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小胶质细胞介导的神经毒性:揭示分子机制

Microglia-mediated neurotoxicity: uncovering the molecular mechanisms.

作者信息

Block Michelle L, Zecca Luigi, Hong Jau-Shyong

机构信息

Neuropharmacology Section, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina 27709, USA.

出版信息

Nat Rev Neurosci. 2007 Jan;8(1):57-69. doi: 10.1038/nrn2038.

DOI:10.1038/nrn2038
PMID:17180163
Abstract

Mounting evidence indicates that microglial activation contributes to neuronal damage in neurodegenerative diseases. Recent studies show that in response to certain environmental toxins and endogenous proteins, microglia can enter an overactivated state and release reactive oxygen species (ROS) that cause neurotoxicity. Pattern recognition receptors expressed on the microglial surface seem to be one of the primary, common pathways by which diverse toxin signals are transduced into ROS production. Overactivated microglia can be detected using imaging techniques and therefore this knowledge offers an opportunity not only for early diagnosis but, importantly, for the development of targeted anti-inflammatory therapies that might slow or halt the progression of neurodegenerative disease.

摘要

越来越多的证据表明,小胶质细胞的激活在神经退行性疾病中会导致神经元损伤。最近的研究表明,在接触某些环境毒素和内源性蛋白质时,小胶质细胞会进入过度激活状态并释放导致神经毒性的活性氧(ROS)。小胶质细胞表面表达的模式识别受体似乎是将多种毒素信号转导为ROS产生的主要常见途径之一。使用成像技术可以检测到过度激活的小胶质细胞,因此这一认识不仅为早期诊断提供了机会,而且重要的是,为开发可能减缓或阻止神经退行性疾病进展的靶向抗炎疗法提供了机会。

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