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 widely known as a neuroprotectant for neurodegenerative diseases such as Alzheimer’s and Parkinson’s. However, the biological mechanisms of how APOE ε2 protects the against neurodegeneration is unknown. The purpose of this study is to investigate APOE ε 2’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 ectopical expression of APOE ε2. The Kaplan-Meier curve indicated that flies carrying APOE ε2 had an increased probability of surviving beyond 20 days post induced TBI compared to nonmutated control group, suggesting a potential neuroprotective benefit. The One-way ANOVA further supports the claim with the injured mutant and uninjured control groups statistically mirroring one another. Flies were then placed in the Drosophila Activity Monitor (DAM) to further evaluate behavioral outcomes and functional resilience. Results of this assay express the functionality and activity levels of the flies remaining intact with similar qualitative results to non-induced flies. A western blot will allow for the probing for proteins to find an increase in amounts of injury-associated TAU. The results suggest that when the ectopically expressed human gene APOE ε2 longevity and activity increases significantly even mimicking the uninjured control group.