阿尔茨海默病（Alzheimer's disease，AD）是一种以近记忆力减退为主要表现伴有其他认知损害的
获得性、持续性、进展性智能减退症候群，在疾病过程中可伴有不同程度的精神行为症状，逐渐影响到患
者的日常生活能力和社会功能。传统病理机制聚焦于β淀粉样蛋白（β-amyloid，Aβ）沉积和tau蛋白神经
纤维缠结。近年来研究表明，血管功能障碍在AD发病机制中起关键驱动作用，大量流行病学、临床和基
础研究支持AD作为一种血管性疾病的新观点。血管危险因素（如高血压、糖尿病和动脉粥样硬化）通过
诱发脑低灌注、破坏血脑屏障及扰乱胰岛素信号通路，直接促进Aβ生成并抑制其清除，从而与Aβ代谢相
互作用共同加剧AD病理进程。本文就血管因素在AD发病机制中的作用展开综述，以期为其诊断和治
疗提供新视角，并为AD研究领域注入新的活力。
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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