Thaddeus S. Nowak, Jr., Ph.D.
Professor, Department of Neurology
Professor, Department of Anatomy and Neurobiology
Director, Neurology Research Laboratories
- B.S. - Massachusetts Institute of Technology, 1971
- Ph.D. - Massachusetts Institute of Technology, 1979
- Staff Fellow/Senior Staff Fellow - LNC, NINDS, NIH, 1980-1986
- Senior Staff Fellow/Special Expert - LNNS, NINDS, NIH, 1986-1992
- Associate Professor/Professor - Neurology, Anatomy & Neurobiology, UTHSC, 1992-present
Clinical Subspecialty Expertise
Multiple Sclerosis, Demyelinating and viral disease of the central nervous system and HTLV-1 associated myelopathy/tropical spastic paraparesis.
Investigations generally focus on the study of brain injury after ischemic insults in animal models. A past interest in selective neuron vulnerability after brief global ischemia has shifted to a recent emphasis on focal brain ischemia (experimental stroke). One area of current research examines protective effects of brain cooling. Recent evidence indicates the particular benefit of temperature reduction at the time of recirculation following transient ischemia, suggesting its potential therapeutic relevance in the context of "reperfusion injury." As a practical spin-off of these studies, the widely used approach to producing experimental stroke by intraluminal filament occlusion has been refined to avoid confounding effects on temperature regulation. A second research focus examines endogenous defense mechanisms activated following prior insults (preconditioning). Although widespread changes in gene expression occur in response to preconditioning insults, ongoing studies indicate that such protection in focal ischemia models arises via synergistic effects on the fundamental parameters of brain blood flow and metabolism. This has led to a new interest in vascular regulation and its response to brain injury.
Nowak T. S. Jr. Synthesis of a stress protein following transient ischemia in the gerbil. Journal of Neurochemistry 45:1635-1641, 1985.
Nowak T. S. Jr. Localization of 70 kDa stress protein mRNA induction in gerbil brain after ischemia. Journal of Cerebral Blood Flow and Metabolism 11:432-439, 1991.
Saito N., Kawai K. and Nowak T. S. Jr. Reexpression of developmentally regulated MAP2c mRNA after ischemia: Colocalization with hsp72 mRNA in vulnerable neurons. Journal of Cerebral Blood Flow and Metabolism 15:205-215, 1995.
Zhou Q., Abe H. and Nowak T. S. Jr. Immunocytochemical and in situ hybridization approaches to the optimization of brain slice preparations. Journal of Neuroscience Methods 59:85-92, 1995.
Yaida Y. and Nowak T. S. Jr. Distribution of phosphodiester and phosphorothioate oligonucleotides in rat brain after intraventricular administration determined by in situ hybridization. Regulatory Peptides 59:193-199, 1995.
Petito C. K., Torres-Munoz J., Roberts B., Olarte J.-P., Nowak T. S. Jr., and Pulsinelli W. A. DNA damage follows delayed neuronal death in CA1 neurons exposed to transient global ischemia in the rat. Journal of Cerebral Blood Flow and Metabolism 17: 967-976, 1997.
Petito C. K., Olarte J.-P., Roberts B., Nowak T. S. Jr. and Pulsinelli W. A. Selective glial vulnerability following transient global ischemia in rat brain. Journal of Neuropathology and Experimental Neurology 57:231-238; 1998.
Suga S. and Nowak T. S. Jr. Postischemic hyperthermia increases expression of hsp72 mRNA after brief ischemia in the gerbil. Neuroscience Letters 243:57-60, 1998.
Yufu K., Yaida Y. and Nowak T. S. Jr. Localization of oligonucleotides in brain by in situ hybridization. In: Antisense Technology (Phillips M. I., ed) Methods in Enzymology, Academic Press pp. 238-247, 2000.
Meade C.A., Figueredo-Cardenas G., Fusco F., Nowak T.S. Jr., Pulsinelli W.A. and Reiner A. Transient global ischemia in rats yields striatal projection neuron and interneuron loss resembling that in Huntington's Disease. Experimental Neurology 166:307-323, 2000.
Marini A. M. and Nowak T. S. Jr Metabolic effects of 1-methyl-4-phenylpyridinium (MPP+) in primary neuron cultures. Journal of Neuroscience Research 62:814-820, 2000.
Abe H. and Nowak T. S. Jr. Postischemic temperature as a modulator of the stress response: dissociation of hsp72 induction from ischemic tolerance in a gerbil model. Neuroscience Letters 295:54-58, 2000.
