The consequences of
cerebrovascular disease are among the leading health issues worldwide. Large and small cerebral vessel disease can trigger
stroke and contribute to the vascular component of other forms of neurological dysfunction and degeneration. Both forms of
vascular disease are driven by diverse risk factors, with
hypertension as the leading contributor. Despite the importance of neurovascular disease and
subsequent injury after ischemic events, fundamental knowledge in these areas lag behind our current understanding of neuroprotection and vascular biology in general. The goal of this review is to address select key structural and functional changes in the vasculature that promote hypoperfusion and
ischemia, while also affecting the extent of injury and effectiveness of
therapy. In addition, as damage to the blood-brain barrier is one of the major consequences of
ischemia, we discuss cellular and molecular mechanisms underlying
ischemia-induced changes in blood-brain barrier integrity and function, including alterations in endothelial cells and the contribution of pericytes, immune cells, and
matrix metalloproteinases. Identification of cell types, pathways, and molecules that control vascular changes before and after
ischemia may result in novel approaches to slow the progression of
cerebrovascular disease and lessen both the frequency and impact of ischemic events.