Un J. Kang, MD

Departments And Divisions

  • Department of Neurology
    Division of Movement Disorders
  • H. Houston Merritt Professor of Neurology
  • Chief, Division of Movement Disorders
Un J. Kang, <span>MD</span>

My academic interest consists of basic science research on pathogenesis and mechanisms of movement disorders using rodent and cellular models.  In my role as the Chief of the Division of Movement Disorders, I spearhead the team effort that consists of basic biology of PD and other movement disorders, clinical characterization of movement disorders, and translational studies including biomarkers, imaging, and therapeutic approaches. 

My research has been focused on understanding the biochemical mechanisms and basal ganglia circuitry of PD and devising novel therapeutic approaches. My earlier work on gene therapy to deliver dopamine in more optimal fashion in animal models is now being applied to human studies by many investigators. Our studies also led to the realization that understanding the mechanisms underlying plasticity of basal ganglia in response to the dopaminergic therapy of Parkinson’s disease is critical to overcome the limitation of the current dopaminergic therapy. We have developed a novel model of PD phenotype utilizing aphakia mouse that lack transcriptional factor pitx3 and show regional loss of dorsolateral nigrostriatal projection as a complementary tool to study PD therapy and dyskinesia. We have also discovered a role of interneurons in basal ganglia plasticity underlying a complication of pharmacological therapy, called dyskinesia. Understanding the contributions of the disease process and dopaminergic therapy to development of dyskinesia has important implications on clinical decisions on when and what to treat patients with. Current projects explore ways to modulate specific cell types to complement the traditional approach of pharmacological manipulation to treat PD abnormalities and its complications. We use pharmacogenetic tools that can express therapeutic genes specifically in particular neuronal types as a potential gene therapy modality. We are also examining selective gene transcription in cholinergic neurons in PD and dyskinesia models in order to understand signal pathway changes and identify new therapeutic targets.

My interests also include understanding the mechanisms of neurodegeneration using both toxic and genetic models of PD.  We have investigated intrinsic factors that make dopamine neurons more susceptible to insults that are hypothesized to contribute to the pathogenesis of PD as well as the mechanisms of PD genes such as DJ-1 and PINK1 in neurodegeneration. These studies are also translated to develop biomarkers of PD.

    Education & Training

  • MD, Johns Hopkins University - Baltimore
  • 1982 Johns Hopkins University School of Medicine
  • Residency: NewYork-Presbyterian Hospital/Columbia University Medical Center
  • Fellowship: NewYork-Presbyterian Hospital/Columbia University Medical Center

Lab Locations

  • William Black Building

    650 West 168th Street
    3rd Floor - room 302
    New York, NY 10032
    Phone:
    (212) 342-3796
    Email:
    ujk2101@cumc.columbia.edu

Past Positions

1992-2013: Assistant Professor, Associate Professor, Full Professor with tenure: Department of Neurology, The University of Chicago

Committees/Societies/Memberships

NIH grant review commitees (since 1994)

Scientific Advisory Board Member: American Parkinson Disease Association (2005 to present), Dystonia Medical Research Foundation (1998-2001)

Director: Parkinson's Disease Foundation Center at Columbia (2013 to present), APDA Advanced Center at U of Chicago (2007-2013)

Fellow, American Academy of Neurology, American Society for Neural Transplantation and Repair

Member, American Neurological Association, Movement Disorders Society, Society for Neuroscience

Research Interests

  • Molecular Mechanisms of Neurodegeneration
  • Models of Parkinson's Disease
  • Basal Ganglia Circuitry and Plasticity

Publications

1. Ding Y, Won L, Britt JP, Lim SAO, McGehee DS, Kang UJ.  Enhanced striatal cholinergic neuronal activity mediates L-DOPA induced dyskinesia in parkinsonian mice.  Proc Natl Acad Sci U S A. 2011 Jan 11;108(2):840-5. PMID: 21187382
2. Zhuang X, Mazzonni P, Kang UJ. The role of plasticity in dopaminergic therapy for Parkinson’s disease.  Nature Review Neurology. 2013 May; 9(5):248-56. PMID: 23588357
3. Won L, Ding Y, Singh P, Kang UJ. Striatal cholinergic cell ablation attenuates L-DOPA induced dyskinesia in Parkinsonian mice. J Neurosci 2014;34:3090-3094. PMID: 24553948
4. Xie T, Vigil J, MacCracken E, Gasparaitis A, Young J, Kang W, Bernard J, Warnke P, Kang UJ. Low-frequency stimulation of STN-DBS reduces aspiration and freezing of gait in patients with PD. Neurology. 2015 Jan 27;84(4):415-20. PMID: 25540305
5. Lin W, Wadlington NL, Chen L, Zhuang X, Brorson JR, Kang UJ. Loss of PINK1 attenuates HIF-1a induction by preventing 4E-BP-dependent switch in protein translation under hypoxia. J Neurosci 2014;34:3079-3089. PMID: 24553947

For a complete list of publications, please visit PubMed.gov