Journal article

Attenuated neurological deficit, cell death and lesion volume in Fas-mutant mice is associated with altered neuroinflammation following traumatic brain injury.

Jenna M Ziebell, Nicole Bye, Bridgette D Semple, Thomas Kossmann, Maria Cristina Morganti-Kossmann

Brain Res | Published : 2011

Abstract

Progressive neurodegeneration following traumatic brain injury (TBI) involves the Fas and TNF-receptor1 protein systems which have been implicated in mediating delayed cell death. In this study, we used two approaches to assess whether inhibition of these pathways reduced secondary brain damage and neurological deficits after TBI. Firstly, we investigated whether the expression of non-functional Fas in lpr mice subjected to TBI altered tissue damage and neurological outcome. Compared to wild-type, lpr mice showed improved neurological deficit (p=0.0009), decreased lesion volume (p=0.017), number of TUNEL+ cells (p=0.011) and caspase-3+ cells (p=0.007). Changes in cellular inflammation and cy..

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