With advancing age, the likelihood of beta-amyloid deposition in the cerebral vasculature increases, particularly in individuals with Alzheimer's disease. The beta-amyloid typically accumulates in the basal lamina of the arteriolar tunica media, and frequently extends into the adjacent neuropil. Cerebrovascular beta-amyloid increases the risk of hemorrhagic stroke, and may also play a role in the pathogenesis of AD. Genetic variations have been identified that are causative or risk factors for cerebrovascular beta-amyloid, including particular mutations in the genes for beta-amyloid precursor protein, presenilins 1 and 2, and possibly cystatin C, as well as polymorphisms in apolipoprotein E. Cerebrovascular amyloidosis is now being studied in a variety of in vitro and in vivo models, including cultured vascular smooth muscle cells, transgenic mice, and aged animals such as nonhuman primates. Methods for delivering agents selectively to vascular amyloid in living subjects are now being developed, and these techniques are paving the way to the development of diagnostic tools and therapies for cerebrovascular amyloidosis.