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在阿尔茨海默氏症中,微质衍生ASC斑交叉粉样蛋白-β

Carmen Venegas¹, Sathish Kumar², Bernardo S Franklin³

¹Department of Neurodegenerative Diseases and Gerontopsychiatry, University of Bonn, Sigmund-Freud-Strasse 25, 53127 Bonn, Germany.

|January 3, 2018

概括

微质释放的炎酶激活的ASC斑块作为交叉种子,在阿尔茨海默病模型中驱动粉样β病理的传播. 阻断ASC斑点可以减少这种病态,突显炎症酶激活的作用.

科学领域:

神经科学
免疫学
病理学

背景情况:

神经退行性疾病的特征是病理分布在大脑区域内和大脑区域之间.
阿尔茨海默病涉及粉样β沉积,先天免疫激活,以及微质中依赖炎症的ASC斑点形成.

研究的目的:

调查由炎体衍生的ASC斑点在化和扩散β粉样蛋白病理中的作用.
确定ASC斑点是否在阿尔茨海默病中起到粉样β病理的作用.

主要方法:

在APP_SwePSEN1_dE9小鼠中注射ASC斑点.
使用ASC缺陷的APP_SwePSEN1_dE9小鼠来评估病理诱导.
使用抗ASC抗体阻止ASC斑点效应.

主要成果:

在APP_SwePSEN1_dE9小鼠中,ASC斑点的内注射诱导了粉样β病理的扩散.
来自APP_SwePSEN1_dE9小鼠的大脑同质物未能在ASC缺乏的小鼠中诱导病理.
同时使用抗ASC抗体抑制了粉样β病理的增加.

结论:

炎症酶激活和ASC斑点形成与粉样β病理的播种和传播有关.
ASC斑点作为一种由炎症驱动的粉素-β病理的交叉种子.
这些发现支持炎症酶激活是阿尔茨海默病进展的关键因素.

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