Sarm1 as a Therapeutic Target for Chronic White Matter Pathology Following Experimental Traumatic Brain Injury

Abstract

Traumatic brain injury (TBI) can have long term consequences that include neurodegeneration and persistent symptoms. White matter tracts, such as the corpus callosum (CC), are particularly vulnerable and are associated with functional outcomes and potential neurodegenerative processes. Treatments are needed to protect axons from early traumatic axonal injury (TAI) and mitigate secondary mechanisms that lead to latest age neurodegeneration and atrophy. The SARM1 (sterile alpha and Toll/interleukin-1receptor motif containing 1) gene has been identified as a master executioner of the axon degeneration pathway and has become a significant target of interest in the development of therapeutic strategies to prevent axonal degradation. Our previous work demonstrated that mice with genetic deletion of Sarm1 exhibit significantly less acute axon damage and demyelination following a model of concussive TBI. This project aimed to determine if the constitutive absence of Sarm1 attenuates chronic white matter pathology and behavioral deficits following experimental TBI.

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Document Details

Document Type
Technical Report
Publication Date
Mar 19, 2021
Accession Number
AD1182968

Entities

People

  • Donald V Jr Bradshaw

Organizations

  • Uniformed Services University of the Health Sciences

Tags

Communities of Interest

  • Biomedical

DTIC Thesaurus Topics

  • Blood
  • Brain
  • Brain Injuries
  • Cells
  • Chemistry
  • Confocal Microscopy
  • Genetics
  • Health Services
  • Medical Personnel
  • Neurodegeneration
  • Neuroglia
  • Neuroimaging
  • Neurosciences
  • Peripheral Nervous System
  • Stem Cells
  • Three Dimensional

Readers

  • Neuroscience
  • Neurotrauma and Rehabilitation Medicine.
  • Traumatic Brain Injury (TBI) and Cognitive Aging in the Guam and Border Populations Affected by Alzheimer's Disease and Tau-Associated Dementias.

Technology Areas

  • Biotechnology