Abstract
Background: Apolipoprotein E (APOE) ɛ4 is associated with poor outcome following moderate to severe traumatic brain injury (TBI). There is a lack of studies investigating the influence of APOE ɛ4 on intracranial pathology following mild traumatic brain injury (MTBI). This study explores the association between APOE ɛ4 and MRI measures of brain age prediction, brain morphometry, and diffusion tensor imaging (DTI). Methods: Patients aged 16 to 65 with acute MTBI admitted to the trauma center were included. Multimodal MRI was performed 12 months after injury and associated with APOE ɛ4 status. Corrections for multiple comparisons were done using false discovery rate (FDR). Results: Of included patients, 123 patients had available APOE, volumetric, and DTI data of sufficient quality. There were no differences between APOE ɛ4 carriers (39%) and non-carriers in demographic and clinical data. Age prediction revealed high accuracy both for the DTI-based and the brain morphometry based model. Group comparisons revealed no significant differences in brain-age gap between ɛ4 carriers and non-carriers, and no significant differences in conventional measures of brain morphometry and volumes. Compared to non-carriers, APOE ɛ4 carriers showed lower fractional anisotropy (FA) in the hippocampal part of the cingulum bundle, which did not remain significant after FDR adjustment. Conclusion: APOE ɛ4 carriers might be vulnerable to reduced neuronal integrity in the cingulum. Larger cohort studies are warranted to replicate this finding.
Highlights
Following mild traumatic brain injury (TBI) (MTBI), most individuals recover quickly; the rate of recovery varies considerably
We report on fractional anisotropy (FA) and mean diffusivity (MD), estimated using dtifit in FMRIB Software Library (FSL)
There were no differences between the Apolipoprotein E (APOE) ε4 groups between complicated or uncomplicated MTBI or in type of injury or location
Summary
Following mild traumatic brain injury (TBI) (MTBI), most individuals recover quickly; the rate of recovery varies considerably. APOE ε4 has been shown to promote amyloid deposition in individuals with TBI [12] and the combination of MTBI and genetic risk for AD may play a role in the degeneration of structural brain integrity [13] These results highlight the intuitive notion that clinical and neuropathological outcomes following MTBI are determined by complex interactions between injury characteristics and genetic factors. By performing brain-age prediction based on sensitive MRI measures of brain morphometry and DTI measures of white matter architecture and coherence, we tested for associations between APOE ε4 status and brain-age gap in patients with MTBI at 12 months after injury. We report results from tests comparing ε4 carriers and non-carriers with regard to more conventional measures of brain morphometry and DTI measures
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