AI Article Synopsis
- Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease marked by abnormal amyloid-β deposits in blood vessels, commonly found in older adults and Alzheimer's patients.
- The underlying processes that lead to blood vessel damage and related issues, like bleeding and cognitive decline, are not well understood yet.
- This review highlights previous research on neuroinflammation's involvement in CAA and suggests future studies focusing on specific targets like matrix metalloproteinases and activated immune cells to improve treatment options.
Article Abstract
Cerebral amyloid angiopathy (CAA) is a cerebrovascular disease characterized by vascular amyloid-β (Aβ) deposition. CAA is often seen in the brains of elderly individuals and in a majority of patients with Alzheimer's disease. The molecular pathways triggered by vascular Aβ, causing vessel wall breakdown and ultimately leading to intracerebral haemorrhage and cognitive decline, remain poorly understood. The occurrence of CAA-related inflammation (CAA-ri) and Amyloid-Related Imaging Abnormalities (ARIA) have sparked interest for a role of neuroinflammation in CAA pathogenesis. This review discusses prior studies of neuroinflammation in CAA and outlines potential future research directions targeting candidates such as matrix metalloproteinases, complement activation, microglial activation, reactive astrocytes and parenchymal border macrophages. Understanding the role of neuroinflammation in CAA pathogenesis could help identify new therapeutic strategies.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11648568 | PMC |
| http://dx.doi.org/10.1016/j.ebiom.2024.105466 | DOI Listing |
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