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嗅觉功能障碍作为C.的早期致病指标. 阿尔茨海默氏症和多重胺胺疾病的 elegans 模型

Weikang Xue¹, Ziyi Lei¹, Bin Liu¹

¹Department of Neurology, Medical Research Institute, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, China.

Frontiers in aging neuroscience

|October 16, 2024

概括

在阿尔茨海默病模型中神经退行早期迹象包括减少气味敏感性和特定神经元中的信号缺陷,先于蛋白质聚合物形成. 激活AMPK通路可以缓解这些嗅觉缺陷.

科学领域:

神经生物学神经生物学神经生物学
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

神经退行性疾病涉及蛋白质错折和神经元死亡.
目前的模型中缺乏综合的分子,形态和功能分析.
在C.I.C.中, 优雅的嗅觉神经元为研究蛋白质静止提供了一个可操作的模型.

研究的目的:

在神经退行性模型中研究早期病原性特征,使用C. 伊莱根斯 (elegans) 是一个词.
描述嗅觉神经元的依赖时间的分子,形态和功能变化.
识别阿尔茨海默病和多重胺胺疾病模型中神经元功能障碍的早期指标.

主要方法:

使用过的C. 优雅的模型表达粉样β 1-42 (Aβ1-42) 和多重氨酸 (Q40).
在嗅觉神经元 (AWB,AWC,AWA) 中评估了气味敏感性,蛋白质聚合,神经元形态 (cilia) 和信号.
研究了ER展开蛋白反应 (UPR) 和AMPK通路的作用.

主要成果:

在AWB和AWC神经元中早在成年第一天就观察到减少的气味敏感性和信号缺陷.
细胞类型特异性功能障碍,AWA神经元不受影响.
年龄相关的蛋白质聚合和神经元形态变化 (眼缩短/扩大) 发生在第6天.
在Aβ1-42模型中观察到ER展开蛋白响应 (UPR) 激活.
AMPK通路的激活改善了嗅觉缺陷,并减少了纤维状Aβ.

结论:

减少信号传递和特定的感觉神经元亚型功能障碍是神经退行症的早期指标.
这些早期事件先于可见的蛋白质聚合物形成.
在C.I.C.中, 嗅觉神经元对于研究神经退行性疾病中的蛋白质稳定机制非常有价值.
该AMPK途径为缓解神经退行性表型提供了潜在的治疗标.

关键词:

阿尔茨海默氏症的疾病是阿尔茨海默氏症.这里是C. elegans.神经退行性疾病的神经退行性疾病神经元神经元的神经元嗅觉嗅觉是一种嗅觉.多重谷氨胺的疾病.

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