Figure 3.

Changes in outcomes after adolescent TBI. Changes in metabolism, behavioral performances, neurodegeneration markers, inflammatory cytokines and hormones after mild-moderate TBI during adolescence are expressed over hours, days, and months post-injury. Changes are expressed as percentages relative to adolescent sham values. Metabolic: early dynamic changes in glucose, cerebral blood flow (CBF) with tendency for hyperemia in younger brain, decreases in adenosine triphosphate (ATP) and N-acetylaspartate (NAA), as well as regionally dynamic changes in calcium accumulation as measured by ⁴⁵Ca⁺⁺ accumulation. Behavior: Adolescent motor deficits (foot faults) and cognitive (novel object recognition, NOR) deficits recovery can be prolonged recovery, additional stressors like substance abuse can further impair cognitive/emotional recovery, social deficits observed early after injury and the normal process of synaptic pruning (i.e., failure to prune) after injury (spine density: M-males, F-females, with insert showing the post-TBI increase in branching and synapses). Neurodegeneration: Following repeat TBI (rTBI), there are acute changes in phosphorylated tau (PTau) and amyloid precursor protein (APP) after injuries. Long-term differences in ßAPP between 24 and 72 h injury intervals are observed in transgenic APP rats. Inflammation: Changes in numerous cytokines are shown along with glial fibrillary acidic protein (GFAP, red line), an astrocyte marker in males (solid) and females (dotted), ionized calcium-binding adaptor molecule-1 (Iba-1, black line) a microglia marker in males (solid) and females (dotted). Hormones: changes in sex hormones after TBI are shown for males and females.