Molecular Mechanisms of GFAP and PTPRC in Alzheimer's Disease: An Analysis of Neuroinflammatory Response and Progression.

Jingyue Huang, Xinping Pang, Hongmei Yang, Chonghao Gao, Dongxiao Wang, Yue Sun, Yezi Taishi, Chaoyang Pang
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Abstract

Introduction: Alzheimer's disease (AD) is a complex neurological disorder that progressively worsens. Although its exact causes are not fully understood, new research indicates that genes related to non-neuronal cells change significantly with age, playing key roles in AD's pathology.

Method: This study focuses on a protein network centered on Glial Fibrillary Acidic Protein (GFAP) and Protein Tyrosine Phosphatase Receptor Type C (PTPRC). The Key Findings of this Study Include: 1. A significant correlation was observed between GFAP and PTPRC expression throughout AD progression, which links closely with clinical phenotypes and suggests their role in AD pathology. 2. A molecular network centered on GFAP and PTPRC, including Catenin Beta 1 (CTNNB1) and Integrin Beta 2 (ITGB2), showed distinct changes in interactions, highlighting its regulatory role in AD. 3. Analysis of GSE5281 data revealed a decline in the interaction strength within this network, pointing to potential desynchronization as a biomarker for AD. 4. SVM diagnostic models comparing GFAP expression and coupling values confirmed this desynchronization, suggesting it worsens with AD progression.

Result: Based on these findings, it is hypothesized that as AD progresses, the GFAP- and PTPRCcentered molecular framework undergoes significant changes affecting key biological pathways. These changes disrupt immune regulation and cellular functions, increasing immune cell activation and inflammation in the brain. This may impair neuronal communication and synaptic functionality, exacerbating AD's pathology.

Conclusion: To verify these findings, Support Vector Machine (SVM) diagnostic models and correlation analyses were used to examine changes in this network, indicating that its dysregulation significantly affects AD progression.

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阿尔茨海默病中 GFAP 和 PTPRC 的分子机制:神经炎症反应和进展分析
导言阿尔茨海默病(AD)是一种复杂的神经系统疾病,会逐渐恶化。虽然其确切病因尚未完全明了,但新的研究表明,与非神经元细胞相关的基因会随着年龄的增长而发生显著变化,在阿尔茨海默病的病理过程中起着关键作用:本研究的重点是以胶质纤维酸性蛋白(GFAP)和蛋白酪氨酸磷酸酶受体 C 型(PTPRC)为中心的蛋白质网络。本研究的主要发现包括1.观察到 GFAP 和 PTPRC 的表达在整个 AD 进展过程中存在明显的相关性,这与临床表型密切相关,并表明它们在 AD 病理中的作用。2.以 GFAP 和 PTPRC 为中心的分子网络(包括 Catenin Beta 1 (CTNNB1) 和 Integrin Beta 2 (ITGB2))显示出明显的相互作用变化,突显了它们在 AD 中的调控作用。3.3. 对 GSE5281 数据的分析表明,该网络中的相互作用强度有所下降,这表明非同步化可能成为 AD 的生物标记物。4.4. 比较 GFAP 表达和耦合值的 SVM 诊断模型证实了这种不同步现象,表明它会随着 AD 的发展而恶化:基于这些发现,我们假设随着 AD 的进展,以 GFAP 和 PTPRC 为中心的分子框架会发生重大变化,影响关键的生物通路。这些变化破坏了免疫调节和细胞功能,增加了免疫细胞的活化和大脑中的炎症。这可能会损害神经元通信和突触功能,从而加剧 AD 的病理变化:为了验证这些发现,研究人员使用支持向量机(SVM)诊断模型和相关性分析来研究该网络的变化,结果表明,该网络的失调会严重影响 AD 的发展。
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