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长非编码RNA UCA1在阿尔茨海默病的诊断价值和认知调节作用

Yongjin Zhang¹, Fangping Wu¹

¹Department of Neurology, The First People's Hospital of Lianyungang, Xuzhou Medical University Affiliated Hospital of Lianyungang, The First Affiliated Hospital of Kangda College of Nanjing Medical University, Lianyungang 222000, China.

Neuroscience letters

|April 7, 2024

概括

血清长非编码RNAUCA1在阿尔茨海默病 (AD) 中升高,并通过调节UCA1/miR-342-3p轴,促进认知衰退,这表明其诊断潜力.

科学领域:

神经科学是一个神经科学.
分子生物学分子生物学
生物化学生物化学

背景情况:

阿尔茨海默病 (AD) 是一种进展性神经退行性疾病.
确定可靠的生物标志物和了解疾病机制对于AD诊断和治疗至关重要.

研究的目的:

研究血清长非编码RNA UCA1在阿尔茨海默病 (AD) 中的诊断作用.
阐明潜在的分子机制,涉及UCA1在AD的发病.

主要方法:

量化逆转录聚合酶链反应 (RT-PCR) 用于UCA1量化.
接收器操作特征 (ROC) 曲线分析用于诊断价值评估.
在SH-SY5Y细胞中进行细胞活力 (CCK-8) 和亡测定 (流细胞计).
在小鼠中进行水迷宫测试以评估认知功能.
双 luciferase 记者测定用于识别 UCA1 目标基因.
对微RNA基因功能和通路的生物信息丰富分析.

主要成果:

在AD组中,血清UCA1水平显著升高,表明了诊断潜力.
在SH-SY5Y细胞中抑制UCA1缓解的粉样β (Aβ) 诱导的活力丧失和亡,通过海绵miR-342-3p.
在AD模型中,UCA1/miR-342-3p轴的淘汰部分恢复了认知功能.
在与AD进展相关的途径中,miR-342-3p的目标基因得到了丰富.

结论:

UCA1/miR-342-3p轴在阿尔茨海默病的发病过程中发挥着重要作用.
这个轴通过调节认知能力来促进AD,突出其作为治疗目标的潜力.

关键词:

阿尔茨海默病的疾病阿尔茨海默病的疾病.认知认知是一种认知.诊断诊断诊断诊断诊断在UCA1中,UCA1是UCA1的.在 miR-342-3p 中使用.

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