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

ABSTRACT:

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

SUBMITTER: Zhang S 

PROVIDER: S-EPMC11770030 | biostudies-literature | 2024

REPOSITORIES: biostudies-literature