转录组与动物模型整合揭示抑制钙稳态相关基因 ITPKB 可缓解淀粉样斑块沉积

IF 2.8 4区 医学 Q3 BIOCHEMISTRY & MOLECULAR BIOLOGY
Yufei Hu, Zijun Zhao, Fang Xu, Xiaoqin Ren, Menglin Liu, Zilei Zheng, Qiujun Wang
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引用次数: 0

摘要

阿尔茨海默病(AD)是一种严重的神经系统疾病,会导致记忆力衰退,是一个全球性问题。最近,钙假说在阿尔茨海默病中稳步发展。然而,钙稳态疗法的前瞻性靶点有限,与AD中钙稳态相关的基因表达水平研究仍很模糊。在本研究中,我们分析了基因表达总库(GEO)数据库中的微阵列数据集(GSE132903),研究了与AD钙稳态相关的基因。通过免疫印迹分析,我们研究了ITPKB与AD炎症的关联。此外,我们还利用免疫荧光技术评估了药物抑制ITPKB对APP/PS1小鼠淀粉样β(Aβ)斑块沉积的影响。本文对钙稳态相关基因的进一步探索推动了钙稳态理论在AD中的验证。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Transcriptome and Animal Model Integration Reveals Inhibition of Calcium Homeostasis-Associated Gene ITPKB Alleviates Amyloid Plaque Deposition

Transcriptome and Animal Model Integration Reveals Inhibition of Calcium Homeostasis-Associated Gene ITPKB Alleviates Amyloid Plaque Deposition

Alzheimer’s disease (AD) is a severe neurological illness that causes memory loss and is a global problem. The calcium hypothesis recently steadily evolved in AD. The prospective targets for calcium homeostasis therapy, however, are limited, and gene expression-level research connected to calcium homeostasis in AD remains hazy. In this study, we analyzed the microarray dataset (GSE132903) taken from the Gene Expression Omnibus (GEO) database to investigate calcium homeostasis-related genes for AD. Using immunoblot analysis, we examined the association of ITPKB with inflammation in AD. Additionally, the immunofluorescence technique was employed to assess the impact of pharmacological inhibition of ITPKB on the amyloid-β (Aβ) plaque deposition in APP/PS1 mice. This article’s further exploration of calcium homeostasis-related genes has propelled the validation of the calcium homeostasis theory in AD.

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来源期刊
Journal of Molecular Neuroscience
Journal of Molecular Neuroscience 医学-神经科学
CiteScore
6.60
自引率
3.20%
发文量
142
审稿时长
1 months
期刊介绍: The Journal of Molecular Neuroscience is committed to the rapid publication of original findings that increase our understanding of the molecular structure, function, and development of the nervous system. The criteria for acceptance of manuscripts will be scientific excellence, originality, and relevance to the field of molecular neuroscience. Manuscripts with clinical relevance are especially encouraged since the journal seeks to provide a means for accelerating the progression of basic research findings toward clinical utilization. All experiments described in the Journal of Molecular Neuroscience that involve the use of animal or human subjects must have been approved by the appropriate institutional review committee and conform to accepted ethical standards.
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