Abstract #2394
DTI to Genetics: The Role of HFE H63D gene mutation in White Matter degeneration in APOE4 carrier of Alzheimer’s disease
Ran Pang1, Jianli Wang2, Prasanna Karunanayaka2, Samgan Kanekar2, Gela Beselia3, Samika Kanekar3, James R. Connor3, and Qing X. Yang4
1Departments of Neurosurgery, Pennsylvania State University College of Medicine, PA, United States; Department of Radiology, Dongfang Hospital, Beijing University of Chinese Medicine, Beijing, China, Hershey, PA, United States, 2Departments of Radiology, Pennsylvania State University Colle, Hershey, PA, United States, 3Departments of Neurosurgery, Pennsylvania State University College of Medicine, PA, United States, Hershey, PA, United States, 4Departments of 1Neurosurgery and 2Radiology, Pennsylvania State University College of Medicine, PA, United States, Hershey, PA, United States
Synopsis
HFE gene mutation involves iron metabolism, which is shown to directly contribute to myelination process. White matter degeneration in bi-genetic mutation (HFEH63D and ApoE4 allele) carriers was investigated using DTI from the AD Neuroimaging Initiative (ADNI) database. Comparing to the HFEWT/ApoE4+ group, mean diffusivity and radial diffusivity of inferior longitudinal fasciculus in the HFEH63D/ApoE4+ group demonstrated less integrity damage and fewer late-myelination loss with aging reflecting a possible mechanism as HFE polymorphism protective role in partly eliminating ApoE4 being the high-risk factor for AD progressing.
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