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小胶质细胞和星形胶质细胞激活在阿尔茨海默病神经炎症发病机制中的作用:治疗方法的合理见解

Influence of microglia and astrocyte activation in the neuroinflammatory pathogenesis of Alzheimer's disease: Rational insights for the therapeutic approaches.

作者信息

Ahmad Mir Hilal, Fatima Mahino, Mondal Amal Chandra

机构信息

Cellular and Molecular Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

Cellular and Molecular Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi 110067, India.

出版信息

J Clin Neurosci. 2019 Jan;59:6-11. doi: 10.1016/j.jocn.2018.10.034. Epub 2018 Oct 29.

Abstract

Alzheimer's disease (AD), the most common progressive neurodegenerative disorder is characterized by the formation of extracellular amyloid plaques and intracellular neurofibrillary tangles (NFTs). Increasing evidences suggest a link between neuroinflammation and neuronal dysfunction in AD, orchestrated by the progressive activation of microglial cells and astrocytes with the consequent overproduction of proinflammatory molecules. The concomitant release of anti-inflammatory mediators antagonizes the inflammatory processes and leading to the severity of the AD pathology. The simultaneous detection of these inflammatory molecules in the pre-symptomatic stage may help in the early diagnosis of the AD. We have discussed the impact of microglia and astrocytic cells, the principal agents in the neuroinflammation process, in relation to the progression of the AD. Modulation of the risk factors and targeting of these immune mechanisms could lead to better therapeutic or preventive strategies for the AD. Further studies need to determine, how the inhibition of inflammatory factors could be used for the AD alternative therapies.

摘要

阿尔茨海默病(AD)是最常见的进行性神经退行性疾病,其特征是细胞外淀粉样斑块和细胞内神经原纤维缠结(NFTs)的形成。越来越多的证据表明,神经炎症与AD中的神经元功能障碍之间存在联系,这是由小胶质细胞和星形胶质细胞的逐渐激活所协调的,随之而来的是促炎分子的过度产生。抗炎介质的同时释放拮抗炎症过程,并导致AD病理学的严重程度。在症状前期同时检测这些炎症分子可能有助于AD的早期诊断。我们已经讨论了小胶质细胞和星形胶质细胞(神经炎症过程中的主要介质)对AD进展的影响。对危险因素的调节以及针对这些免疫机制可能会带来更好的AD治疗或预防策略。进一步的研究需要确定,如何将炎症因子的抑制用于AD的替代疗法。

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