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甲状腺功能过高对认知功能,神经炎症和APP/PS1小鼠中的亡的影响

Kai Lou¹, Shudong Liu², Fengxia Zhang³

¹Department of Endocrinology, Jinan Central Hospital Affiliated to Shandong First Medical University, Jinan, 250013, China.

Journal of translational medicine

|September 22, 2023

概括

甲状腺功能障碍,特别是格雷夫斯病,在阿尔茨海默病 (AD) 鼠群中加剧认知缺陷和粉样蛋白-β (Aβ) 沉积. 这通过神经炎症和RIPK3 / MLKL介导的亡发生,突出显示甲状腺功能障碍和痴呆症进展之间的联系.

科学领域:

神经科学是一个神经科学.
内分泌学在内分泌学.
病理学病理学病理学

背景情况:

甲状腺功能障碍越来越多地与痴呆症的发病有关.
甲状腺功能低下症与更高的痴呆症风险有关.
甲状腺功能障碍对痴呆症的影响在很大程度上仍未被探索.

研究的目的:

为了研究甲状腺功能过高对认知功能和粉样β (Aβ) 在阿尔茨海默病 (AD) 鼠标模型中的积累的影响.
探索关联甲状腺功能障碍与AD病理学的潜在机制.

主要方法:

在APP/PS1 AD模型小鼠中利用腺病毒载体诱导Graves病 (GD) 现型.
在GD诱导的AD小鼠中评估认知功能和Aβ沉积.
采用单细胞RNA测序来分析微质功能和炎症途径.

主要成果:

GD小鼠表现出持续的甲状腺功能障碍,认知缺陷和Aβ沉积增加.
在GD小鼠中,微质功能障碍,神经炎症和M1/M2两极分化是至关重要的.
激活受体相互作用的血清蛋白/氨酸蛋白激酶3 (RIPK3) /混合系激酶域类伪激酶 (MLKL) 介导的亡导致了Aβ沉积和神经元损失.
一种RIPK3抑制剂减轻了GD诱导的Aβ积累和神经元损失.

结论:

格雷夫斯病诱导的甲状腺功能障碍症加剧了AD小鼠的认知衰退.
甲状腺功能障碍症通过神经炎症和RIPK3 / MLKL介导的亡促进Aβ沉积和神经元损失.
这些发现确立了甲状腺功能升高和AD进展之间的机制联系.

关键词:

阿尔茨海默氏症是阿尔茨海默氏症的一种疾病.格雷夫斯的疾病.尸体灭 (Necroptosis) 是一种死亡的过程.神经炎症是一种神经炎症.一个单细胞RNA测序.

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