The University of Texas Health Science Center at Houston
McGovern Medical School
Department of Neurology
Clinically, stroke is increasingly recognized as a sexually dimorphic disease. Most international databases demonstrate that women enjoy lower stroke incidence relative to men until advanced age. This native neuroprotection is lost after menopause, often attributed to the loss of estrogen. Emerging data suggest that cell death mechanisms in the brain follow differing mechanistic paths that are dependent on sex chromosome compliment in addition to exposure to sex steroids. We have now established that tissue damage and functional outcome after experimental brain injury are shaped by biologic sex (XX vs. XY). We have found that these sex differences also exist at the cellular level, for example XY-derived (male) hippocampal slice cultures exhibited increased caspase-independent cell death after exposure to oxygen-glucose deprivation compared to those derived from XX (female) neurons.
Our laboratory also has been investigating differences in inflammatory signaling. Other areas of active investigation in the laboratory include the examination of age-related inflammation in both the brain and peripheral tissues after stroke, peripheral post-stroke immunosuppression, and studies investigating the detrimental effects of social isolation on the immune response to stroke during chronic recovery. We are currently attempting to modulate peripheral age-related inflammation in an attempt to reduce brain injury using bone marrow replacement, and manipulation of the microbiome. Very new work in our laboratory is examining a new model of multi-infarct dementia in aged animals.
Education & Training
PhD, University of Connecticut, 1992
MD, University of Connecticut, 1996