Kathryn E. Saatman

TL;DR: A new, multidimensional classification system should be developed for TBI clinical trials and it was agreed that preclinical models were vital in establishing pathophysiologic mechanisms relevant to specific pathoanatomic types of TBI and verifying that a given therapeutic approach improves outcome in these targeted TBI types.

TL;DR: The results suggest that this new model of parasagittal CCI in the mouse mimics a number of well-established sequelae observed in previously characterized brain injury models using other rodent species.

TL;DR: This paper will review the literature suggesting that alterations in intracellular calcium with resulting changes in gene expression, activation of reactive oxygen species (ROS), activation of intrACEllular proteases (calpains), expression of neurotrophic factors, and activation of cell death genes (apoptosis) may play a role in mediating delayed cell death after trauma.

TL;DR: This review focuses on the current state of knowledge of the role of calpains in TBI-induced neuropathology and effectiveness of calpain as a therapeutic target in the acute post-traumatic period.

TL;DR: Increasing the depth of impact led to similar structural alterations in neurons, astrocytes and the vasculature, but resulted in greater behavioral deficits and cortical and hippocampal cell death.