Mild Cognitive Impairment: At the Crossroad of Neurodegeneration and Vascular Dysfunction
Mild Cognitive Impairment: At the Crossroad of Neurodegeneration and Vascular Dysfunction
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DOI：
10.2174/1567205012666150530202508
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发表时间：
2015-01-01
影响因子：
2.1
通讯作者：
Ihara, Masafumi
中科院分区：
文献类型：
--
作者：
Saito, Satoshi;Yamamoto, Yumi;Ihara, Masafumi
轻度认知障碍（MCI）的概念最初是为了识别处于无认知障碍和阿尔茨海默病（AD）之间的中间状态的个体而引入的。最近，MCI的异质性引起了人们的关注，因为已经清楚的是，其他疾病，如脑血管疾病和帕金森病也可以引起轻度认知障碍，促使MCI的重新定义。神经病理学检查证实了MCI的异质性。大多数MCI患者不仅具有淀粉样斑块和神经元tau蛋白缠结，而且还具有脑血管病理学，如动脉硬化和脑淀粉样血管病（CAA）。CAA诱发不同大小和类型的脑梗死或出血，导致进一步的认知障碍。散发性AD和CAA被认为是A β消除失败的结果，主要由血管周围引流系统紊乱引起。由于重度CAA是痴呆的独立危险因素，因此已建议促进A β清除作为AD和MCI的潜在治疗。许多流行病学研究表明，血管危险因素增加MCI的发病率及其向AD的进展。因此，控制这些因素已被证明可以降低AD转化的风险并改善AD患者的认知障碍。因此，在预防神经病学的时代，神经血管方法可能有望治疗痴呆症。
The concept of mild cognitive impairment (MCI) was first introduced for the purpose of identifying individuals in an intermediate state between no cognitive impairment and Alzheimer's disease (AD). Recently, the heterogeneity of MCI has attracted attention as it has become clear that other diseases, such as cerebrovascular disease and Parkinson disease can also cause mild cognitive deficits, prompting a redefinition of MCI. Heterogeneity of MCI has been confirmed by neuropathological examinations. Most MCI patients not only possess amyloid plaques and neurofibrillary tau tangles, but also cerebral vascular pathology such as arteriosclerosis and cerebral amyloid angiopathy (CAA). CAA induces cerebral infarcts or hemorrhage of varying size and type, attributing to further cognitive impairment. Sporadic AD and CAA has been suggested to be the consequence of A beta elimination failure, mainly caused by disturbance of the perivascular drainage system. Since severe CAA is an independent risk factor for dementia, facilitation of A beta clearance has been suggested as a potential treatment of AD and MCI. Many epidemiological studies have shown that vascular risk factors increase incidence of MCI and its progression to AD. Accordingly, control of such factors has been shown to reduce risk of conversion to AD and ameliorate cognitive impairment in AD patients. Neurovascular approaches may therefore hold promise for the treatment of dementia in an era of preventive neurology.