Dr. Michal Kraszpulski:
Tel: (937) 775- 4489
Office: 325B Fawcett Hall
E-Mail: michal.kraszpulski@wright.edu
Dr. Michal Kraszpulski
Bio
Dr. Michał Kraszpulski received his Master Degree in Biology from University of Gdańsk (Poland) in 1980. After graduating, years he worked as a research assistant at the Laboratory of Electron Microscopy of the Medical University of Gdańsk (Poland), as well as at the Laboratory of Clinical Neuropathology of the N.Y.S. Institute for Basic Research in Developmental Disabilities. In 1995, he received his Ph.D. Degree in Neuroscience from Medical University of Gdańsk (Poland). His dissertation research, under the guidance of Dr. Teresa Żawrocka-Wrzołkowa, focused on the effects of chronic ethanol intoxication on the hippocampal structures. During his postdoctoral training at the Department of Neurology of the University of Kuopio (Finland), Dr. Michał Kraszpulski was participating in Alzheimer’s disease studies, concentrating mostly on different factors affecting the distribution of β-amyloid load in the brain.
Dr. Michał Kraszpulski came to Wright State University in fall of 2007, first to the Department of Neuroscience, Cell Biology and Physiology, where he was involved in studies of axonal regeneration. In 2010, he has joined the Behavioral Neurosciences group in the Department of Psychology where he participates in the research focusing on the effects of elevated glucocorticoids on hippocampal learning during development. He also teaches several undergraduate courses and is involved in graduate teaching in the Master of Anatomy program.
Research Interests
The center of my research interests are the pathological changes related to the different kind (chemical, mechanical, stress, HIV infection, Alzheimer’s disease) of brain injuries. Together with my collaborators, I have combined different methods (stereology, histology, brain imaging, molecular biology) to achieve some novel and interesting results.
Among others, we have found that in the microencephaly observed as a frequent sequel in pediatric AIDS, the loss of brain tissue is global and includes an almost proportional loss of cortex, subcortical gray matter and white matter.
In chronically ethanol-intoxicated rats, we observed age and regional differentiation of ethanol-related microvascular changes, which did not correlate well with the damaging effects of alcohol on corresponding neuronal elements, emphasizing the very complicated pathogenesis of ethanol-induced injuries.
Studying the Alzheimer’s disease-related changes, we have found that not only the load but also the vertical distribution of b-amyloid within cortex is influenced by risk factors such as ApoE genotype and gender. We reported also an increase in the count of TUNEL-labelled cells as the pathology of AD intensifies.
In prenatally stressed rats, we have found differences in the developmental trajectories of amygdala nuclei, which may be the harbinger of their different functioning in adulthood. These data may have direct import for the effect of adverse early life experiences and the etiology of anxiety disorders in humans.
In the studies of chemotherapy-related cognitive dysfunction, we have indicated that chemotherapeutic agents alone, i.e., in the absence of malignancy, damage the brain resulting in memory dysfunction. Moreover, our results strongly indicate that the damaging effect is mediated by oxidative stress, as memory dysfunction is preventable by the co-administration of an antioxidant.
I am currently engaged in research with Dr. Dragana Claflin focusing on the development of learning and memory. Of my special interests are the effects of elevated glucocorticoids on hippocampal learning during development.
