Vascular Dementia (VaD) is the second leading cause of cognitive impairment in the elderly, often co-occurring with Alzheimer's disease (AD). VaD is characterized by heterogeneity in clinical phenotype and pathogenetic mechanisms, ranging from multiple cortical infarctions to subcortical ischemic changes. Clinical symptoms vary based on the location and size of the stroke lesion, and no single neuropsychological profile is characteristic of VaD, although dysexecutive function is common. VaD has a slightly higher mortality rate and slower progression compared to AD. Prevention of VaD is potentially achievable through rigorous identification and treatment of cardiovascular disease risk factors. Modest symptomatic improvement with cholinesterase inhibitors has been reported. Key factors contributing to VaD include age, low education level, vascular risk factors (such as hypertension, diabetes, hyperlipidemia, and smoking), and ethnic background. VaD can be classified into post-stroke dementia, including multi-infarct dementia (MID), strategic infarct dementia, subcortical vascular dementia (SVD), and hypoperfusion dementia. MID is characterized by transient ischemic attacks and stroke episodes, while SVD is marked by insidious onset and slow progression, with cognitive deterioration, gait disturbance, and urinary dysfunction being common symptoms. Neuroimaging plays a crucial role in diagnosing VaD, with MRI being more sensitive than CT for ischemic damage and vascular lesions. Treatment options include cholinesterase inhibitors and N-methyl-d-aspartate receptor antagonists, with varying degrees of efficacy and side effects. The prognosis of VaD varies, but it generally shortens life expectancy and has a similar or slightly worse impact on mortality compared to AD. Early identification and management of vascular risk factors are essential for preventing VaD.Vascular Dementia (VaD) is the second leading cause of cognitive impairment in the elderly, often co-occurring with Alzheimer's disease (AD). VaD is characterized by heterogeneity in clinical phenotype and pathogenetic mechanisms, ranging from multiple cortical infarctions to subcortical ischemic changes. Clinical symptoms vary based on the location and size of the stroke lesion, and no single neuropsychological profile is characteristic of VaD, although dysexecutive function is common. VaD has a slightly higher mortality rate and slower progression compared to AD. Prevention of VaD is potentially achievable through rigorous identification and treatment of cardiovascular disease risk factors. Modest symptomatic improvement with cholinesterase inhibitors has been reported. Key factors contributing to VaD include age, low education level, vascular risk factors (such as hypertension, diabetes, hyperlipidemia, and smoking), and ethnic background. VaD can be classified into post-stroke dementia, including multi-infarct dementia (MID), strategic infarct dementia, subcortical vascular dementia (SVD), and hypoperfusion dementia. MID is characterized by transient ischemic attacks and stroke episodes, while SVD is marked by insidious onset and slow progression, with cognitive deterioration, gait disturbance, and urinary dysfunction being common symptoms. Neuroimaging plays a crucial role in diagnosing VaD, with MRI being more sensitive than CT for ischemic damage and vascular lesions. Treatment options include cholinesterase inhibitors and N-methyl-d-aspartate receptor antagonists, with varying degrees of efficacy and side effects. The prognosis of VaD varies, but it generally shortens life expectancy and has a similar or slightly worse impact on mortality compared to AD. Early identification and management of vascular risk factors are essential for preventing VaD.