedical Science and Master of Chinese Medicine programmes; Director, Mr. & Mrs. Ko Chi Ming Centre for Parkinson's Disease Research

 

2007Distinguished Female Chinese Medicine Practitioner by the China Association of Chinese medicine, Beijing, China
2011Municipal Science and Technology Project Award from Shenzhen Virtual University Park, Shenzhen, China
2012School's Award for Outstanding Performance in Scholarly Work, HKBU
2013President's Award for Outstanding Performance in Teaching, HKBU

 

Achievements

Prof. Li's current research directions are:

Investigation of the Efficacy and Safety of TCM in the Treatment of Neurodegenerative Diseases including Parkinson's Disease (PD) and Alzheimer's Disease (AD) based on Randomized Controlled Clinical Trials, as well as the Interaction of TCM and Western Medicine.
Understanding the Neuroprotective Effects and Underlying Mechanisms of TCM on Neurodegenerative Diseases including PD and AD.
Studying the Protective Effects and Underlying Mechanisms of TCM on Vascular Endothelial Cells by in Vitro and in Vivo Models.

 

Project 1: Curcumin analogue C1 ameliorates APP and Tau pathology and improves cognitive deficits in Alzheimer disease transgenic mice via TFEB activation 

  • (Funding sources:  RGC/HKBU121006/18, RGC/HKBU121014/17, HMRF/15163481, HMRF14150811, HKBU/RC-IRCs/17-18/03 and FRG II/16-17/018)
  • Previously we identified a novel TFEB activator named curcumin analog C1 which directly binds to and activates TFEB (Song et al., Autophagy 2016; US patent: US9540299 and US9351946). Importantly, this small molecule has good brain permeability and promotes autophagy-lysosome pathway (ALP) in vivo. Here, we found that C1 efficiently activated TFEB, enhanced autophagy and lysosomal activity, and reduced beta-amyloid precursor protein (APP), APP C-terminal fragments (CTF-β/α), Aβ and Tau aggregates in 5xFAD mice, P301S mice and 3xTg-AD mice accompanied by improved learning and memory. Knockdown of TFEB and inhibition of lysosomal activity significantly inhibited the effects of C1 on APP and Tau degradation in vitro. In summary, curcumin analog C1 is a potent TFEB activator with promise for use in the treatment of AD. (Song et al., Aging Cell 2020).

 

Project 2: Nuclear receptor binding factor 2 (NRBF2) is involved in the degradation process of APP-CTFs in Alzheimer disease models 

  • (Funding sources: RGC/HKBU121014/17, FDCT-024-2017-AMJ, FDCT-022/2015/A1 and FRG II/15-16/034)
  • Autophagy plays an important role in AD pathogenesis by regulating amyloid precursor protein (APP) processing and intra-neuronal amyloid beta (Aβ) homeostasis. However, the mechanism whereby autophagy modulates APP metabolism is poorly understood. In this study, we found that NRBF2, a key component and regulator of the PtdIns3K, is involved in APP-CTFs homeostasis. We found that NRBF2 interacts with APP in vivo and its expression levels are reduced in hippocampus of 5XFAD AD mice. We further demonstrated that NRBF2 modulates APP C-terminal fragments (APP-CTFs), and Aβ1-40 and Aβ1-42 levels in human mutant APP overexpression cells. Furthermore NRBF2 positively regulates autophagy in neuronal cells and NRBF2-mediated reduction of APP-CTFs levels is autophagy-dependent. Importantly, NRBF2 knockout attenuates the recruitment of APP/APP-CTFs into autophagosome/autolysosome and the sorting of APP/APP-CTFs into endosomal intraluminal vesicles, which is accompanied by the accumulation of the APP/APP-CTFs into RAB5-positive early endosomes. Collectively, our results demonstrate that NRBF2 plays an important role in regulating degradation of AD-associated APP-CTFs through modulating autophagy. (Yang et al., Autophagy 2017)

 

