Dr Anuska Andjelkovic-Zochowski is Professor of Pathology and Research Professor of Neurosurgery. She received her MD degree from University of Nis (Yugoslavia/Serbia) in 1990 and MS degree in Neuroscience from University of Belgrade (Yugoslavia/Serbia) in 1995. Dr Andjelkovic-Zochowski did her PhD project on the origin and characterization of microglial/macrophages cells during human brain development (University of Connecticut) 1996-1997 and earned her PhD degree in developmental neuroscience and neuroimmunology from University of Belgrade in 1999. She completed her postdoctoral fellowship at University of Connecticut from 1997-2000 focusing the chemokine and chemokine receptor biology, and leukocytes transmigration at Blood brain barrier and become Assistant Professor (in residence) in 2000. Dr Andjelkovic-Zochowski join the Department of Neurosurgery at University of Michigan in 2001, first as Assistant Research scientist and then Research Assistant professor in 2003. In 2005 Dr Andjelkovic-Zochowski join the faculty of Pathology as Assistant professor (tenure track) and got promoted to Associate professor with tenure (2012), to Professor of Pathology (tenure) and Research professor of Neurosurgery (2020). She is an active member of two graduate programs, Molecular and Cellular pathology and Neuroscience. Dr Andjelkovic-Zochowski is member of several professional organizations Society of Neuroscience, International Blood brain barrier society, American Heart association.

Since 2000 she developed research program focused on Blood brain barrier dysfunction in neuroinflammation and cerebrovascular disease. She published more than 50 manuscripts in several prominent journals. Dr Andjelkovic-Zochowski is a member of multiple national (NIH, American heart association, and Department of Defense Medical Research Program) and international grant review committees. Dr Andjelkovic-Zochowski is also a member of the editorial boards in Tissue Barrier, Atherosclerosis, Neurochemical research, Fluid and barrier in CNS, International Journal of Medicine.

The Blood Brain Barrier (BBB) is unique entity of barrier endowed capillary endothelial cells and perivascular cells suited on the interface of blood and brain. The failure of BBB structural integrity and function plays pivotal role in the pathogenesis of many diseases of the central nervous system (CNS) (i.e ischemia, inflammation, trauma, neoplasia and epilepsy). Our research is focused on the understanding molecular mechanisms of regulation of barrier permeability, remodeling and rapier in the cerebrovascular diseases.

My laboratory is taking multidisciplinary approach to investigate protein-protein interactions and multi-protein assemblies within the brain endothelial tight junction and barrier formation. We are particularly interested in how tight junction is affected and impaired in stroke, cerebral small vessel diseases, and cerebral cavernous malformation with goal to develop novel means to correct barrier function and restore health.

Over the past two decades we have dissected signaling pathways (Rho kinase, protein kinase-C) tight junction protein-protein interactions and process (internalization) that take role in inflammatory remodeling of tight junctional complex and “opening” of BBB. These results were ground for ongoing research focused on the pattern of tight junction complex remodeling in the aging, cerebral small vessels diseases and chronic stroke condition, to identify cause of tight junctional complex defects and potential underlaying signaling and epigenetic mechanism involved in remodeling.

As junctional proteins are not sole structure proteins, we are also focused on understanding the non-canonical role of these proteins in regulation of brain endothelial cell phenotype and barrier integrity Our current project in the laboratory is concentrated on the dissecting the non-canonical role of role of JAM-A, claudin-1 and connexin43 in guiding the inflammatory response, cause the vascular injury and affecting the Blood brain barrier repair in setting of stroke, aging and small vessels disease (cerebral amyloid angiopathy).

Parallel project in the laboratory is focused on understanding the molecular basis underlying vessel dysfunction that causes hemorrhagic stroke and particularly inherited hemorrhaging stroke in humans -cerebral cavernous malformation. We are aiming to define how mutation of CCM3 protein affects the tight junction complex stability and dissect pathways involved in microvascular permeability and hemorrhagic transformation in CCM3 lesion progression.

Our ultimate goal is to develop the platform for repear the Tight junctional defect and BBB permeability as well to manipulate of tight junction cell-cell contacts, for improving drug delivery to the brain.