A recently conducted scientific study uncovers significant connections between repetitive head impacts (RHI), chronic traumatic encephalopathy (CTE), and hippocampal sclerosis (HS), a brain condition characterized by loss of neurons and hardening of the ventricles in the hippocampus. This important research emphasizes the role of head trauma in facilitating severe neurological conditions.
CTE, a neurodegenerative disease, is widely linked to instances of RHI, which often occur in contact sports or professions with a high risk of head injury. In this study, researchers investigated the presence and prevalence of HS and the protein known as transactive response DNA-binding protein with 43 kDa (TDP-43) in cases of CTE. TDP-43 is associated with several neurodegenerative disorders and is often found in abnormal aggregates in patients’ brain cells.
The team examined two distinct groups: 401 participants with a history of RHI and confirmed CTE at autopsy, and a smaller cohort of 33 participants with HS-aging, a condition characterized by cognitive impairment associated with aging, but without CTE.
The findings revealed that HS was present in 23.4% of the CTE group, and TDP-43 inclusions were observed in 43.3% of the same participants. Interestingly, the occurrence of HS in the CTE group was at a relatively young age (with a mean of 77.0 years), indicating a potential correlation with years of exposure to RHI. This finding suggests that repetitive head injuries may accelerate the onset of HS.
The presence of TDP-43 inclusions was noted more frequently in the frontal cortex, a brain region often linked to cognitive functions such as decision making and social behavior. These inclusions were observed in both the presence and absence of limbic TDP-43, another form of the protein found in the limbic system, which manages emotions and memory.
A structural equation model, a sophisticated statistical model used for hypothesis testing, further reinforced the link between RHI and neurological damage. The model showed that exposure years to RHI were associated with an increase in hippocampal TDP-43 inclusions, a connection mediated by an increased CTE stage.
In conclusion, the study provided substantial evidence that repetitive head impacts and the resultant CTE pathology may contribute to the deposition of TDP-43 and development of hippocampal sclerosis. Further research is needed to fully understand these relationships and the potential for therapeutic interventions.
