RT Journal Article SR Electronic T1 Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice JF eneuro JO eNeuro FD Society for Neuroscience SP ENEURO.0220-16.2016 DO 10.1523/ENEURO.0220-16.2016 VO 3 IS 5 A1 Terry C. Yin A1 Jaymie R. Voorhees A1 Rachel M. Genova A1 Kevin C. Davis A1 Ashley M. Madison A1 Jeremiah K. Britt A1 Coral J. Cintrón-Pérez A1 Latisha McDaniel A1 Matthew M. Harper A1 Andrew A. Pieper YR 2016 UL http://www.eneuro.org/content/3/5/ENEURO.0220-16.2016.abstract AB Axonal degeneration is a prominent feature of many forms of neurodegeneration, and also an early event in blast-mediated traumatic brain injury (TBI), the signature injury of soldiers in Iraq and Afghanistan. It is not known, however, whether this axonal degeneration is what drives development of subsequent neurologic deficits after the injury. The Wallerian degeneration slow strain (WldS) of mice is resistant to some forms of axonal degeneration because of a triplicated fusion gene encoding the first 70 amino acids of Ufd2a, a ubiquitin-chain assembly factor, that is linked to the complete coding sequence of nicotinamide mononucleotide adenylyltransferase 1 (NMAT1). Here, we demonstrate that resistance of WldS mice to axonal degeneration after blast-mediated TBI is associated with preserved function in hippocampal-dependent spatial memory, cerebellar-dependent motor balance, and retinal and optic nerve–dependent visual function. Thus, early axonal degeneration is likely a critical driver of subsequent neurobehavioral complications of blast-mediated TBI. Future therapeutic strategies targeted specifically at mitigating axonal degeneration may provide a uniquely beneficial approach to treating patients suffering from the effects of blast-mediated TBI.