John Ravits, MD
Title:
Research Associate Scientist
Email Address:
Phone Number:
206-341-1944
Background
Dr. Ravits graduated from Yale University where he studied English literature and pre-medicine. He attended the Mayo Clinic School of Medicine and did his internship and residency in Neurology at the University of California, San Diego. He did fellowships in Neurophysiology at the Brigham and Women’s Hospital, Harvard Medical School and at the National Institute of Neurological Diseases and Stroke, National Institutes of Health. He joined the Neurology Section at the Virginia Mason Medical Center in 1986 and specializes in Neurophysiology and Neuromuscular Disorders. He is a Clinical Professor (Neurology) at the University of Washington School of Medicine. He is an Associate Research Scientist at the Benaroya Research Institute, which he joined in 2004 to pursue research in amyotrophic lateral sclerosis and genome science.
Areas of Research
Dr. Ravits laboratory is devoted to translational research of amyotrophic lateral sclerosis (“Lou Gehrig’s disease”) and is focused on identifying and understanding molecular mechanisms contributing to select motor neuron degeneration and the 3-dimensional anatomic spread of disease. The research is moving in several directions involving in vitro and in vivo models and molecular pathology. Much of the work employs discovery techniques of new genomic technologies such as laser capture microdissection, RNA amplification, and the rapidly advancing techniques for whole genome transcriptome profiling. The data is processed using computational biology to seek unique signals within the data, correlations between human sporadic disease and models of genetic disease, and correlations between whole genome SNP data and the transcriptional profiles. This work is done in collaboration with and is supported by investigators at the Microsoft Research (Microsoft’s research division, http://research.microsoft.com/en-us/ ) as well as a number of other collaborators at the University of Washington, National Institute of Aging, and various other institutions. The mechanisms and pathways identified through computational biology are then sought using a variety of technologies such as immunohistochemistry, PCR, and biochemistry in the tissues and disease models. The hope is that with fundamental understanding of disease mechanisms, rationally-based therapies will develop.
Selected Publications
1. Ravits J, Laurie P, and Stone B: Amyotrophic lateral sclerosis microgenomics. Phys Med Rehabil Clin N Am. 2005;16 (4):909-24.
2. Mackenzie IRA, Bigio EH, Ince PG, Geser F, Neumann M, Cairns NJ, Kwong LW, Forman MS, Ravits J, Shaw PJ, Stewart H, McClusky L, Kretzschmar HA, Monoranu C, Highley R, Kirby J, Siddique T, Lee V M-Y, Trojanowski JQ: Pathological TDP-43 distinguishes sporadic ALS from ALS with SOD-1 mutations. Ann Neurol 2007;61:427-434.
3. Ravits J, Paul P, Jorg C: Focality of upper and lower motor neuron degeneration at the clinical onset of ALS. Neurology 2007;68:1571-1575.
4. Ravits J, Laurie P, Fan Y, and Moore DH: Implications of ALS focality: rostral-caudal distribution of lower motor neuron loss postmortem. Neurology 2007;68:1576-1582.
5. Ravits J, Traynor B: Current and Future Directions in Genomics of ALS. Phys Med Rehabil Clin N Am (2008, in press).
6. Ravits J, LaSpada A: Motor phenotype heterogeneity, focality, and spread in ALS: deconstructing motor neuron degeneration. Neurology 2009; 73: 805– 811.
7. Rabin S, Kim H, Baughn M, Libby R, Kim Y, Fan Y, La Spada A, Libby RT, Stone B, Ravits J: Sporadic ALS has compartment-specific aberrant exon splicing and perturbation of cell-matrix adhesion biology. Human Molecular Genetics 2010;19:313–328.
8. Bodansky A, Kim H, Tempest L, Velagupudi A, Libby RT, Ravits J: TDP-43 and ubiquitinated cytoplasmic aggregates in ALS are low frequency and widely distributed in the lower motor neuron columns independent of disease spread. Amyotroph Lateral Scler (Jan 2010, in press).
Translational Research Program