The relatively preliminary studies described here have begun to delineate aspects of the neurogenic response to TBI that should determine whether this phenomenon can be manipulated for therapeutic purposes. Clarifying the time course over which NPC proliferation, migration, differentiation, and integration occur after injury is necessary for defining therapeutic windows in which to attempt to augment these processes. From studies thus far, it is known that there are an increased number of neurons added to the rodent hippocampal circuitry, which survive for at least several weeks after injury. Without longer outcome data, it is still not certain that this event is not transitory, and, of course, its verification in the human brain is still pending. Likewise, it seems that neuroblasts from the rodent SVZ migrate toward damaged cortical areas; however, the verification of this phenomenon in the human brain would be even more remarkable, because, thus far, there is no evidence for baseline long-distance SVZ NPC migration in the human brain (along the lines of the rodent rostral migratory stream). It is likely that human NPCs do proliferate in response to TBI, but measuring this occurrence must be the first step in assessing the applicability of findings in rodent studies to the potential development of neurogenic therapies to be tested in clinical trials. Additionally, it remains challenging to attribute any improvement in neurologic function to the augmentation of neurogenesis by therapeutic agents, because many neurogenic compounds have complex effects on central nervous system physiology. Nonetheless, neurogenesis remains an exciting prospect for exploration in TBI research.
ASJC Scopus subject areas
- Clinical Neurology