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尖端RBD通过微质-神经元交叉介导的RTP801上调调节驱动持续的帕金森病进展

Sha-Sha Wang¹, Ruo-Lan Yuan², Wen-Fei Wang¹

¹Hunan Engineering Technology Center of Standardization and Function of Chinese Herbal Decoction Pieces, College of Pharmacy, Hunan University of Chinese Medicine, Changsha 410208, China; State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica & Neuroscience Center, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China.

Journal of advanced research

|August 5, 2025

概括

SARS-CoV-2尖端RBD通过激活涉及微质和神经元的有害反循环,使帕金森病 (PD) 恶化. 准RTP801或STING通路可以治疗长期COVID对PD的影响.

科学领域:

神经科学是一个神经科学.
免疫学免疫学免疫学
病毒学病毒学

背景情况:

新出现的证据将COVID-19与恶化的帕金森病 (PD) 进展联系起来.
SARS-CoV-2 尖端受体结合域 (RBD) 可能会在大脑中持续存在并驱动神经病理学,但机制尚不清楚.

研究的目的:

研究SARS-CoV-2 RBD加剧PD的机制.
确定导致COVID-19后PD持续进展的关键途径.

主要方法:

在α-synuclein (αSyn) A53T小鼠的黑质体中注射SARS-CoV-2 RBD的立体注射.
评估运动和非运动行为,功能连接 (fMRI),电生理学和αSyn聚合.
利用RNA测序,电子显微镜,微质枯竭和RTP801淘汰模型来阐明机制.

主要成果:

RBD加速了PD症状恶化,大脑连接功能受损,神经元刺激性降低.
RBD加剧了多巴胺基神经元损失和αSyn聚合,RTP801被确定为关键调解者.
涉及线粒体功能障碍,mtDNA释放,微质激活和cGAS-STING-IFNβ/RTP801轴的反循环驱动了神经退行.

结论:

SARS-CoV-2 RBD通过微质和神经元之间的病原性交叉声加剧了PD.
一个与线粒体损伤相关的分子模式 (DAMPs) -cGAS-STING-IFNβ/RTP801轴调解神经毒性.
准RTP801或STING通路为长期COVID相关PD提供了潜在的治疗策略.

关键词:

长时间的COVID.帕金森病是帕金森氏症的一种疾病.心理上的压力是心理上的压力.在RBD中,RBD是RBD.在RTP801中使用.cGAS-STING 的使用情况.

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