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Article type: Review Article
Authors: Abisambra, Jose F.; * | Scheff, Stephen
Affiliations: Sanders Brown Center on Aging, University of Kentucky, Lexington, KY, USA
Correspondence: [*] Correspondence to: Jose F. Abisambra, Sanders Brown Center on Aging, University of Kentucky, 800 S Limestone Street, Lexington, KY 40536-0230, USA. Tel.: +1 859 323 6040/Ext. 488; E-mail: joe.abisambra@uky.edu.
Abstract: Traumatic brain injury (TBI) is the most common form of head injury and is a leading cause of death worldwide. Due to the vast variability in the types and severity of trauma, the cellular consequences of head injury are not completely understood. The development of reliable models of TBI will aid in understanding the molecular consequences of head trauma, and they will assist in identifying biological surrogate markers of the degree of damage and prognosis. In doing so, effective therapeutic strategies can be applied. Current in vivo experimental models yield important information, but they too have a significant amount of variation. The goal of this review is to re-evaluate the use of these in vivo models of TBI and assess whether they correlate with the consequence of TBI in humans from the perspective of tau, an axonal microtubule-stabilizing protein. We present and discuss the current models of traumatic head injury, and we focus on those that assess changes in tau. We evaluate reports of TBI in humans that measured changes in tau and that were detectable in serum and cerebrospinal fluid, and as a pathological consequence in brain tissue.
Keywords: Alzheimer's disease, chronic traumatic encephalopathy, tau, tau post-translational modification, traumatic brain injury
DOI: 10.3233/JAD-131019
Journal: Journal of Alzheimer's Disease, vol. 40, no. 3, pp. 495-518, 2014
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