Vascular Dementia

Although vascular dementia (VaD) represents the second most common cause of dementia after Alzheimer’s disease (AD) in the elderly, and is referred to as the ‘‘silent epidemic of the twenty‐first century,’’ there is still a controversy on terminology, classification, and diagnostic criteria of VaD. The diagnosis of VaD resides on diagnostic clinical criteria determining (1) a cognitive impairment, (2) the presence of cerebrovascular disease, and (3) specifically in poststroke or multi‐infarct dementia, a temporal relationship between these. The search for a reliable biochemical test helping in the diagnosis of VaD is so far not available. Several vascular risk factors have a role in the development of VaD and their identification and treatment are among the major aspects of VaD management. A new line of research in this field is the study of genetic factors underlying vascular cognitive impairment which are: (1) genes predisposing to cerebrovascular disease, and (2) genes that influence brain tissue responses to cerebrovascular lesions. Evidence in favor of a coexistence of vascular and degenerative components in the pathogenesis of dementia in an elderly population comes from neuropathological and epidemiological studies. There is now a great debate whether VaD and AD are more than common coexisting unrelated pathologies or, instead, represent different results of synergistic pathological mechanisms. Current available medications for the treatment of VaD include acetylcholinesterase inhibitors for mild to moderate cases, and memantine, an NMDAreceptor antagonist. However, therapeutic preventive approaches aiming at reducing incident VaD by targeting patients at risk of cerebrovascular disease (primary prevention), or acting on patients after a stroke (secondary prevention) to prevent stroke recurrence and the progression of brain changes associated with cognitive impairment are the mandatory strategies.