Physician Photo

Vikram (Vik) Khurana, MBBS, PhD

Vik Khurana is an attending neurologist at Massachusetts General Hospital and a Visiting Scientist at the Whitehead Institute for Biomedical Research at MIT.

  • Phone: 855-644-6387
Departments
Department of Neurology
Clinical Interests
Parkinson's disease
Ataxia/gait disorders
Atypical parkinsonism
Multiple System Atrophy
Locations
Boston: Massachusetts General Hospital
Medical Education
PhD, Harvard University
MBBS, University of Sydney School of Medicine
Residency, Brigham and Women's Hospital
Residency, Prince of Wales Hospital
Fellowship, Massachusetts General Hospital
Board Certifications
Neurology, American Board of Psychiatry and Neurology
Gender
Male
Patient Gateway
Yes, learn more
Patient Age Group
Adult
Accepting New Patients
Yes

BiographyVik Khurana is on the faculty at Harvard Medical School and Massachusetts General Hospital, and a Visiting Scientist at the Whitehead Institute for Biomedical Research. His clinical and research interests relate to  neurodegenerative movement disorders, including Parkinson's disease, multiple system atrophy and the cerebellar ataxias. He is a medical graduate of the University of Sydney, Australia, and came to Boston as a Fulbright Scholar and Merck Company Foundation Fellow in 2001, obtaining his Ph.D. in neurobiology from Harvard University in 2006. He completed his residency in Neurology at Brigham and Womens and Massachusetts General Hospitals, and Fellowship training in Movement Disorders and Ataxia at Massachusetts General Hospital. His research efforts at the Whitehead Institute aim to develop novel therapies for neurodegenerative diseases by using diverse model systems including patient-derived stem cells. This work is supported by funding from the Howard Hughes Medical Institute and JPB Foundation,  and a Clinician Scientist Development Award to Dr Khurana from the American Brain and Parkinson's Disease Foundations.

ResearchVik Khurana is interested in the molecular mechanisms underlying nerve cell death in neurodegenerative parkinsonism, ataxias and dementia.  The overarching goal of his research is to develop therapies tailored to individual patients. His research uses diverse model systems to understand these diseases and to test drugs and small molecules, from patient-derived human stem cells (induced pluripotent stem cells) to simpler systems including rodent neurons, fruit flies and yeast cells.

Publications

View my most recent publications at PubMed

    1. Khurana V, Merlo P, Duboff B, Fulga TA, Sharp KA, Campbell SD, G?tz J, Feany MB. A neuroprotective role for the DNA damage checkpoint in tauopathy. Aging Cell. 2012 Apr; 11(2):360-2.
    2. Soldner F, Lagani?re J, Cheng AW, Hockemeyer D, Gao Q, Alagappan R, Khurana V, Golbe LI, Myers RH, Lindquist S, Zhang L, Guschin D, Fong LK, Vu BJ, Meng X, Urnov FD, Rebar EJ, Gregory PD, Zhang HS, Jaenisch R. Generation of isogenic pluripotent stem cells differing exclusively at two early onset Parkinson point mutations. Cell. 2011 Jul 22; 146(2):318-31.
    3. Khurana V, Elson-Schwab I, Fulga TA, Sharp KA, Loewen CA, Mulkearns E, Tyynel? J, Scherzer CR, Feany MB. Lysosomal dysfunction promotes cleavage and neurotoxicity of tau in vivo. PLoS Genet. 2010 Jul; 6(7):e1001026.
    4. Khurana V, Lindquist S. Modelling neurodegeneration in Saccharomyces cerevisiae: why cook with baker's yeast? Nat Rev Neurosci. 2010 Jun; 11(6):436-49.
    5. Khurana V. Modeling Tauopathy in the fruit fly Drosophila melanogaster. J Alzheimers Dis. 2008 Dec; 15(4):541-53.
    6. Fulga TA, Elson-Schwab I, Khurana V, Steinhilb ML, Spires TL, Hyman BT, Feany MB. Abnormal bundling and accumulation of F-actin mediates tau-induced neuronal degeneration in vivo. Nat Cell Biol. 2007 Feb; 9(2):139-48.
    7. Khurana V, Lu Y, Steinhilb ML, Oldham S, Shulman JM, Feany MB. TOR-mediated cell-cycle activation causes neurodegeneration in a Drosophila tauopathy model. Curr Biol. 2006 Feb 7; 16(3):230-41.
    8. Khurana V, Fulga TA, Feany MB. Senseless makes sense for spinocerebellar ataxia-1. Nat Neurosci. 2005 Nov; 8(11):1422-4.



 

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Phone: 855-644-6387
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