Ren Y., Hashimoto M., Pulsinelli W. A. and Nowak T. S. Jr. Hypothermic protection in rat focal ischemia models: strain differences and relevance to "reperfusion injury." Journal of Cerebral Blood Flow and Metabolism 24:42-53, 2004.
Abe H. and Nowak T. S. Jr. Induced hippocampal neuron protection in an optimized gerbil ischemia model: insult thresholds for tolerance induction and altered gene expression defined by ischemic depolarization. Journal of Cerebral Blood Flow and Metabolism 24:84-97, 2004.
Nishino K. and Nowak T. S. Jr. Time course and cellular distribution of hsp27 and hsp72 stress protein expression in a quantitative gerbil model of ischemic injury and tolerance: thresholds for hsp72 induction and hilar lesioning in the context of ischemic preconditioning. Journal of Cerebral Blood Flow and Metabolism 24:167-178, 2004.
Sorimachi T. and Nowak T. S. Jr. Pharmacological manipulations of ATP-dependent potassium channels and adenosine A1 receptors do not impact hippocampal ischemic preconditioning in vivo: evidence in a highly quantitative gerbil model. Journal of Cerebral Blood Flow and Metabolism 24:556-563, 2004.
Halaby I. A., Takeda Y., Yufu K., Nowak T. S. Jr. and Pulsinelli W. A. Depolarization thresholds for hippocampal damage, ischemic preconditioning, and changes in gene expression after global ischemia in the rat. Neuroscience Letters 372:12-16, 2004.
Ueda M. and Nowak T. S. Jr. Protective preconditioning by transient global ischemia in the rat: components of delayed injury and lasting protection distinguished by comparisons of depolarization thresholds for cell loss at long survival times. Journal of Cerebral Blood Flow and Metabolism 25:949-958, 2005.
Kamiya T., Jacewicz M., Nowak T. S. Jr. and Pulsinelli W. A. CBF thresholds for mRNA synthesis after focal ischemia and the effect of MK-801. Stroke 36:2463-2467, 2005.
Zhao L. and Nowak T. S. Jr. CBF changes associated with focal ischemic preconditioning in the Spontaneously Hypertensive Rat. Journal of Cerebral Blood Flow and Metabolism 26:1128-1140, 2006 http://www.nature.com/doifinder/10.1038/sj.jcbfm.9600269.
Ma J., Zhao L. and Nowak T. S. Jr. Selective, reversible occlusion of the middle cerebral artery in rats by an intraluminal approach. Journal of Neuroscience Methods 156:76-83, 2006 doi:10.1016/jneumeth.2006.02.006.
Nowak T. S. Jr. Animal models of global brain ischemia. In: Acute Stroke: Bench to Bedside (Bhardwaj A., Alkayed N. J., Kirsch J. R., Traystman R. J. eds.) Marcel Dekker, New York pp. 275-292, 2007.
Kurasako T., Zhao L., Pulsinelli W. A., Nowak T. S. Jr. Transient cooling during early reperfusion attenuates delayed edema and infarct progression in Spontaneously Hypertensive Rats. Distribution and time course of regional brain temperature in a model of postischemic hypothermic protection. Journal of Cerebral Blood Flow and Metabolism 27:1919-1930, 2007 (doi:10.1038/sj.jcbfm.9600492).
Hashimoto M., Zhao L., Nowak T. S. Jr. Temporal thresholds for infarction and hypothermic protection in Long-Evans rats. Factors affecting apparent "reperfusion injury" after transient focal ischemia. Stroke 39:421-426, 2008 (doi:10.1161/strokeaha.107.495788).
Zhao Y., Xiao J., Ueda M., Wang Y., Hines M., Nowak T. S. Jr., LeDoux M. S. Glial elements contribute to stress-induced torsinA expression in the CNS and peripheral nervous system. Neuroscience 155:439-453, 2008 (doi:10.1016/j.neuroscience.2008.04.053).
Jacewicz M., Nowak T. S. Jr., Giraldo E. and Pulsinelli W. A. Ischemic Stroke. In: Principles of Drug Therapy in Neurology (Gilman S., Johnston M. V., Gross R. eds.) Oxford University Press, New York, pp. 173-203, 2008.
Department of Neurology
855 Monroe Ave, Suite 415
Memphis, Tennessee 38163
Phone: (901) 448-6199
Fax: (901) 448-7440
Andrei V. Alexandrov, M.D.
Department of Neurology
Adult Neurology Residency
Phone: (901) 448-6661
Fax: (901) 448-7440