Abstract
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.