神经炎症
医学
神经科学
认知
痴呆
认知障碍
炎症
血脑屏障
血管性痴呆
发病机制
先天免疫系统
脑血流
认知功能衰退
免疫系统
冲程(发动机)
生物信息学
免疫学
临床实习
生物标志物
小胶质细胞
白质
机制(生物学)
炎症反应
过程(计算)
脑灌注不足
多发性硬化
治疗方法
作者
Akane Mizutani,Carlos Parra-Pérez,Akihiro Shindo,Ignacio Lizasoaín,Maria Angeles Moro,Ken Arai
标识
DOI:10.1177/0271678x261437523
摘要
Vascular cognitive impairment and dementia (VCID) encompasses a heterogeneous group of disorders in which cerebrovascular pathology contributes to cognitive decline. Accumulating evidence from both clinical and basic studies suggests that neuroinflammation is one of the major mechanisms underlying VCID pathogenesis. However, its clinical evaluation remains challenging, and how it influences the process of VCID pathogenesis is still not fully understood. Experimental models of chronic cerebral hypoperfusion have demonstrated that decreased cerebral blood flow can activate innate immune responses and trigger inflammatory cascades. These cascades may contribute to white matter damage and cognitive deficits, and anti-inflammatory interventions have shown therapeutic potential in mitigating these outcomes. In this mini-review, we summarize recent findings on neuroinflammation from both clinical and basic studies, and discuss its role in VCID progression. A deeper understanding of the multifaceted mechanisms involved in inflammatory signaling will be essential for advancing VCID research and developing effective therapeutic strategies.
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