Cerebrovascular disease is the second leading cause of cognitive impairment in late life. The manifestations of vascular cognitive impairment (VCI) are widely heterogeneous in severity, pathophysiology, and neurobehavioral phenotype depending upon site, size, and sum of vascular brain injury (VBI). One-third of patients experience poststroke dementia (PSD) and if not initially affected are at twice the risk of developing subsequent cognitive impairment over the ensuing 10 years. CADASIL is a prototypical example of “pure” subcortical vascular dementia (SVD) and has greatly advanced our understanding of underlying pathophysiology and brain–behavior correlations. At the present time, structural MRI provides the most sensitive and specific measure of VBI (e.g., silent brain infarcts (SBI) and white matter hyperintensities (WMH)), which is associated with impairment in executive function even in individuals without cognitive symptoms. Neuropathology studies show that Alzheimer's disease (AD) and VBI often occur together and exert additive adverse effects on cognition. Many risk factors for sporadic VBI (e.g., hypertension, diabetes mellitus, dyslipidemia) are modifiable, although double-blind placebo-controlled trials are often inconclusive because they are started too late, are too short in duration, or lack sufficiently sensitive cognitive outcome measures. Cholinesterase inhibitors and memantine show mild benefits for cognitive, but not global endpoints, in treatment trials. By and large, the means for early detection and prevention of VCI are known. The major challenge remains one of diligent clinical practice and public health implementation.