Torgeir Hellstrøm1, Nada Andelic1,2, Ann-Marie G de Lange3,4,5, Eirik Helseth6,7, Kristin Eiklid8, Lars T Westlye3,9,10. 1. Department of Physical Medicine and Rehabilitation, Oslo University Hospital, 0424 Oslo, Norway. 2. Research Center for Habilitation and Rehabilitation Models and Services (CHARM), Institute of Health and Society, University of Oslo, 0318 Oslo, Norway. 3. Department of Psychology, Faculty of Social Sciences, University of Oslo, 0317 Oslo, Norway. 4. LREN, Centre for Research in Neurosciences-Department of Clinical Neurosciences, CHUV and University of Lausanne, 1011 Lausanne, Switzerland. 5. Department of Psychiatry, University of Oxford, Oxford OX3 7JK, UK. 6. Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0318 Oslo, Norway. 7. Department of Neurosurgery, Oslo University Hospital, 0424 Oslo, Norway. 8. Department of Medical Genetic, Oslo University Hospital, 0424 Oslo, Norway. 9. NORMENT, Division of Mental Health and Addiction, Oslo University Hospital, 0424 Oslo, Norway. 10. K.G Jebsen Center for Neurodevelopment Disorders, Faculty of Medicine, University of Oslo, 0318 Oslo, Norway.
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.
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.
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