Protein changes in cerebral cortex following a mild traumatic brain injury (mTBI) identified herein will help in the development of monitoring and response biomarkers that may translate to clinical mTBI.

A head concussion model in fruit flies reveals that early-life exposure to mild concussions significantly increases the risk of late-life neurodegeneration, with females especially vulnerable due to reproductive factors.

Use of a newly developed experimental model in fruit flies reveals that death following traumatic brain injury is largely due to a mechanism by which brain damage triggers disruption of the intestinal barrier, leading to elevated levels of glucose in the circulatory system with deleterious consequences.

Three-dimensional imaging and automated, brain-wide cell counting yield new insight into the diversity of neurons that connect the brain to the spinal cord and their different sensitivity to spinal cord damage.

Transcriptional analyses provide an atlas of how traumatic brain injury and aging shape meningeal cell composition and gene expression.

Local deep hypothermia combined with hibernation-mimicking cold protection is neuroprotective in a translatable large animal model of traumatic optic neuropathy.

Veterans with PTSD show increased attention to a history of unexpected outcomes during loss learning, both as measured by computational model-derived behavioral parameters and in increased neural signaling in amygdala and insula.

High mortality following traumatic brain injury in mice carrying a human mutation for familial hemiplegic migraine type 1 (FHM1) is caused by a decreased threshold for cortical spreading depolarizations (CSDs) and subsequent brain edema formation.

Traumatic injury leads to functional defects in nucleocytoplasmic transport and TDP-43 pathology in multiple model systems.

Promoting a Warburg-like shift in astrocytic metabolism through reduced mitochondrial electron transport accommodates the energetic burden caused by brain trauma without overwhelming cellular respiration and redox to salvage dopaminergic neurons.