APOE ε2 Potential Protection Against Long-Term Consequences of Traumatic Brain Injury

Traumatic brain injury (TBI) can alter the quality of life, often resulting in cognitive decline, neurodegeneration, or death. There have been no biological advances to resolve the long-term consequences of TBI. The APOE ε2 gene is well known as a neuroprotectant against neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. However, the biological mechanisms of how APOE ε2 protects against neurodegeneration are unknown. The purpose of this study is to investigate APOE ε2’s response to an environmental stimulus that leads to neurodegeneration, TBI, and further investigate APOE ε2’s biological mechanisms. After inflicting blunt force trauma to our model organism, Drosophila melanogaster, longevity, activity, and molecular analyses allowed quantitative data to conclude the effects of the ectopic expression of APOE ε2. The Kaplan-Meier survival curve indicated that flies carrying APOE ε2 had a higher probability of surviving beyond 20 days post-induced TBI than the non-mutated control group, suggesting a potential neuroprotective benefit. Flies were then placed in the Drosophila Activity Monitor (DAM) to further evaluate behavioral outcomes and functional resilience. The results suggest that when the ectopically expressed human APOE ε2 gene is present, it confers longevity and mitigates activity.