Research Outputs

Ten Most Representative Publications

  • Song JX, Malampati S, Zeng Y, Durairajan SSK, Yang CB, Tong BC, Iyaswamy A, Shang WB, Sreenivasmurthy SG, Zhu Z, Cheung KH, Lu JH, Tang C, Xu N, Li M*. A small molecule transcription factor EB activator ameliorates beta-amyloid precursor protein and Tau pathology in Alzheimer's disease models. Aging Cell. 2020 Feb;19(2):e13069.doi: 10.1111/acel.13069.
  • Yang C, Zhu Z, Tong BC, Iyaswamy A, Xie WJ, Zhu Y, Sreenivasmurthy SG, Senthilkumar K, Cheung KH, Song JX, Zhang HJ, Li M*. A stress response p38 MAP kinase inhibitor SB202190 promoted TFEB/TFE3-dependent autophagy and lysosomal biogenesis independent of p38. Redox Biol. 2020 Jan 28:101445. doi: 10.1016/j.redox.2020.101445.
  • Ji F, Sreenivasmurthy SG, Wei J, Shao X, Luan H, Zhu L, Song J, Liu L, Li M*, Cai Z*. Study of BDE-47 induced Parkinson's disease-like metabolic changes in C57BL/6 mice by integrated metabolomic, lipidomic and proteomic analysis. J Hazard Mater. 2019 Oct 15;378:120738.  doi: 10.1016/j.jhazmat.2019.06.015.
  • Yang CB, Cai CZ, Song JX, Tan JQ, Iyaswamy A, Wu MY, Durairajan SSK, Chen LL, Yue ZY, Li M*, Lu JH*. NRBF2 is involved in the autophagic degradation process of APP-CTFs in Alzheimer disease models. Autophagy, 2017;13(12):2028-2040.  doi:10.1080/15548627.2017.1379633.
  • Chen LL, † Wang YB, † Song JX, † Deng WK, Lu JH, Ma LL, Yang CB, Li M*, Xue Y*. Phosphoproteome-based kinase activity profiling reveals the critical role of MAP2K2 and PLK1 in neuronal autophagy.  Autophagy, 2017;13(11):1969-1980.  doi:10.1080/15548627.2017.1371393.
  • Song JX, YR, Peluso I, Zeng Y, Yu X, Lu JH, Xu Z, Wang MZ, Liu LF, Huang YY, Chen LL, Durairajan SS, Zhang HJ, Zhou B, Zhang HQ, Lu A, Ballabio A, Medina D*, Guo Z*, Li M*. A Novel Curcumin Analog Binds to and Activates TFEB in Vitro and in Vivo Independent of MTOR Inhibition. Autophagy, 2016; 12(8):1372-89.doi: 10.1080/15548627.2016.1179404.
  • Lu JH, He L, Behrends C, Araki M, Araki K, Jun Wang Q, Catanzaro JM, Friedman SL, Zong WX, Fiel MI, Li M, Yue ZY*. NRBF2 Regulates Autophagy and Prevents Liver Injury Through Modulating Beclin Atg14L-Linked Phosphatidylinositol-3 Kinase III Activity. Nat. Commun. 2014; 5:3920.   doi: 10.1038/ncomms4920.
  • Song JX, Lu JH, Liu LF, Chen LL, Durairajan SS, Yue Z, Zhang HQ, Li M*. HMGB1 is involved in Autophagy Inhibition Caused by SNCA/alpha-synuclein Overexpression: a Process Modulated by the Natural Autophagy Inducer Corynoxine B. Autophagy. 2014;10(1):144-154. doi: 10.4161/auto.26751.
  • Lu JH, Tan JQ, Durairajan, Liu LF, Zhang ZH, Ma L, Shen HM, Chan HY*, Li M*. Isorhynchophylline, a Natural Alkaloid, Promotes the Degradation of Alpha-synuclein in Neuronal Cells via Inducing Autophagy. Autophagy. 2012; 8(1):98-108. doi: 10.4161/auto.8.1.18313. (Erratum in Autophagy. 2012; 8 (5):864-866.) 
  • Durairajan SSK, Liu LF, Lu JH, Chen LL, Yuan Q, Chung SK, Huang L, Li XS, Huang JD, Li M*. Berberine Ameliorates Beta-amyloid Pathology, Gliosis, and Cognitive Impairment in an Alzheimer's disease Transgenic Mouse Model. Neurobiol Aging. 2012; 33(12): 2903- 2919.  doi: 10.1016/j.neurobiolaging.2012.02.016.