PT  - JOURNAL ARTICLE
AU  - Terry C. Yin
AU  - Jaymie R. Voorhees
AU  - Rachel M. Genova
AU  - Kevin C. Davis
AU  - Ashley M. Madison
AU  - Jeremiah K. Britt
AU  - Coral J. Cintrón-Pérez
AU  - Latisha McDaniel
AU  - Matthew M. Harper
AU  - Andrew A. Pieper
TI  - Acute Axonal Degeneration Drives Development of Cognitive, Motor, and Visual Deficits after Blast-Mediated Traumatic Brain Injury in Mice
AID  - 10.1523/ENEURO.0220-16.2016
DP  - 2016 Sep 01
TA  - eneuro
PG  - ENEURO.0220-16.2016
VI  - 3
IP  - 5
4099  - http://www.eneuro.org/content/3/5/ENEURO.0220-16.2016.short
4100  - http://www.eneuro.org/content/3/5/ENEURO.0220-16.2016.full
SO  - eNeuro2016 Sep 01; 3
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.