TY  - JOUR
PY  - 2015//
TI  - Blast traumatic brain injury-induced cognitive deficits are attenuated by preinjury or postinjury treatment with the glucagon-like peptide-1 receptor agonist, exendin-4
JO  - Alzheimer's and dementia
A1  - Tweedie, David
A1  - Rachmany, Lital
A1  - Rubovitch, Vardit
A1  - Li, Yazhou
A1  - Holloway, Harold W.
A1  - Lehrmann, Elin
A1  - Zhang, Yongqing
A1  - Becker, Kevin G.
A1  - Perez, Evelyn
A1  - Hoffer, Barry J.
A1  - Pick, Chaim G.
A1  - Greig, Nigel H.
SP  - 34
EP  - 48
VL  - 12
IS  - 1
N2  - 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>
LA  - en
SN  - 1552-5260
UR  - http://dx.doi.org/10.1016/j.jalz.2015.07.489
ID  - ref1
ER  -