About 1.5 million Americans acquire a traumatic brain injury every year, and an estimated 5.3 million people in the United States alone are living with disabilities that are related to traumatic brain injury. After sustaining such injuries, many would think of the cost of treatment— but the impairments in cognition and emotional/sensory systems are perhaps the worst cost. Luckily, many scientists and medical professionals around the world are currently doing research on possible therapeutic methods for the treatment of traumatic brain injury-- specifically through molecular and cellular neuroscience research.
In “CCR5 Is a Therapeutic Target for Recovery after Stroke and Traumatic Brain Injury,” a research team explored how interventions at the molecular level can help potentially aid in the recovery of neurological impairments and cognitive function caused by stroke or traumatic brain injury. In this research study, the team specifically focused on CCR5 signaling, which plays a role in recovery after both stroke and TBI brain injury. The team knew that increased CCR5 signaling is associated with both learning and memory reduction (Zhoi et al., 2016). They also knew that neuronal plasticity in the pre-motor-to-motor circuits after a case of stroke in the motor cortex is associated with motor recovery. This team’s experiment centered around pharmacological blockage, to test if CCR5 antagonists could potentially lead to recovery in learning and cognition in mice. The two tasks at the center of this experiment were a novel object recognition task, where the mice had to identify a novel object and were timed while doing so. The other task was a Barnes maze, where the mice were tested on spatial learning through their ability to spot the hole in the maze leading to a goal box. It was shown that animals that received maraviroc treatment (a CCR5 antagonist) after TBI had better and improved performances in the novel object recognition task after TBI, as well as better latency to find a hole leading to the goal box in a Barnes maze task. These results show how the knockdown of CCR5 in CA1 and CA3 and/or the pharmacological blockage of CCR5 can help aid in the recovery of learning and cognition following a traumatic brain injury.
However, is this the only potential therapeutic intervention for traumatic brain injury? Not quite. In “Neuromodulatory Interventions for Traumatic Brain Injury,” Theresa Pape and her colleagues explored different interventions for patients who have experienced traumatic brain injury. Similar to the previous science journal, these approaches explore interventions at the molecular and cellular level, which could then possibly help with the recovery of TBI-induced symptoms in both cognition and behavior. In this particular case, an intervention called “neuromodulatory intervention” was emphasized. In neuromodulatory intervention, signal transmission between neurons is altered— to be specific, this is done via mechanisms similar to the acquisition of LTP (or, long term potentiation), as well as LTD (long-term depression). By either initiating or enhancing signaling, we can modulate the activity between the neurons that make up the neural pathways that support sensorimotor functions, cognitive functions, and behavior, among other important aspects of functioning. This helps to partially restore and initiate the recovery of somatosensory and higher order cortically-based skills for patients who have experienced traumatic brain injury. Another potential therapeutic intervention explored was repetitive transcranial magnetic stimulation (rTMS). Through this intervention, stimulation of neurons is emphasized. Through three different parameters (focality of stimulation based on coils used, stimuli strength determined by pulse frequency, as well as pulse intensity and temporal patterns), manipulation can be induced, causing more rapid or slower neuronal activity, and therefore greater or slower neuronal depolarization. This is important, because neuronal activation can induce spreading from the surface of the brain to other regions of the brain in a “white matter connectivity-dependent matter,” as described by the team. This is extremely promising, as white matter is crucial for both cognitive and behavioral function. This can potentially help treat mild TBI neurocognitive and neuropsychiatric symptoms, such as disordered consciousness and attention impairments.
Therefore, while there is no permanent cure to the unfathomable effects of traumatic brain injury on human beings with real feelings and stories, it is clear to see that there is a possible light at the end of the tunnel with all of the research that is being implemented in order to help find treatments for such situations. Hopefully, with such findings as the results discussed in this summary, more funding can be put towards research in TBI recovery and experiments on the molecular/cellular level— especially since TBI can affect people from all walks of life, whether it be through sports injuries or car accidents. It is moments like these when we realize why science is important— to not only advance society, but to also enrich the lives of the people that make up society.
References:
1. Centers for Disease Control and Prevention. (2016, January 22). Report to congress: Traumatic brain injury in the United States. Centers for Disease Control and Prevention. https://www.cdc.gov/traumaticbraininjury/pubs/tbi_report_to_congress.html
2. Joy, M. T., Ben Assayag, E., Shabashov-Stone, D., Liraz-Zaltsman, S., Mazzitelli, J., Arenas, M., Abduljawad, N., Kliper, E., Korczyn, A. D., Thareja, N. S., Kesner, E. L., Zhou, M., Huang, S., Silva, T. K., Katz, N., Bornstein, N. M., Silva, A. J., Shohami, E., & Carmichael, S. T. (2019). CCR5 is a therapeutic target for recovery after stroke and Traumatic Brain Injury. Cell, 176(5). https://doi.org/10.1016/j.cell.2019.01.044
3. Bender Pape, T. L., Herrold, A. A., Guernon, A., Aaronson, A., & Rosenow, J. M. (2020). Neuromodulatory interventions for traumatic brain injury. Journal of Head Trauma Rehabilitation, 35(6), 365–370. https://doi.org/10.1097/htr.0000000000000643
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