A Role for Myelin in Traumatic Brain Injury Deficits and Recovery
Abstract
Impact-acceleration forces to the head can cause traumatic brain injury (TBI). In many cases, including mild injuries, TBI produces traumatic axonal injury (TAI) within long axons of white matter tracts. In addition to TAI, we have shown that experimental TBI causes distinct myelin pathologies in the corpus callosum (CC), a large white matter tract commonly affected in human TBI cases. These pathologies include demyelination, defined as myelin loss along intact axons. Little is known about how these myelin pathologies arise or how they may affect patient deficits and eventual recovery. We explored to what extent demyelination may persist in an experimental mouse model of TBI where axonal pathology is attenuated. SARM1 activation is essential for execution of the conserved axon death pathway through which axon damage progresses to full degeneration. We assessed axon and myelin pathology in mice with genetic deletion of Sarm1 (Sarm1-/-) using ultrahigh resolution structural analysis in the CC at three days after TBI. Sarm1-/- mice had reduced axon degeneration as compared to littermate mice with the wild type gene. Furthermore, TBI-induced demyelination did not occur inSarm1-/- mice, suggesting a relationship between axon degeneration and demyelination.
Document Details
- Document Type
- Technical Report
- Publication Date
- Mar 22, 2019
- Accession Number
- AD1127963
Entities
People
- Christina M. Marion
Organizations
- Uniformed Services University of the Health Sciences