Dr. Burke's research focus is on basic neuroscience related to the cause and treatment of degenerative neurological disease, particularly Parkinson's Disease. His early work demonstrated that a genetically programmed form of cell death, called apoptosis, occurs in dopaminergic neurons of the substantia nigra. He demonstrated that this form of cell death can be induced in models of parkinsonism and it can be effectively blocked by pharmacologic or genetic approaches that inhibit cell death signaling.
Recent work has shown that axonal degeneration, which is mediated by non-apoptotic pathways, can also be inhibited by genetic approaches. His laboratory has also recently shown that, contrary to the long-held belief that axons of the mature central nervous system are incapable of re-growth, they can be induced to grow by the kinase Akt and the GTPase Rheb expressed in dopamine neurons by viral vector transfer.
Dr. Burke's early clinical research included important work in dystonia and the tardive dyskinesias, and led to the first descriptions of the delayed-onset dystonias and tardive dystonia.
His publications have appeared in The Journal of Neuroscience, Nature Neuroscience, Neuron, The Proceedings of the National Academy of Sciences (USA), The Annals of Neurology, The Journal of Comparative Neurology, Molecular Therapy and other leading neuroscience journals.
Li Y, Liu W, Oo TF, Wang L, Tang Y, Jackson-Lewis V, Zhou C, Geghman K, Bogdanov M, Przedborski S, Beal MF, Burke RE, Li C. Mutant hR1441G LRRK2 BAC transgenic mice recapitulate cardinal features of Parkinson’s Disease. Nature Neuroscience, 2009, 12:826-828.
Cheng H-C, Kim SR, Oo TF, Kareva T, Yarygina O, Rzhetskaya M, Wang C, During MJ, Talloczy Z, Tanaka K, Komatsu M, Kobayashi K, Okano H, Kholodilov N, Burke RE. Akt suppresses retrograde degeneration of axons by inhibition of macroautophagy. Journal of Neuroscience, 2011, 31:2125-2135.
Kim SR, Chen X, Oo TF, Kareva T, Yarygina O, Wang C, During MJ, Kholodilov N, Burke RE. Dopaminergic pathway reconstruction by Akt/Rheb-induced axon regeneration. Annals of Neurology, 2011, 70:110-120.
Kim SR, Kareva T, Yarygina O, Kholodilov N, Burke RE. AAV transduction of dopamine neurons with constitutively active Rheb protects from neurodegeneration and mediates axon re-growth. Molecular Therapy, 2012, 20:275-286.
Chen X, Tagliaferro P, Kareva T, Yarygina O, Kholodilov N, Burke RE. Neurotrophic effects of Serum- and Glucocorticoid-Inducible Kinase (SGK) on adult murine mesencephalic dopamine neurons. J Neuroscience, 2012, 32: 11299-11308.
Padmanabahn S, Kareva T, Kholodilov N, Burke RE. Quantitative morphological comparison of axon targeting strategies for gene therapies directed to the nigro-striatal projection. Gene Therapy, 2014, 21:115-122.
Wu D, Klaw M, Conners T, Kholodilov N, Burke RE, Tom V. Expressing constitutively-active Rheb in adult neurons after a complete spinal cord injury enhances axonal regeneration beyond a chondroitinase-treated glial scar. J Neuroscience, 2015, 35: 11068-80.
Tagliaferro P, Kareva T, Oo TF, Yarygina O, Kholodilov N, Burke RE. An early axonopathy in a hLRRK2(R1441G) transgenic model of Parkinson disease. Neurobiology of Disease, 2015, 82:359-371.
Honors and Awards
1970 Phi Beta Kappa
2004 President’s Award, The Dystonia Medical Research Foundation
2006 First Recipient of the J. William Langston Award of the Michael J Fox Foundation for Parkinson’s Research
2015 Fellow, American Association for the Advancement of Science
Committees , Council, and Professional Society Memberships
American Academy of Neurology
American Association for the Advancement of Science
American Neurological Association
American Society of Gene and Cell Therapy
Association for Research in Nervous and Mental Disease
International Brain Research Organization
Movement Disorder Society
New York Academy of Sciences
Society for Neuroscience
apoptosis, developmental neurobiology, neurogenesis, neurotrophic factor, substantia nigra, biological signal transduction, gene expression, gene mutation, growth factor receptor, laboratory mouse, laboratory rat, transgenic animal