Kang Lai, Class of 2026

Traumatic Brain Injury (TBI) is one of the most common causes of cognitive defects affecting both physical and mental functions of the brain. Its implications span from cognitive defects to motor dysfunction to behavioral disorders–all of which permanently and severely diminish quality of life. TBI also greatly disrupts neurogenesis–the formation of new neurons– and neuronal stem cell regeneration. At the Department of Anesthesiology at Stony Brook University, researchers investigated TBI-induced neurodegeneration in mice and determined the fate of dividing cells in various brain regions. Using neuronal markers for astrocytes, microglia and oligodendrocytes, the mice were analyzed after 1-7 weeks following a lateral fluid percussion injury (LFPI). 

Mice were divided into 3 groups; intact control, trauma, and sham. Within each group, the mice were randomly divided into two subgroups to label for dividing cells. Click Histochemistry and immunohistochemistry were performed on brain sections to label EdU+ and DCX+ cells alongside other cell markers. These various cell markers are indicators of astrogliosis, neurogenesis, oligodendrogenesis, microgliosis, all terms to indicate the formation of new neuronal cell types. EdU-labeling specifically marked proliferating cells; in combination with other markers, this allowed for colocalization and visualization of the specific neuronal phenotype of dividing cells in weeks 1 and 7. 

Lateral fluid percussion injury triggered extensive proliferative responses. Through the aforementioned staining procedures, it was found that oligodendrogenesis occurred in the striatum and optic tract. This finding suggests that there are potential self-repair abilities in the nerve fibers occurring via remyelination in these regions, which is important for the regeneration of oligodendrocytes as well as determining factors for nervous tissue recovery and nerve fiber conductivity. Seven weeks post-LFPI, there was an increase in cell proliferation and dividing cells specifically in the optic tract. These results suggest that newborn cells potentially play a role in repairing damaged retinal axons. This, however, was not seen in the thalamus, where there was no increase in dividing cells. In addition to oligodendrogenesis, similar post-TBI neurogenesis was detected in the striatum, implicating the striatum as a potential neurogenic area despite the effects of TBI. 

From the results of this study, it is important to emphasize that LFPI triggers widespread neuronal proliferative response in non-neurogenic cortical and subcortical brain regions involving various glial cells. This suggests these specific brain regions may be most significant in neurogenesis, and they may be potential targets for repair mechanisms following TBI in future treatments or studies.

Figure 1: MRI of a brain with a TBI.

Works Cited: 

[1] Astakhova, O., Ivanova, A., Komoltsev, I., Gulyaeva, N., Enikolopov, G., & Lazutkin, A. (2025). Traumatic Brain Injury Promotes Neurogenesis and Oligodendrogenesis in Subcortical Brain Regions of Mice. Cells, 14(2), 92. https://doi.org/10.3390/cells14020092

[2] Image retrieved from: https://commons.wikimedia.org/wiki/File:Brain_injury_with_herniation_MRI.jpg