Diabetes drugs activate neuroprotective pathways in neonatal hypoxic-ischemic encephalopathy models

ABSTRACT: Hypoxic-ischemic encephalopathy (HIE) arises from diminished blood flow and oxygen to the neonatal brain during labor, leading to infant mortality or severe brain damage, with a global incidence of 1.5 per 1000 live births. Glucagon-like Peptide 1 Receptor (GLP1-R) agonists, used in type 2 diabetes treatment, exhibit neuroprotective effects in various brain injury models, including HIE. In this study, we observed enhanced neurological outcomes in post-natal day 10 mice with surgically induced hypoxic-ischemic (HI) brain injury after immediate systemic administration of exendin-4 or semaglutide. Short- and long-term assessments revealed improved neuropathology, survival rates, and locomotor function. We explored the mechanisms by which GLP1-R agonists trigger neuroprotection and reduce infl

SUBMITTER: Dr. Laura Poupon-Bejuit 

PROVIDER: S-SCDT-10_1038-S44321-024-00079-1 | biostudies-other |

REPOSITORIES: biostudies-other