Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects
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...
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MDPI AG
2022-06-01
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Online Access: | https://www.mdpi.com/1422-0067/23/11/6224 |
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author | Zhengming Tian Xunming Ji Jia Liu |
author_facet | Zhengming Tian Xunming Ji Jia Liu |
author_sort | Zhengming Tian |
collection | DOAJ |
description | 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. |
first_indexed | 2024-03-10T01:14:30Z |
format | Article |
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issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-10T01:14:30Z |
publishDate | 2022-06-01 |
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spelling | doaj.art-bbf2b0f66647468c88ec1320a9edd9512023-11-23T14:11:50ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-06-012311622410.3390/ijms23116224Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and ProspectsZhengming Tian0Xunming Ji1Jia Liu2Laboratory of Brain Disorders, Beijing Institute of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Capital Medical University, Beijing 100069, ChinaLaboratory of Brain Disorders, Beijing Institute of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Capital Medical University, Beijing 100069, ChinaLaboratory of Brain Disorders, Beijing Institute of Brain Disorders, Ministry of Science and Technology, Collaborative Innovation Center for Brain Disorders, Beijing Advanced Innovation Center for Big Data-Based Precision Medicine, Capital Medical University, Beijing 100069, ChinaVascular 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.https://www.mdpi.com/1422-0067/23/11/6224hypoxiaischemiamicroglianeuroinflammationvascular cognitive impairment and dementia |
spellingShingle | Zhengming Tian Xunming Ji Jia Liu Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects International Journal of Molecular Sciences hypoxia ischemia microglia neuroinflammation vascular cognitive impairment and dementia |
title | Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects |
title_full | Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects |
title_fullStr | Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects |
title_full_unstemmed | Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects |
title_short | Neuroinflammation in Vascular Cognitive Impairment and Dementia: Current Evidence, Advances, and Prospects |
title_sort | neuroinflammation in vascular cognitive impairment and dementia current evidence advances and prospects |
topic | hypoxia ischemia microglia neuroinflammation vascular cognitive impairment and dementia |
url | https://www.mdpi.com/1422-0067/23/11/6224 |
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