| dc.description.abstract | Ischemic stroke, accounting for 87% of stroke cases globally is a considerable source of morbidity and mortality. After the initial thromboembolism of a cerebral vessel, secondary injuries such as oedema and reactive gliosis occur as a part of the pathophysiology of stroke. Aquaporin-4 (AQP4) is the primary water channel found in the brain and is highly expressed on astrocyte endfeet surrounding blood vessels in the brain. Disruption of this perivascular expression of AQP4 is seen across multiple chronic and acute neurologic illnesses, including ischemic stroke. As AQP4 is a water channel it has been studied as an important factor in stroke pathology, especially in the context of oedema. More recently, it is becoming apparent that AQP4 also has a role in reactive gliosis. Therefore, a literature review was conducted to compile our current knowledge on the expression and disruption of AQP4 after both experimental stroke in mice, and in clinical and pathohistological research on humans. Data from experimental stroke in mice show changes in AQP4 expression as well as perivascular polarization in the first hours to days after infarction. These changes follow logically as responses to oedema formation. While studies on human samples show a loss of perivascular AQP4 and an increase in the total amounts of Aquaporin 4 in the glial scar in the chronic stages after stroke, which could have structural implications for the glial scar. Overall, AQP4 expression changes on the temporal and spatial dimensions in relation to the secondary injuries seen after stroke. | eng |