Exendin-4 ameliorates traumatic brain injury-induced cognitive impairment in rats

Katharine Eakin, Yazhou Li, Yung Hsiao Chiang, Barry J. Hoffer, Hilary Rosenheim, Nigel H. Greig, Jonathan P. Miller

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Traumatic brain injury represents a major public health issue that affects 1.7 million Americans each year and is a primary contributing factor (30.5%) of all injury-related deaths in the United States. The occurrence of traumatic brain injury is likely underestimated and thus has been termed "a silent epidemic". Exendin-4 is a long-acting glucagon-like peptide-1 receptor agonist approved for the treatment of type 2 diabetes mellitus that not only effectively induces glucose-dependent insulin secretion to regulate blood glucose levels but also reduces apoptotic cell death of pancreatic β-cells. Accumulating evidence also supports a neurotrophic and neuroprotective role of glucagon-like peptide-1 in an array of cellular and animal neurodegeneration models. In this study, we evaluated the neuroprotective effects of Exendin-4 using a glutamate toxicity model in vitro and fluid percussion injury in vivo. We found neuroprotective effects of Exendin-4 both in vitro, using markers of cell death, and in vivo, using markers of cognitive function, as assessed by Morris Water Maze. In combination with the reported benefits of ex-4 in other TBI models, these data support repositioning of Exendin-4 as a potential treatment for traumatic brain injury.

Original languageEnglish
Article numbere82016
JournalPLoS One
Volume8
Issue number12
DOIs
Publication statusPublished - Dec 2 2013

ASJC Scopus subject areas

  • Agricultural and Biological Sciences(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Medicine(all)

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    Eakin, K., Li, Y., Chiang, Y. H., Hoffer, B. J., Rosenheim, H., Greig, N. H., & Miller, J. P. (2013). Exendin-4 ameliorates traumatic brain injury-induced cognitive impairment in rats. PLoS One, 8(12), [e82016]. https://doi.org/10.1371/journal.pone.0082016