PiN Faculty Member - Vikram Khurana, PhD

Vikram Khurana, PhD

Assistant Professor of Neurology

Brigham and Women's Hospital
Building for Transformative Medicine, BTM 10016L
60 Fenwood Road
Boston, MA 02115
Tel: 617-525-5218
Email: vkhurana@bwh.harvard.edu
Visit my lab page here.



Neurodegenerative diseases like Alzheimer’s and Parkinson’s disease are diseases caused when proteins abnormally fold and aggregate in specific celltypes of the central nervous system. Cellular pathology results from a complex interplay of the host (genome and cellular proteome) with a protein folded into a specific, toxic conformation or “strain." The Khurana Lab (khuranalab.bwh.harvard.edu) utilizes unbiased genetic and spatial mapping methods to systematically dissect this host-strain interaction. These approaches include genome editing and genome-wide genetic screens, in conjunction with proteome and protein-protein interaction mapping techniques. We predominantly use neurons and organoids derived from patient induced pluripotent stem (iPS) cells as a model system. However, we frequently study proteinopathies in the genetically tractable baker’s yeast system (Saccharomyces cerevisiae) to guide our hypotheses and experimentation. The lab is particularly interested in the misfolding of alpha-synuclein, the protein that underlies a group of degenerative brain diseases known as synucleinopathies, that includes Parkinson’s disease, multiple system atrophy and dementia with Lewy bodies. In 2013, we succeeded in identifying and reversing early, innate cellular pathologies in Parkinson patient-derived neurons harboring alpha-synuclein mutations (Chung, Khurana et al., Science 2013; Tardiff et al. Science 2013). We have more recently completed the first comprehensive genetic and spatial mapping of alphasynuclein proteinopathy in living cells (Khurana, Chung, Peng et al., Cell Systems 2017; Chung, Khurana et al., Cell Systems 2017). In these studies, we uncovered an unexpected connection between alpha-synuclein and perturbed mRNA metabolism, as well as genetic interactions between alpha-synuclein and other proteins underlying distinct neurodegenerative diseases. These relationships are now being actively investigated in the lab, and our molecular networks are being harnessed to better understand the genetic architecture and host-strain relationships of synucleinopathies in humans.



Last Update: 12/11/2018



Publications

For a complete listing of publications click here.

 


 



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