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存在淀粉样蛋白和tau蛋白时缺血后脑的神经炎症

Neuroinflammation in the Post-Ischemic Brain in the Presence of Amyloid and Tau Protein.

作者信息

Pluta Ryszard

机构信息

Department of Pathophysiology, Medical University of Lublin, 20-090 Lublin, Poland.

出版信息

Discov Med. 2025 Jan;37(192):1-18. doi: 10.24976/Discov.Med.202537192.1.

DOI:10.24976/Discov.Med.202537192.1
PMID:39851219
Abstract

Ischemia-induced brain neurodegeneration is a leading cause of mortality and permanent disability worldwide, with no definitive cure. The development of neuroinflammation following ischemic events plays a dual role; it is essential for brain repair and homeostasis and can also exacerbate post-ischemic damage and worsen neurological outcomes. Neuroinflammation represents a complex process involving interactions between infiltrating immune cells from the bloodstream and resident immune cells within the affected brain regions. This inflammatory response begins immediately after ischemia and can persist for years. This review focuses on the intricate relationship between neuroinflammation, amyloid accumulation, tau protein pathology and glial cells in the post-ischemic brain. Notably, it examines whether amyloid and tau protein amplify neuroinflammation and whether neuroinflammatory responses influence the behavior and aggregation of these molecules. Understanding these interactions is critical, as they contribute to the progression of post-ischemic brain neurodegeneration. Additionally, this review highlights the role of neuroinflammation as a functionally complex immune response regulated by transcription factors and mediated by cytokines. It explores how the presence of amyloid and modified tau protein may shape the inflammatory landscape. This review aims to advance our understanding of post-ischemic neuroinflammation and its implications for long-term brain health and neurodegenerative diseases.

摘要

缺血性脑神经元变性是全球死亡率和永久性残疾的主要原因,目前尚无确切的治愈方法。缺血事件后神经炎症的发展具有双重作用;它对脑修复和内环境稳定至关重要,但也会加剧缺血后损伤并恶化神经学结果。神经炎症是一个复杂的过程,涉及来自血液的浸润免疫细胞与受影响脑区的常驻免疫细胞之间的相互作用。这种炎症反应在缺血后立即开始,并可持续数年。本综述重点关注缺血后脑神经炎症、淀粉样蛋白积累、tau蛋白病理与神经胶质细胞之间的复杂关系。值得注意的是,它研究了淀粉样蛋白和tau蛋白是否会放大神经炎症,以及神经炎症反应是否会影响这些分子的行为和聚集。理解这些相互作用至关重要,因为它们会导致缺血后脑神经变性的进展。此外,本综述强调了神经炎症作为一种由转录因子调节并由细胞因子介导的功能复杂的免疫反应的作用。它探讨了淀粉样蛋白和修饰的tau蛋白的存在如何塑造炎症格局。本综述旨在增进我们对缺血后神经炎症及其对长期脑健康和神经退行性疾病影响的理解。

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