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Un J. Kang, MD

  • H. Houston Merritt Professor of Neurology
  • Chief, Division of Movement Disorders
Un J. Kang, MD

Dr. Kang is a physician scientist who just returned to the Department of Neurology as H. Houston Merritt Professor of Neurology and chief of the Division of Movement Disorders in 2013. Dr. Kang completed his medical training at Johns Hopkins University and his neurology residency and fellowship in movement disorders here at Columbia, under the mentorship of his legendary predecessor, Dr. Stanley Fahn. Following his clinical education, Dr. Kang obtained his basic science training in catecholamine molecular biology and gene therapy for Parkinson's disease (PD), before joining the faculty of the University of Chicago School of Medicine, where he served as professor of neurology and director of the Parkinson's Disease and Movement Disorders Center until 2013. Funded by the National Institutes of Health and private foundations, Dr. Kang's research focuses on the elucidation of mechanisms of long term plasticity of basal ganglia in PD that manifest as either in detrimental ways or beneficial ways. His laboratory also studies mechanisms underlying degeneration in PD, including the role of genes involved in familial forms of PD. He is striving to translate some of his research findings to patient-based studies such as biomarker studies in PD to diagnose and stratify the patients better and aid in therapy development.

He directs the Division of Movement Disorders in a team effort to understand the disorders better through both basic and translational research and also to provide the best possible clincal care of patients with movement disorders. The division founded by Dr. Fahn has contributed to the development of the field of movenent disorders in a major way and to education of leaders who continue to make contributions all over the world and Dr. Kang will carry on with the tradition.

Dr. Kang is a specialist in movement disorders and provides clinical services for diagnosis, management and consultation for patients with Parkinson's disease, parkinsonian disorders (including multiple system atrophy, progressive supranuclear palsy, and corticobasal syndrome), tremors, chorea (including Huntington's disease), dystonia (including blepharospasm, cervical dystonia, writer's cramp), tics, tardive dyskinesias, and other abnormal involuntary movements.

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.

Departmental Appointments

  • Department of Neurology
    Division of Movement Disorders

Board Certifications

  • Neurology

Areas of Expertise

  • Movement Disorders
  • Parkinson's Disease
  • Dystonia
  • Tremor
  • Huntington Disease
  • Botulinum Toxin (Botox Injection)

Languages Spoken

(in addition to English)

  • Korean

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

Locations

  • Neurological Institute of New York

    710 West 168th Street
    Floor: 3rd floor
    New York, NY 10032
    For new and current patient appointments, call:
    (212) 305-1303

Provider Affiliations

  • NewYork-Presbyterian/Columbia

Insurance Programs

Please contact the provider's office directly to verify that your particular insurance is accepted.

  • Aetna [EPO, HMO, Medicare Managed Care, NY Signature, POS, PPO, Signature Administrators, Student Health]
  • Cigna [EPO, Great West, HMO, POS, PPO]
  • Emblem/HIP [ConnectiCare, EPO, Essential Plan, HMO, Medicaid Managed Care, Medicare Managed Care, POS, PPO, Select Care (Exchange), Vytra]
  • Empire Blue Cross Blue Shield [Blue Priority, EPO, HMO, Medicare (Mediblue), NYP Employee Plan, Pathway (Exchange), POS, PPO]
  • Local 1199 [Local 1199]
  • MagnaCare [MagnaCare]
  • Multiplan [Multiplan]
  • Oxford Health Plans [Freedom, Liberty, Medicare Managed Care]
  • POMCO [POMCO]
  • UnitedHealthcare [Columbia University Employee Plan, EPO, Essential Plan, HMO, Medicaid (Community Plan), Medicare Managed Care, POS, PPO]

This provider accepts new patients

Appointment Phone Number: (212) 305-1303

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

NIH Grants

  • TARGETING LEWY BODY SPECIFIC PATHOLOGY USING BIOMARKERS (Federal Gov)

    Sep 30 2016 - Aug 31 2021

    THE STRIATAL CHOLINERGIC INTERNEURONS IN PARKINSON S DISEASE AND TREATMENT (Federal Gov)

    May 1 2017 - Feb 28 2021

    STRIATAL CHOLINERGIC INTERNEURON ABLATION DYSTONIA MODEL (Federal Gov)

    Jun 1 2017 - Nov 30 2018

    THE EDMOND J. SAFRA FELLOWSHIP IN MOVEMENT DISORDERS (Private)

    Jul 1 2015 - Jun 30 2018

    PLASTICITY OF BRIDGE COLLATERALS IN PARKINONIAN STATE AND TREATMENT (Federal Gov)

    May 15 2016 - Mar 31 2018

    PBMC AND URINE EXOSOSMES IN LRRK2 AND IDIOPATHIC PD (Private)

    Jan 1 2016 - Dec 31 2017

    INSTITUTIONAL MOVEMENT DISORDERS FELLOWSHIP AWARD AT COLUMBIA UNIVERSITY (Private)

    Jul 1 2016 - Jun 30 2017

    PARKINSON S DISEASE FOUNDATION (PDF) RESEARCH CENTER GRANT (Private)

    Jul 1 2016 - Jun 30 2017

    NANO TOOLS VALIDATION PROJECT FOR ANTI-DJ-1 MONOCLONAL ANTIBODIES FOR BIOMARKER ASSAY DEVELOPMENT (Private)

    Jan 1 2016 - Dec 31 2016

    THE ROLE OF STRIATAL CHOLINERGIC INTERNEURONS IN PARKINSON S DISEASE (Federal Gov)

    Dec 1 2015 - Nov 30 2016

    PARKINSONS DISEASE FOUNDATION RESEARCH CENTER GRANT (Private)

    Jul 1 2000 - Jun 30 2016

    COLLABORATIVE VALIDATION OF OXIDIZED DJ-1 ANTIBODIES FOR PD BIOMARKER STUDY - SUPPLEMENT 2014 (Private)

    Oct 1 2014 - Jan 31 2016

    WRITING AND ANALYSIS AWARD-BIOFIND (Private)

    Jul 1 2015 - Dec 31 2015

    GENE EXPRESSION CHANGES IN STRIATAL CHOLINERGIC INTERNEURONS ASSOCIATED WITH L-DOPA-INDUCED DYSKINESIA IN PD. (Private)

    Aug 7 2014 - Aug 6 2015

    THE ROLE OF STRIATAL CHOLINERGIC INTERNEURONS IN PD DYSKINESIA (Private)

    Aug 7 2014 - Aug 6 2015

    PARKINSONS DISEASE FOUNDATION RESEARCH CENTER GRANT (Private)

    Jul 1 2000 - Jun 30 2015

    STRIATAL CHOLINERGIC NEURONS AND L-DOPA INDUCED DYSKENESIA (Federal Gov)

    May 1 2013 - Apr 30 2015

    FOX INVESTIGATION FOR NEW DISCOVERY OF BIOMARKERS (BIOFIND) (Private)

    Aug 12 2013 - Aug 11 2014

    PARKINSON S DISEASE FOUNDATION RESEARCH CENTE (Private)

    Jul 1 2000 - Jun 30 2014

    PARKINSON S DISEASE FOUNDATION RESEARCH CENTE (Private)

    Jul 1 2000 - Jun 30 2014

    PARKINSON S DISEASE FOUNDATION RESEARCH CENTE (Private)

    Jul 1 2000 - Jun 30 2014

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