%0 Journal Article
%T Blast traumatic brain injury-induced cognitive deficits are attenuated by preinjury or postinjury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4
%J Alzheimer's and dementia
%D 2015
%A Tweedie, David
%A Rachmany, Lital
%A Rubovitch, Vardit
%A Li, Yazhou
%A Holloway, Harold W.
%A Lehrmann, Elin
%A Zhang, Yongqing
%A Becker, Kevin G.
%A Perez, Evelyn
%A Hoffer, Barry J.
%A Pick, Chaim G.
%A Greig, Nigel H.
%V 12
%N 1
%P 34-48
%X BACKGROUND: Blast traumatic brain injury (B-TBI) affects military and civilian personnel. Presently, there are no approved drugs for blast brain injury. <br><br>METHODS: Exendin-4 (Ex-4), administered subcutaneously, was evaluated as a pretreatment (48 hours) and postinjury treatment (2 hours) on neurodegeneration, behaviors, and gene expressions in a murine open field model of blast injury. <br><br>RESULTS: B-TBI induced neurodegeneration, changes in cognition, and genes expressions linked to dementia disorders. Ex-4, administered preinjury or postinjury, ameliorated B-TBI-induced neurodegeneration at 72 hours, memory deficits from days 7-14, and attenuated genes regulated by blast at day 14 postinjury. <br><br>CONCLUSIONS: The present data suggest shared pathologic processes between concussive and B-TBI, with end points amenable to beneficial therapeutic manipulation by Ex-4. B-TBI-induced dementia-related gene pathways and cognitive deficits in mice somewhat parallel epidemiologic studies of Barnes et al. who identified a greater risk in US military veterans who experienced diverse TBIs, for dementia in later life.<p /> <p>Language: en</p>
%G en
%I Elsevier Publishing
%@ 1552-5260
%U http://dx.doi.org/10.1016/j.jalz.2015.07.489