Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea. ; Department of Anatomy and Cell Biology, Cell Dysfunction Research Center (CDRC), University of Ulsan College of Medicine, Seoul, Korea.
Department of Neurology, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
J Stroke. 2014 Jan;16(1):18-26. doi: 10.5853/jos.2014.16.1.18. Epub 2014 Jan 31.
Vascular dementia (VaD) is a history-laden disease entity that dates back to the 19th century when arteriosclerotic brain atrophy due to hardening of the arteries was perceived as the major cause of senile dementia. Its existence had been overshadowed by the emergence of Alzheimer's disease (AD) in the past century and research on AD dominated the field of dementia. Interest in VaD has been revived in recent years as vascular lesions have been shown to make great contributions to the development of dementia, particularly in the elderly. VaD has now evolved into the concept of vascular cognitive impairment (VCI), which encompasses not only VaD but also AD with cerebrovascular disorder and VCI with no dementia. The concept of VCI is intended to maximize the therapeutic potential in dementia management because the vascular component may be amenable to therapeutic intervention particularly in the early stages of cognitive impairment. Subcortical ischemic vascular dementia (SIVD) is pathologically driven by severe stenosis and the occlusion of small vessels that culminate into white matter ischemia and multiple lacunar infarctions in the subcortical structures. The relatively slow progression of symptoms and clinical manifestations associated with cholinergic deficits often make the differentiation of SIVD from AD difficult. The recent development of in vivo amyloid imaging enabled further pathological breakdown of SIVD into pure SIVD and mixed dementia with subcortical ischemia based on the absence or existence of amyloid pathology in the brain. In this article, the authors reviewed the emerging concepts of VaD/VCI and the clinical manifestations, biomarkers, treatments, and preclinical models of SIVD based on the pathophysiologic mechanisms of the disease.
血管性痴呆（VaD）是一种历史悠久的疾病实体，可以追溯到 19 世纪，当时由于动脉硬化导致的脑萎缩被认为是老年痴呆症的主要原因。在过去的一个世纪里，阿尔茨海默病（AD）的出现使它黯然失色，AD 的研究主导了痴呆领域。近年来，由于血管病变对痴呆的发展有很大的贡献，尤其是在老年人中，对 VaD 的兴趣又重新燃起。VaD 现在已经演变成血管性认知障碍（VCI）的概念，它不仅包括 VaD，还包括伴有脑血管疾病的 AD 和无痴呆的 VCI。VCI 的概念旨在最大限度地发挥痴呆管理的治疗潜力，因为血管成分可能对治疗干预有反应，特别是在认知障碍的早期阶段。皮质下缺血性血管性痴呆（SIVD）主要由严重狭窄和小血管闭塞引起，导致皮质下白质缺血和皮质下结构多发性腔隙性梗死。与胆碱能缺陷相关的症状和临床表现的相对缓慢进展，往往使 SIVD 与 AD 难以区分。最近，体内淀粉样蛋白成像的发展使我们能够根据大脑中是否存在淀粉样蛋白病理学，将 SIVD 进一步细分为纯 SIVD 和伴有皮质下缺血的混合性痴呆。在本文中，作者根据疾病的病理生理机制，综述了 VaD/VCI 的新观念以及 SIVD 的临床表现、生物标志物、治疗方法和临床前模型。
