摘要
传统上,大脑被认为是一个有免疫特权的器官,然而,内源性刺激如存在错误折叠或聚集的蛋白质,以及全身的炎症反应等可能会导致小胶质细胞和脑先天免疫系统的活化,接着到神经发炎。阿尔茨海默氏病,是老年痴呆症的主要原因,是由β-淀粉样蛋白沉积和tau蛋白过度磷酸化导致的。神经炎症已被确定为阿尔茨海默氏病发病机制的主要原因。一旦被激活,小胶质细胞会释放一些促或抗炎因子,它们会影响大脑的功能和结构,阿尔兹海默病中小胶质细胞的调整激活也许会开启新的治疗纪元。
关键词: 阿尔茨海默病;淀粉样蛋白β;细胞因子;神经炎症;神经退行性病变;小胶质细胞。
Current Alzheimer Research
Title:Microglia in Alzheimer's Disease: The Good, the Bad and the Ugly
Volume: 13 Issue: 4
Author(s): Dario Tejera, Michael T. Heneka
Affiliation:
关键词: 阿尔茨海默病;淀粉样蛋白β;细胞因子;神经炎症;神经退行性病变;小胶质细胞。
摘要: Traditionally the brain has been viewed as being an immune-privileged organ. However, endogenous stimuli such as the presence of misfolded or aggregated proteins, as well as systemic inflammatory events may lead to the activation of microglial cells, the brain´s innate immune system, and, subsequently, to neuroinflammation. Alzheimer's disease, the leading cause of dementia, is characterized by amyloid beta deposition and tau hyperphosphorylation. Neuroinflammation in Alzheimer's disease has been identified as major contributor to disease pathogenesis. Once activated, microglia release several pro and anti-inflammatory mediators of which several affect the function and structure of the brain. Modulation of this microglial activation in Alzheimer's disease might open new therapeutic avenues.
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Cite this article as:
Dario Tejera, Michael T. Heneka , Microglia in Alzheimer's Disease: The Good, the Bad and the Ugly, Current Alzheimer Research 2016; 13 (4) . https://dx.doi.org/10.2174/1567205013666151116125012
DOI https://dx.doi.org/10.2174/1567205013666151116125012 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
Call for Papers in Thematic Issues
Current updates on the Role of Neuroinflammation in Neurodegenerative Disorders
Neuroinflammation is an invariable hallmark of chronic and acute neurodegenerative disorders and has long been considered a potential drug target for Alzheimer?s disease (AD) and dementia. Significant evidence of inflammatory processes as a feature of AD is provided by the presence of inflammatory markers in plasma, CSF and postmortem brain ...read more
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