Blast traumatic brain injury-induced cognitive deficits are attenuated by preinjury or postinjury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4.

Exendin-4 administered subcutaneously either 48 hours before or 2 hours after blast traumatic brain injury significantly reduced neurodegeneration at 72 hours, improved cognitive deficits observed between days 7 and 14, and attenuated blast-induced changes in dementia-related gene expression at day 14 postinjury in a mouse model.

Using a murine open field model of blast injury, exendin-4 was administered subcutaneously either as a pretreatment 48 hours before injury or as a postinjury treatment 2 hours after blast exposure. Neurodegeneration, cognitive behavior, and gene expression changes were assessed at multiple time points up to 14 days postinjury.

This study identifies exendin-4 as a potential therapeutic agent for blast traumatic brain injury, a condition currently lacking approved treatments, and links blast injury effects to dementia-related pathways, highlighting new avenues for intervention.

The study was conducted in mice, so results may not fully translate to humans. The exact study type and strength of evidence were not specified, limiting assessment of reliability.