PhD Anatomy, 1978 Univ of Cal Davis
MS Anatomy, 1974 Univ of Cal Davis
BS Zoology, 1973 Univ of Cal Davis
POST-DOCTORAL TRAINING AND RESIDENCY:
1979 John Hopkins University School of Medicine: Research Associate, Department of Neurology.
1978 - 1980 Johns Hopkins University School of Medicine: Postdoctoral Fellow, Department of Cell Biology and Anatomy.
1978 - 1980 NIH Postdoctoral Fellowship; Johns Hopkins University School of Medicine, Department of Anatomy; Study of catecholamine fibers within the developing cerebellum.
1989 - Present Associate Professor, Dept. Neurobiology and Anatomy, Univsity of Rochester.
1983 - 1989 Assistant Professor, Neurobiology and Anatomy, University of Rochester
APPOINTMENTS ACADEMIC - EXTERNAL:
1980 - 1983 National Institute of Mental Health, Staff Fellow, Section on Histopharmacology, Laboratory of Clinical Science.
AWARDS AND HONORS:
2004 Commendation for excellence in medical education, University of Rochester School of Medicine and Dentistry.
2003 Commendation for excellence in medical education, University of Rochester School of Medicine and Dentistry.
2001 Commendation for excellence in medical education, University of Rochester School of Medicine and Dentistry.
2000 Commendation for excellence in medical education, University of Rochester School of Medicine and Dentistry.
1996 Commendation for excellence in medical education, University of Rochester School of Medicine and Dentistry.
1995 Student (undergraduate) Advisor of the Year, University of Rochester.
1994 Alumni Award for Excellence in Graduate Education, University of Rochester School of Medicine and Dentistry.
1992 George W. Merck Dean's Teaching Scholar Award, University of Rochester School of Medicine and Dentistry.
1978 Outstanding Teaching Award, Graduate Division, University of California, Davis.
1974 Sigma Xi Honor Society
Models of CNS inflammation.
The inflammatory processes that follow injury (trauma, stroke, seizure, infection, radiation, etc.) to the central nervous system (CNS) dramatically amplify the damage. For example, reduction of the inflammatory process following stroke has been shown to limit the volume of damaged tissue by 2/3's. Our laboratory is currently working to better understand the mechanisms of inflammation within the CNS. Currently we are examining several clinically relevant areas of CNS inflammation, most in collaboration with Dr. Kerry O'Banion. First, we are using a model of damage to the CNS caused by gamma-irradiation. Treatment of brain tumors with radiation leads to long-term damage of the normal brain tissue, damage caused by a massive inflammatory response. This model will be expanded beginning in the fall of 2008 by a NIAID funded pilot project as we examine the effects of combined injuries, radiation and a peripheral injury, on the functioning of both brain and lung. In a related model, we are examining the effect of cosmic radiation (similar to the exposure received in space) on the CNS. Third, using several transgenic mouse models of Alzheimer's disease coupled with a model of chronic inflammation, we are exploring the possible beneficial effects of inflammation in the clearing of Aß plaque pathology. Fourth, in a project begun this year, we are examining the potential brain injuring effects of underwater sound exposure. This project funded by the Office of Naval Research is interested in the use of sound exposure as a non-lethal weapon. Our final and newest area of research examines late appearing cytokines following brain injury. While suppression of acute pro-inflammatory cytokines has worked well in animal models, they have not proven useful clinically. We are now examining the late appearing cytokine HMGB-1 and its receptors (RAGE, TLR4 and TLR2) in a model of traumatic brain injury. With a better understanding, we hope to limit the inflammatory response and thus improve the effectiveness of therapy. Using techniques such as light microscopic immunocytochemistry, in situ hybridization, computerized image analysis, quantitative real time RT-PCR, and the immunohistochemical methods for detection of apoptosis, we have begun to unravel the cell types, cytokines, chemokines, apoptotic genes, and adhesion molecules involved in CNS inflammation.
With the aid of a pilot grant from the Schmitt Foundation, we are now beginning to examine to role of CNS inflammation in the development of seizure activity. Following a variety of inflammation models (radiation-induced, Alzheimer's transgenic mice, peripheral inflammation, etc), we have begun to record EEG's from mice to determine alterations in susceptibility to seizure activity.
Matousek, S.B., A.M. Hein, S.S. Shaftel, J.A. Olschowka, S. Kyrkanides, and M.K. O'Banion. Cyclooxygenase-1 mediates prostaglandin E2 elevation and contextual memory impairment in a model of sustained hippocampal interleukin-1? expression. J. Neurochem. In press.
Hein AM, Stasko, MR, Matousek SB, Scott-McKean JJ, Maier SF, Olschowka JA, Costa AC, O'Banion MK. Sustained hippocampal IL-1ß overexpression impairs contextual and spatial memory in transgenic mice. Brain Behav. Immun. 2009, PMCID: PMC2818290
Kyrakanides S, Miller AW, Miller JN, Tallents RH, Brouxhon SM, Olschowka ME, O'Banion MK, Olschowka JA. Peripheral blood mononuclear cell infiltration and neuroinflammation in the HexB-/- mouse model of neurodegeneration. J Neuroimmunol. 203 (2008):50-57,.
Shaftel, S. S.; Carlson, T. J.; Olschowka, J. A.; Kyrkanides, S.; Matousek, S. B.; O'Banion, M. K.;. "Chronic interleukin-1beta expression in mouse brain leads to leukocyte infiltration and neutrophil-independent blood brain barrier permeability without overt neurodegeneration". J Neurosci 27 (2007): 9301-9.