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Rudy J. Castellani, is professor of pathology at the University of Maryland in Baltimore, Maryland, where he also serves as Director of Neuropathology, Director of Autopsy Services, Program Director of the Pathologist's Assistant Graduate Program, and Associate Director of the Pathology Residency Program. Dr. Castellani serves as Chair of the Veterans Administration, Neurobiology Study Section. He is the former Vice President (2006–2008) and former President (2008–2010) of the Maryland Society of Pathologists. He is recognized in the field of Alzheimer's disease and prion disease research, particularly for his work on oxidative stress, mitochondria dysfunction, cell cycle re-entry, and genotype-phenotype correlations.He is distinguished as one of the top Neuropathologists in the world. His many honors include the Alzheimer Medal, the Golden Chair Award from the American Association of Neuropathologists, the Wall of Fame award for excellence in teaching at the University of Maryland School of Medicine, and Educator of the Year from the Michigan State University Department of Neurology and Ophthalmology.
Castellani's research is dedicated to the study of neurodegenerative disease pathogenesis, including Alzheimer’s disease and so-called prion diseases. They have extensively characterized sporadic Creutzfeldt-Jakob disease in terms of clinical phenotype, pathological alterations, prion chemistry, and molecular genetics, and have found that specific features of the PrPsc molecule are remarkable predictors of phenotype. Further, they have recently characterized a form of human prion disease characterized by “protease-sensitive PrPsc,” expanding the spectrum of disease and drawing even closer overlap with more common neurodegenerative diseases. His studies on Alzheimer’s disease relate to early events in disease progression; as such, they have found a number of adducts related to oxidative stress in vulnerable, but pathologically normal, neurons in Alzheimer’s disease, as well as in control brains several decades prior to the onset of neurodegeneration. Their findings have significant implications in terms of therapeutic intervention.
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