Maintaining the homeostasis of the brain microenvironment is essential for proper neuronal function. This homeostasis is maintained, in large part, thanks to the presence of the blood-brain barrier (BBB) and the blood-cerebrospinal fluid barrier (BCSFB). The endothelium of brain capillaries forms the BBB, whereas the epithelial cells of the choroid plexus constitute the BCSFB. The function and integrity of these barriers are affected in various CNS disorders (such as ischemia, trauma, neurodegenerative diseases) and cancer, which has an important impact on the progression of these CNS disorders and on the efficacy of potential therapies.
I am interested in the function of the BBB and BCSFB in the context of brain injury and aging. Traumatic brain injury (TBI) is the leading cause of death of young Americans, accounting for around 100,000 fatalities each year. TBI is usually accompanied by cerebral edema, a life-threatening condition characterized by excessive brain swelling. Despite the importance of this medical condition, very limited progress has been made in the past decades in our understanding of the cellular and molecular mechanisms underlying edema formation, which has resulted in a paucity of effective therapies available for clinical use. Brain barriers control the movement of blood-borne molecules and inflammatory cells into the CNS, and the dysfunction of these barriers plays an important role in the formation of post-traumatic brain edema. In my laboratory, we investigate how neuropeptides, growth factors, and cytokines affect the function of brain barriers in the injured CNS. This research is aimed at finding new therapeutic approaches for cerebral edema.
Another aspect of our research is to understand how and why the function of the BBB and BCSFB changes in advanced age. Although TBI is most prevalent in the youth population, the incidence of brain injury is also high in the elderly. The outcome in the elderly population is usually worse, compared to young patients, with prolonged recovery and permanent neurological deficits. However, the underlying mechanisms are not well characterized. Our studies focus on defining the age-related factors that cause the dysfunction of brain barriers and on identifying potential targets for effective TBI treatment in the elderly.