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Ted M. Dawson, M.D., Ph.D.

Director, Institute for Cell Engineering
Professor of Neurology

See Research on Pubmed

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The Johns Hopkins Hospital

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  • Director, Institute for Cell Engineering
  • Director, Morris K. Udall Parkinson's Disease Research Center
  • Leonard and Madlyn Abramson Professor in Neurodegenerative Diseases
  • Professor of Neurology
  • Professor of Neuroscience
  • Professor of Pharmacology and Molecular Sciences

Centers & Institutes

  • Cell Engineering, Institute for
  • Parkinson's Disease and Movement Disorders Center


Neurological Disease, Neurology, Parkinson's Disease

Research Interests

Molecular and Cellular Signals Controlling Neurodegeneration; Neuronal Survival and Cell Death


Dr. Ted Dawson focuses on movement disorders with many advances in neurobiology of disease have stemmed from Dr. Dawson''s identification of the mechanisms of neuronal cell death and the elucidation of the molecular mechanisms of neurodegeneration. He pioneered the role of nitric oxide in neuronal injury in stroke and excitotoxicity and elucidated the molecular mechanisms by which nitric oxide and poly (ADP-ribose) polymerase kills neurons. His studies of nitric oxide led to major insights into the neurotransmitter functions of this gaseous messenger molecule. He co-discovered the neurotrophic properties of non-immunosuppressant immunophilin ligands. Dr. Dawson''s discoveries have led to innovative approaches and enhanced the development of new agents to treat neurologic disorders, such as Parkinson''s disease and Alzheimer''s disease as well as other neurodegenerative disorders.

Dr. Ted Dawson received his medical degree and Ph.D. in pharmacology from the University of Utah School of Medicine. He then completed an internship in medicine at the University of Utah Affiliated Hospitals before going to the Hospital of the University of Pennsylvania for a neurology residency. Next, he came to The Johns Hopkins where he completed a fellowship in neuroscience and senior clinical fellowship in movement disorders.
Additional Resources +
  • Education +


    • The University of Utah ( Salt Lake City UT ) (1986)


    • University of Pennsylvania/ Neurology ( Philadelphia PA ) (1990)


    • The Johns Hopkins Hospital/ Sr Clinical Fellow / Neurology ( Baltimore MD ) (1993)
    • Johns Hopkins University School of Medicine/ Post Doc Fellow in Neuroscience ( Baltimore MD ) (1992)


    • Neurology, American Board of Psychiatry & Neurology (1991)
  • Research & Publications +

    Selected Publications View all on PubMed

    1. Andrabi SA, Umanah GK, Chang C, Stevens DA, Karuppagounder SS, Gagné JP, Poirier GG, Dawson VL, Dawson TM. Poly(ADP-ribose) polymerase-dependent energy depletion occurs through inhibition of glycolysis. Proc Natl Acad Sci U S A. 2014 Jul 15;111(28):10209-14. doi: 10.1073/pnas.1405158111. Epub 2014 Jul 1. PMID: 24987120 
    2. Sagal J, Zhan X, Xu J, Tilghman J, Karuppagounder SS, Chen L, Dawson VL, Dawson TM, Laterra J, Ying M. Proneural transcription factor atoh1 drives highly efficient differentiation of human pluripotent stem cells into dopaminergic neurons. Stem Cells Transl Med. 2014 Aug;3(8):888-98. doi: 10.5966/sctm.2013-0213. Epub 2014 Jun 5. PMID: 24904172 
    3. Chen YC, Umanah GK, Dephoure N, Andrabi SA, Gygi SP, Dawson TM, Dawson VL, Rutter J. Msp1/ATAD1 maintains mitochondrial function by facilitating the degradation of mislocalized tail-anchored proteins. EMBO J. 2014 Jul 17;33(14):1548-64. doi: 10.15252/embj.201487943. Epub 2014 May 19. PMID: 24843043 [PubMed - in process] 
    4. Karuppagounder SS, Brahmachari S, Lee Y, Dawson VL, Dawson TM, Ko HS. The c-Abl inhibitor, nilotinib, protects dopaminergic neurons in a preclinical animal model of Parkinson's disease. Sci Rep. 2014 May 2;4:4874. doi: 10.1038/srep04874.
      PMID: 24786396 [PubMed - in process] 
    5. Chi Z, Byrne ST, Dolinko A, Harraz MM, Kim MS, Umanah G, Zhong J, Chen R, Zhang J, Xu J, Chen L, Pandey A, Dawson TM, Dawson VL. Botch is a γ-glutamyl cyclotransferase that deglycinates and antagonizes Notch. Cell Rep. 2014 May 8;7(3):681-8. doi: 10.1016/j.celrep.2014.03.048. Epub 2014 Apr 24. PMID: 24767995


    The Dawson lab studies molecular mechanisms of neurodegeneration of Parkinson’s disease, nitric oxide signaling and neuronal cell death and neuroprotective and neurorestorative strategies in neurodegenerative diseases, stroke and trauma.

    Parkinson’s disease is a common neurodegenerative disorder and the Dawson lab is studying the genetic basis of PD by investigating the mechanisms by which mutations in familial-linked genes cause PD, with hopes of identifying potential therapeutic targets for developing PD treatments. Current projects include the study of alpha-synuclein, LRRK2, parkin and PINK1.

    Nitric oxide is a major player in neuronal cell death and the Dawson team has discovered parthanatos, a caspase-independent programmed cell death pathway involving apoptosis inducing factor (AIF) downstream of NO and its major target poly (ADP-ribose) polymerase (PARP). The team now is further characterizing that pathway to identify targets of AIF and the roles of other cell death effectors with the hope of identifying new signaling pathways that might be amenable to therapeutic intervention. NO also activates the Ras-cell survival signaling pathway and the team is characterizing novel cell survival genes targeted by this pathway.

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    The Johns Hopkins Hospital
    600 N. Wolfe Street
    Sheikh Zayed Tower
    Baltimore, MD 21287
    Phone: 410-614-1307
    Appointment Phone: 410-955-9441
    Location Map
    Johns Hopkins Outpatient Center
    601 N. Caroline Street
    Baltimore, MD 21287
    Phone: 410-614-1307
    Appointment Phone: 410-955-9441
    Location Map


    • Neurology - Movement Disorders
    • Pharmacology and Molecular Sciences
    • Neuroscience

    For Research Inquiries Contact

    Miller Research Building,
    Suite 731,
    733 N. Broadway,
    Baltimore, MD 21205

    Phone: 410-614-3359
    Fax: 410-614-9568

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