Open AccessWallerian degeneration as a therapeutic target in traumatic brain injury
Author(s) -
Vassilis E. Koliatsos,
Athanasios Alexandris
Publication year - 2019
Publication title -
current opinion in neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 119
eISSN - 1473-6551
pISSN - 1350-7540
DOI - 10.1097/wco.0000000000000763
Subject(s) - wallerian degeneration , neuroscience , traumatic brain injury , medicine , degeneration (medical) , axon , neuroinflammation , astrogliosis , context (archaeology) , atf3 , disconnection , biology , pathology , central nervous system , disease , gene , paleontology , biochemistry , gene expression , promoter , psychiatry , political science , law
Diffuse or traumatic axonal injury is one of the principal pathologies encountered in traumatic brain injury (TBI) and the resulting axonal loss, disconnection, and brain atrophy contribute significantly to clinical morbidity and disability. The seminal discovery of the slow Wallerian degeneration mice (Wld) in which transected axons do not degenerate but survive and function independently for weeks has transformed concepts on axonal biology and raised hopes that axonopathies may be amenable to specific therapeutic interventions. Here we review mechanisms of axonal degeneration and also describe how these mechanisms may inform biological therapies of traumatic axonopathy in the context of TBI.