Vascular dementia (VaD) is the second most common cause of cognitive impairment in the elderly, often co-occurring with Alzheimer's disease (AD). It is heterogeneous, resulting from various cerebrovascular pathologies such as large vessel infarcts or small artery disease leading to subcortical ischemic changes. Clinical symptoms vary based on stroke location and size, with dysexecutive function being common. VaD has a slightly higher mortality rate and slower progression than AD. Prevention is possible through managing cardiovascular risk factors, and cholinesterase inhibitors show modest symptomatic improvement. VaD is classified into types such as multi-infarct dementia (MID), strategic infarct dementia, and subcortical vascular dementia (SVD). MID involves multiple cortical infarcts and is associated with atherothrombotic strokes. SVD, more common, results from lacunar infarcts and ischemic white matter lesions, often without a history of stroke. Cognitive and behavioral changes in SVD are due to frontal-subcortical circuit disruption, leading to dysexecutive syndrome. Diagnosis of VaD requires clinical, imaging, and pathological evidence. Current criteria include DSM-IV, ICD-10, ADDTC, and NINDS-AIREN guidelines. Neuroimaging, particularly MRI, is crucial for identifying infarcts and white matter lesions. MRI is more sensitive than CT for detecting ischemic damage. Treatment includes controlling cardiovascular risk factors, anti-platelet therapy, and medications like cholinesterase inhibitors and NMDA receptor antagonists. Memantine and cholinesterase inhibitors are effective for symptom management. Prognosis varies, with MID having a poorer outcome. VaD is associated with higher mortality than AD but can be managed with early diagnosis and treatment. Prevention is key, with early identification of vascular cognitive impairment and modification of vascular risk factors in midlife being crucial for preventing VaD. VaD is distinct from AD, with subcortical frontal and executive dysfunction as its hallmark, rather than amnesia. Early detection and management are essential for improving outcomes.Vascular dementia (VaD) is the second most common cause of cognitive impairment in the elderly, often co-occurring with Alzheimer's disease (AD). It is heterogeneous, resulting from various cerebrovascular pathologies such as large vessel infarcts or small artery disease leading to subcortical ischemic changes. Clinical symptoms vary based on stroke location and size, with dysexecutive function being common. VaD has a slightly higher mortality rate and slower progression than AD. Prevention is possible through managing cardiovascular risk factors, and cholinesterase inhibitors show modest symptomatic improvement. VaD is classified into types such as multi-infarct dementia (MID), strategic infarct dementia, and subcortical vascular dementia (SVD). MID involves multiple cortical infarcts and is associated with atherothrombotic strokes. SVD, more common, results from lacunar infarcts and ischemic white matter lesions, often without a history of stroke. Cognitive and behavioral changes in SVD are due to frontal-subcortical circuit disruption, leading to dysexecutive syndrome. Diagnosis of VaD requires clinical, imaging, and pathological evidence. Current criteria include DSM-IV, ICD-10, ADDTC, and NINDS-AIREN guidelines. Neuroimaging, particularly MRI, is crucial for identifying infarcts and white matter lesions. MRI is more sensitive than CT for detecting ischemic damage. Treatment includes controlling cardiovascular risk factors, anti-platelet therapy, and medications like cholinesterase inhibitors and NMDA receptor antagonists. Memantine and cholinesterase inhibitors are effective for symptom management. Prognosis varies, with MID having a poorer outcome. VaD is associated with higher mortality than AD but can be managed with early diagnosis and treatment. Prevention is key, with early identification of vascular cognitive impairment and modification of vascular risk factors in midlife being crucial for preventing VaD. VaD is distinct from AD, with subcortical frontal and executive dysfunction as its hallmark, rather than amnesia. Early detection and management are essential for improving outcomes.