Alzheimer's disease (AD) is an acquired, persistent, and progressive intellectual deterioration
syndrome characterized primarily by recent memory impairment accompanied by other cognitive deficits.
During the course of the disease, it can be accompanied by varying degrees of psychiatric and behavioral
symptoms, gradually affecting patients' activities of daily living and social functioning. Traditional
pathological mechanisms have focused on the deposition of β-amyloid (Aβ) and the formation of neurofibrilla
ry tangles composed of tau protein. In recent years, studies have indicated that vascular dysfunction plays a
crucial driving role in the pathogenesis of AD, with extensive epidemiological, clinical, and basic research
supporting the novel perspective that AD can be considered a vascular disease. Vascular risk factors (such as
hypertension, diabetes, and atherosclerosis) directly promote A β production and inhibit its clearance by
inducing cerebral hypoperfusion, disrupting the blood-brain barrier, and interfering with insulin signaling
pathways, thereby interacting with Aβ metabolism to collectively exacerbate the pathological progression of
AD. This review discusses the role of vascular factors in the pathogenesis of AD, aiming to provide new
perspectives for its diagnosis and treatment and inject fresh vitality into the field of AD research.
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