Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects

Abstract

Vascular cognitive impairment and dementia (VCID) is a major heterogeneous brain disease caused by multiple factors, and it is the second most common type of dementia in the world. It is caused by long-term chronic low perfusion in the whole brain or local brain area, and it eventually develops into severe cognitive dysfunction syndrome. Because of the disease’s ambiguous classification and diagnostic criteria, there is no clear treatment strategy for VCID, and the association between cerebrovascular pathology and cognitive impairment is controversial. Neuroinflammation is an immunological cascade reaction mediated by glial cells in the central nervous system where innate immunity resides. Inflammatory reactions could be triggered by various damaging events, including hypoxia, ischemia, and infection. Long-term chronic hypoperfusion-induced ischemia and hypoxia can overactivate neuroinflammation, causing apoptosis, blood–brain barrier damage and other pathological changes, triggering or aggravating the occurrence and development of VCID. In this review, we will explore the mechanisms of neuroinflammation induced by ischemia and hypoxia caused by chronic hypoperfusion and emphasize the important role of neuroinflammation in the development of VCID from the perspective of immune cells, immune mediators and immune signaling pathways, so as to provide valuable ideas for the prevention and treatment of the disease.

Chronic Neuroinflammation and Cognitive Decline in Patients with Cardiac Disease: Evidence, Relevance, and Therapeutic Implications

“…Recent data from brain imaging support the association of increased neuroinflammation during the progression of MCI and AD [ 70 ]. In contrast to ‘classical’ AD, VCID is a heterogeneous brain disease, where chronic cerebral hypoperfusion and persistence of an ischemic and hypoxic micro-environment leads to neuroinflammation, oxidative stress, neurotrophic uncoupling, destruction of the blood–brain barrier, and eventually to cognitive dysfunction [ 71 ]. In several animal models of VCID, neuroinflammation caused by chronic cerebral hypoperfusion induced white matter damage, while microglia and astrocytes were activated [ 71 , 72 ].…”

Research progress on acupuncture treatment in central nervous system diseases based on NLRP3 inflammasome in animal models

“…Although it has a high incidence rate, it is the only one among various types of dementia that can be prevented and treated early. The latest research has found that immune and neuroinflammation have gradually attracted the attention of researchers, excluding common risk factors for cerebrovascular diseases (Finger et al, 2022;Tian et al, 2022). Many studies have shown that acupuncture has a certain effect on VD (Chen et al, 2022b), but there are differences in efficacy due to different acupuncture methods, and there is no unified clinical standard.…”

SM22α Deletion Contributes to Neurocognitive Impairment in Mice through Modulating Vascular Smooth Muscle Cell Phenotypes

“…Unfortunately, despite hundreds of research studies over recent decades, there is no cure in sight. Considerable evidence now indicates that diseases with cognitive impairment, such as Alzheimer’s disease (AD), which is primarily a vascular disorder that precedes neuronal dysfunction, could be prevented or delayed by targeting the vascular component [ 3 , 4 , 5 , 6 ].…”