Neuroinflammation mediates the progression of neonate hypoxia-ischemia brain damage to Alzheimer’s disease: a bioinformatics and experimental study

作者：Shengjie Zhang, Ruqiu Zhang, Zhaoqin Chen, Zihan Shao, An Li, Fan Li, Fang Huang · 发表于：Frontiers in Aging Neuroscience · 年份：2025 · DOI：10.3389/fnagi.2024.1511668 · 被引用次数：4 · 研究领域：S100 Proteins and Annexins、Traumatic Brain Injury and Neurovascular Disturbances、Neonatal and fetal brain pathology

Background: Traumatic brain injury (TBI) can generally be divided into focal damage and diffuse damage, and neonate Hypoxia-Ischemia Brain Damage (nHIBD) is one of the causes of diffuse damage. Patients with nHIBD are at an increased risk of developing Alzheimer's disease (AD). However, the shared pathogenesis of patients affected with both neurological disorders has not been fully elucidated. Purpose: We here aim to identify the shared molecular signatures between nHIBD and AD. We used an integrated analysis of the cortex gene expression data, targeting differential expression of genes related to the mechanisms of neurodegeneration and cognitive impairment following traumatic brain injury. Methods: The gene expression profiles of Alzheimer's disease (GSE203206) and that of Neonate Hypoxia-Ischemia Brain Damage (GSE23317) were obtained from the Gene Expression Omnibus (GEO) database. After identifying the common differentially expressed genes (DEGs) of Alzheimer's disease and neonate Hypoxia-Ischemia Brain Damage by limma package analysis, five kinds of analyses were performed on them, namely Gene Ontology (GO) and pathway enrichment analysis, protein-protein interaction network, DEG-transcription factor interactions and DEG-microRNA interactions, protein-drug interactions and protein-disease association analysis, and gene-inflammation association analysis and protein-inflammation association analysis. Results: In total, 12 common DEGs were identified including HSPB1, VIM, MV...