Abstract:
The central nervous system (CNS) and the immune system collectively coordinate cellular functionalities, sharing common developmental mechanisms. Immunity-related molecules exert an influence on brain development, challenging the conventional view of the brain as immune-privileged. Chronic inflammation emerges as a key player in the pathophysiology of Alzheimer\'s disease (AD), with increased stress contributing to the disease progression and potentially exacerbating existing symptoms. In this study, the most significant gene signatures from selected RNA-sequencing (RNA-seq) data from AD patients and healthy individuals were obtained and a functional analysis and biological interpretation was conducted, including network and pathway enrichment analysis. Important evidence was reported, such as enrichment in immune system responses and antigen processes, as well as positive regulation of T-cell mediated cytotoxicity and endogenous and exogenous peptide antigen, thus indicating neuroinflammation and immune response participation in disease progression. These findings suggest a disturbance in the immune infiltration of the peripheral immune environment, providing new challenges to explore key biological processes from a molecular perspective that strongly participate in AD development.
摘要:
中枢神经系统(CNS)和免疫系统共同协调细胞功能,共享共同的发展机制。免疫相关分子对大脑发育有影响,挑战传统观点的大脑免疫特权。慢性炎症在阿尔茨海默病(AD)的病理生理学中发挥关键作用,压力增加导致疾病进展,并可能加剧现有症状。在这项研究中,从AD患者和健康个体的选定RNA测序(RNA-seq)数据中获得了最重要的基因特征,并进行了功能分析和生物学解释,包括网络和路径富集分析。报告了重要证据,如免疫系统反应和抗原过程的富集,以及T细胞介导的细胞毒性和内源性和外源性肽抗原的正调控,从而表明神经炎症和免疫反应参与疾病进展。这些发现提示了外周免疫环境的免疫浸润紊乱,从强烈参与AD发展的分子角度探索关键生物过程提供了新的挑战。