New York University School of Medicine, 1991
Landon Center on Aging, MS 2012
3901 Rainbow Blvd
Kansas City, KS 66160-7401
Phone: 913-588-6970
Fax: 913-588-0681
Email: rswerdlow@kumc.edu
My laboratory focuses on the role mitochondria play in aging and neurodegeneration. In particular, the influence of mitochondrial genes on aging and neurodegenerative diseases (in particular, Alzheimer’s disease and Parkinson’s disease) is explored. The laboratory also investigates the relationship between mitochondrial dysfunction and neurodegenerative disease histopathology, adaptation responses that help cells survive mitochondrial dysfunction, and the treatment of mitochondrial dysfunction. Techniques commonly used in the lab include cell culture, PCR, Western blotting, DNA sequencing, generation of gene constructs, cell transfection, mitochondrial enzyme activity determinations, and fluorescence-based measurements of mitochondrial integrity/oxidative stress.
Swerdlow RH, Parks JK, Miller SW, Tuttle JB, Trimmer PA, Sheehan JP, Bennett JP, Davis RE, Parker WD. Origin and functional consequences of the complex I defect in Parkinson’s disease. Ann Neurol 1996; 40:663-670.
Swerdlow RH, Parks JK, Cassarino DS, Maguire DJ, Maguire RS, Bennett JP, Parker WD. Cybrids in Alzheimer’s disease: A cellular model of the disease? Neurology 1997; 49:918-925.
Swerdlow RH, Parks JK, Davis JN, Cassarino DS, Trimmer PA, Currie LJ, Dougherty J, Bridges S, Bennett JP, Wooten GF, Parker WD. Matrilineal inheritance of complex I dysfunction in a multigenerational Parkinson’s disease family. Ann Neurol 1998; 44:873-881.
Swerdlow RH, Miller SW, Parks JK, Sheehan JP, Cassarino DS, Maguire DJ, Maguire RS, Bennett JP, Juel VC, Phillips LH, Trimmer PA, Pattee G, Tuttle JB, Davis RE, Parker WD. Mitochondria in sporadic amyotrophic lateral sclerosis. Exp Neurol 1998; 153:135-142.
Parker WD Jr, Swerdlow RH. Mitochondrial dysfunction in idiopathic Parkinson disease. Am J Hum Gen 1998; 62:758-762.
Cardoso SM, Santos S, Swerdlow RH, Oliveira CR. A functional mitochondria is the target for amyloid-$ mediated toxicity. FASEB J 2001; 15:1439-1441.
Swerdlow RH and Khan S. A “Mitochondrial Cascade Hypothesis” for sporadic Alzheimer’s disease. Med Hypoth 2004;63:8-20.
Barrett MJ, Alones V, Wang KX, Phan L, Swerdlow RH. Mitochondria-Derived Oxidative Stress Induces a Heat Shock Protein Response. J Neurosci Res 2004;78:420-429.
Binder DR, Dunn WH Jr, Swerdlow RH. Molecular characterization of mtDNA depleted and repleted NT2 cell lines. Mitochondrion 2005;5:255-265.
Swerdlow RH, Weaver B, Grawey A, Wenger C, Freed E, Worrall BB. Complex I polymorphisms, bigenomic heterogeneity, and family history in Virginians with Parkinson’s disease. J Neurol Sci 2006;247:224-230.
Swerdlow RH. Is aging part of Alzheimer’s disease, or is Alzheimer’s disease part of aging? Neurobiol Aging 2007;28:1465-1480.
Swerdlow, RH. Mitochondria in cybrids containing mtDNA from persons with mitochondriopathies. J Neurosci Res 2007 [Epub ahead of print] PMID: 17243174.
Swerdlow RH. Treating neurodegeneration by modifying mitochondria: Potential solutions to a “complex” problem. Antiox Redox Signal 2007 [Epub ahead of print] PMID: 17663643.
Ghosh S, Patel N, Rahn D, McAllister J, Sadeghi S, Horwitz G, Berry D, Wang KX, Swerdlow RH. The thiazolidinedione pioglitazone alters mitochondrial function in human neuronal-like cells. Molecular Pharmacology 2007;71:1695-1702.
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The University of Kansas Medical Center