Vascular cognitive impairment (VCI) is the phenotypic outcome of a cascade of events: vascular risk factors lead to vascular disease, which causes vascular brain injury (VBI) in networks important for cognition. Both VCI and Alzheimer’s disease (AD) increase exponentially with age, and their interactions are common and controversial. The ability of current consensus criteria to distinguish VCI from AD is limited. Currently, the primary and secondary prevention of VCI is essentially the same for stroke, whereas symptomatic treatment of VCI is similar to AD. An emerging database suggests that VBI contributes significantly to mild VCI and can accelerate the appearance of dementia when AD pathology is mild. Early evidence suggests that the adverse effects of VBI are submerged once AD pathology spreads into isocortex. Recently, epidemiologic studies reported associations between vascular risk factors and clinically diagnosed AD as well as stroke. If hypertension, diabetes, and hyperlipidemia truly accelerate β-amyloidosis and tauopathy, as well as VBI, the importance of their early identification and treatment will be greatly magnified.