About IEC

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Weidong Le

Title: Professor, MD, PhD
Email: wdle@sibs.ac.cn
Major: Neurology

Working Experience

19891990: Postdoctoral, Department of Neurology, Baylor College of Medicine

1991-1992 : Research Associate, Department of Neurology, Baylor College of Medicine

1992-1993:Instructor, Department of Neurology, Baylor College of Medicine

1993-1999:Assistant Professor, Department of Neurology, Baylor College of Medicine

2000-2005:Associate Professor, Department of Neurology, Baylor College of Medicine

2006-2013:Professor of Neurology, Baylor College of Medicine, Unites States

12/2013-Present:Senior Member and Adjunct Professor of Neuroscience ResearchProgram, Houston Methodist Research Institute and Weill Cornell Medical College of Cornell University, USA


Participation in the Academic Community

1984 - Member of Neurology Society, Chinese Medical Association

1986 - Member of Neuroscience Society, Chinese Academy of Sciences

1991 - Member of American Society for Neuroscience

1997 - Member of Movement Disorder Society

2000 - Member of American Academy of Neurology

2007 - Committee Member of Chinese Parkinson’s Disease and Movement Disorders Society

2008 - Board Member of Chinese Neuroscience Society

2010 - Vice Director of Chinese of Cell Therapy Committee


Research Direction

1.Determine the epigenetic mechanisms of chronic hypoxia induced learning and memory deficiency and Alzheimer’s disease neuropathology

2.Understanding the molecular mechanisms of transcription factors Nurr1 and Pitx3, and microRNA-132 regulation in dopaminergic cell differentiation

3.Define the role of dopaminergic neuron development gene defects in Parkinson’s disease

4.Assess the pathological effect of reactive microglia and astrocytes in Parkinson’s disease

5.Investigate the pathological role of autophagy defects in motor neuron degeneration in ALS and other neurodegenerative disorders


Thesis or Articles Published

1.Le W, Xu P.Y, Jiang H, et al. (2003) Mutations in NNR4A2 associated with familial Parkinson’s disease. Nature Genetics. 33:85-89.

2. Deng H, Le W, Jankovic J (2004). Parkinson’s Disease, Essential Tremor, and Premutation Alleles of theFMR1Gene. JAMA  292:1685-1686

3. Jankovic J, Chen S, Le W. (2005) Role of Nurr1 in dopamine neuron development and Parkinson disease. Progress in Neurobiology. 77:128-138

4. Peng CG, Aron L, Klein R, Li M, Wurst W, Prakash N, Le W (2011) Pitx3 is a critical mediator of GDNF-induced BDNF expression in nigrostriatal dopaminergic neurons. J Neurosci. 31(36):12802-12815

5. Zhang X, Li L, Chen S, Yang D, Wang Y, Zhang X, Wang Z, Le W. (2011) Rapamycin treatment augments motor neuron degeneration in SOD1 (G93A) mouse model of amyotrophic lateral sclerosis. Autophagy.7(4):412-425

6. Wang Y, Yang D, Song L, Li T, Yang J, Zhang X, Le W (2012) Mifepristone inducible caspase-1 expression in mouse embryonic stem cells eliminates tumor formation but spares differentiated cells in vitro and in vivo. Stem Cells. 30(2):169-79

7. Le W, Sayana P, Jankovic J (2014) Animal models of Parkinson's disease: A Gateway to Therapeutics? Neurotherapeutics, 11(1), 92-110

8. Le W, Zhang X (2014 ) Novel Therapeutic Strategies for Amyotrophic Lateral Sclerosis, Science, special edition: Neurodegenerative Disease in China, 59-62

9. Tang Y, Li T, Li J, Yang J, Liu H, Zhang X, Le W (2014) Jmjd3 is essential for the epigenetic modulation of microglia phenotypes in the immune pathogenesis of Parkinson's disease, Cell Death Differ, 21, 369–80

10. Zhang X, Chen S, Song L, Tang Y, Shen Y, Jia L, Le W (2014) ependent, autophagic enhancer trehalose prolongs motor neuron survival and ameliorates the autophagic flux defect in a mouse model of amyotrophic lateral sclerosis, Autophagy, 10(4), 1-15

11. Li J, Li T, Zhang X, Tang Y, Yang J, Le W (2014) Human SOD1 overexpression in motor neurons of Caenorhabditis elegans causes axon guidance defect and neurodegeneration, Neurobiol Aging, 35(4), 837-46

12.Yang D, Li T, Xu M, Gao F, Yang J, Yang Z, Le W (2014) Graphene oxide promotes the differentiation of mouse embryonic stem cells to dopamine neurons, Nanomedicine, posted online on February 24


Scientific Research Project

1.National Natural Science Foundation:Hypoxia affects the Alzheimer’s disease development and epigenetic study. 2014-2017 the amount of patronage: 700,000 RMB

2. National Natural Science Foundation: Study on molecular mechanism of p38α regulating UPS and ALP system and affecting function of dopamine neurons. 2012-2015 the amount of patronage: 600,000RMB

3. Subtopic of Project 973: IPS cells based investigation on serious disease models and pathogenesis. 2010-2015 the amount of patronage: 2,000,000 RMB

4. Subtopic of Project 973: Regulation of autophagy to dopamine neurons damage. 2010-2015 he amount of patronage: 2,500,000 RMB