Proteomic analysis of hippocampus reveals metabolic reprogramming in a piglet model of mild hypoxic ischemic encephalopathy.

ABSTRACT: Neonatal hypoxic-ischemic encephalopathy (HIE) remains a leading cause of long-term neurologic morbidity. Fifty percent of HIE cases are mild and do not have clearly defined therapeutic interventions. Emergent evidence now demonstrates that up to 25% of children with mild HIE suffer motor and developmental delay by 18 months and 35% have cognitive impairments by age 5 years. Interestingly, the hippocampus, which is responsible for learning and memory, does not show overt injury but does demonstrate volume changes on imaging that correlate with cognitive and behavioral outcomes. Although there is extensive data regarding pathophysiological changes following moderate and severe HIE, there is a paucity of understanding regarding the extent, duration, and compensatory adaptations in the mild n

SUBMITTER: Lammert DB 

PROVIDER: S-EPMC12021231 | biostudies-literature | 2025

REPOSITORIES: biostudies-literature