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小胶质细胞与β-淀粉样肽清除中的炎症机制

Microglia and inflammatory mechanisms in the clearance of amyloid beta peptide.

作者信息

Rogers Joseph, Strohmeyer Ron, Kovelowski C J, Li Rena

机构信息

Sun Health Research Institute, Sun City, Arisona.

出版信息

Glia. 2002 Nov;40(2):260-269. doi: 10.1002/glia.10153.

DOI:10.1002/glia.10153
PMID:12379913
Abstract

There is now abundant evidence that brain microglia, when activated, have the lineage, receptors, and synthetic capacity to participate in both potentially neurotoxic inflammatory responses and potentially beneficial phagocytic responses. Amyloid beta peptide (Abeta) forms highly insoluble, beta-pleated aggregates that are widely deposited in the Alzheimer's disease (AD) cortex and limbic system. Aggregated Abeta also activates the classical and alternative complement cascades. These properties make Abeta an excellent target for microglial phagocytosis, a view supported by multiple reports, through well established mechanisms of phagocyte clearance.

摘要

现在有充分的证据表明,脑小胶质细胞在被激活时,具有参与潜在神经毒性炎症反应和潜在有益吞噬反应的谱系、受体和合成能力。β淀粉样肽(Aβ)形成高度不溶性的β折叠聚集体,广泛沉积于阿尔茨海默病(AD)的皮质和边缘系统。聚集的Aβ还激活经典和替代补体级联反应。这些特性使Aβ成为小胶质细胞吞噬作用的理想靶点,这一观点得到了多篇报道的支持,通过成熟的吞噬细胞清除机制。

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