As with spinal cord injury, the damaged tissue environment after traumatic brain injury heavily favors activation of proinflammatory M1 microglia [70]. Several studies demonstrating a protective effect of anti-inflammatory treatment indicate that the inflammatory response after trauma contributes to the ensuing damage [71-73]. The aftermath of traumatic brain injury results in a mixed profile of activated microglia and macrophages exhibiting a range of phenotypes [74]. However after one week, just like with spinal cord injury, the concentration of Arg1+ cells decreased to non-detectable levels [74], and other studies showed the presence of M1 microglia and proinflammatory cytokines weeks to months after traumatic brain injury [74-76]. This suggests that M1 microglia are the dominant phenotype and M2 cells are not present to repair damage. To highlight the importance M2 microglia might play after traumatic brain injury, it was observed in aged mice where the M2 response is impaired (discussed in a later section) that lesion size was increased relative to young animals with a more functional M2 response [70]. The M2 microglia observed during traumatic brain injury do seem to possess
