Vascular dementia (VaD) is defined as cognitive impairment that affects the ability to perform daily living activities as a result of cerebrovascular disease, including hemorrhagic and ischemic cerebrovascular disease. The two core elements of Vascular Dementia are: clinical dementia syndrome and objective evidence of cerebrovascular disease as the cause of dementia. The concept of VaD has been proposed for over a century, but the pathogenesis is still not fully understood and its diagnostic criteria are still not very satisfactory. The NINDS-AIREN criteria, which are currently more widely used, are more stringent than the DSM-IV and California ADDTC criteria. Moreover, the existing diagnostic criteria for VaD are inadequate in distinguishing subtypes, and only the NINDS-AIREN criteria roughly classify vascular dementia into cortical, thalamic, and Binswanger disease. Which diagnostic criteria to use has been the most prominent disagreement and controversy in clinical and epidemiological studies of vascular dementia for many years. In general, the prevalence of vascular dementia ranges from 3-6%, but literature reports vary from 0-20%. It remains uncertain whether the differences in epidemiological data on vascular dementia in different countries are due to differences in ethnicity, geography, socioeconomic factors, or to differences in diagnostic criteria and methodology (ref 6). The diagnostic difficulty in vascular dementia is the determination of the causal relationship between vascular lesions and cognitive impairment. The difficulty in this again lies in the differentiation between vascular and degenerative lesions. In the past, a simple dichotomy was often used to separate vascular dementia from Alzheimer’s disease. However, as research continued, it was discovered that the two pathological changes, vascular factors and degenerative changes, develop in parallel and interact with each other. Moreover, the importance of small vessel disease is increasingly being recognized as a hot topic of research in recent years compared to the previously important infarcts at critical sites of large vessels. In the past, the distinction between AD and VaD relied on vascular risk factors, neuroimaging, and clinical features (e.g., acute onset, stepwise progression, uncontrolled affect, etc.). (ref 5) However, the current view is that, to a large extent, vascular and degenerative pathologies are at opposite ends of a spectrum. At one end of the spectrum is “pure AD”, which is caused exclusively by degenerative pathology, and at the other end is “pure VaD”, which is caused exclusively by vascular pathology. In fact, more patients with dementia or cognitive impairment fall somewhere in between, with both degenerative pathology and vascular factors that are inextricably linked. It is difficult to set a clear artificial line of demarcation between the two. Studies have also shown an interaction between cerebrovascular pathology and AD-like degeneration: cognitive impairment is more severe in patients with both degenerative and vascular disease. Flow surveys show that AD and VaD share common vascular risk factors (e.g., hypertension, diabetes, atherosclerosis, etc.), and that these vascular factors not only contribute to cognitive impairment in conjunction with degeneration, but also participate in the pathogenic pathogenesis of dementia through multiple pathways such as inflammation, infection, and oxidative stress. The converse is also true, which further expands the scope of vascular cognitive impairment. Because of this, the current classification of dementia subtypes and the diagnostic criteria for vascular dementia have been subject to divergent opinions, resulting in reports of the composition ratio of VaD in dementia ranging from 0-85% (ref1). In the author’s opinion, one should abandon the traditional simple “dichotomy” and take a dialectical approach to the problem. The clinician should place the patient within this spectrum, considering that some symptoms may be degenerative and some manifestations may be attributable to vascular factors, and that this integrated clinical thinking can help us to better develop individualized treatment plans for each patient (ref 1). (ref 1).