<p>Vascular dementia (VaD) is a neurocognitive disorder attributed to different types of cerebrovascular disease (CVD) and characterized by complex and multifold pathophysiological mechanisms. The most common forms in the elderly brain are multi-infarct, subcortical and strategic infarct dementias caused by atherosclerosis, small vessel disease, and cerebral amyloid angiopathy (CAA), hereditary forms being rare. VaD prevalence, accounting for 5% to 20% of all dementias, in comparison to Alzheimer disease and mixed dementias declines due to recent improvement of cardiovascular risk factors. Its diagnosis relies on thorough clinical evaluations based on current classification criteria, neuroimaging, and fluid biomarkers. Epidemiological research has delineated multiple risk factors that contribute to the etiology of VaD. Its pathogenesis is complex and multifactorial, brain hypoperfusion and hypoxia being due to cerebrovascular pathologies. The lesions affect neuronal networks involved in many cognitive domains, e.g., thalamo-cortical, striato-subfrontal, and limbic systems. The sequence of events leading to VaD is defined by its clinical subtypes that are influenced by genetic disposition, aging, unhealthy lifestyle, and other factors, many of which are modifiable, highlighting the need for preventive measures and early intervention strategies. Newly developed biomarkers may help differentiate VaD from other dementias and unravel its pathomechanisms. Their integration into clinical practice and pathological assessment presents a prominent strategy for early assessment of VaD. Current treatments mainly target symptoms rather than slowing development and progression of VaD. This review will summarize recent findings about classification, epidemiology, risk factors, pathophysiology, biomarkers, and predictive and therapeutic strategies of VaD, in order to promote better clinical outcomes and enhanced quality of life for affected individuals.</p>