This work demonstrates that HFE mutations in cognitively normal compared to wild-type subjects lead to differences in diffusion and relaxation parametrics, such that HFE mutation carrier parametrics converge towards AD subjects. Furthermore, HFE mutations appeared to be preservative against white matter integrity loss in AD patients. Iron-loading HFE mutations appear to preserve relaxation and diffusion neuroimaging biomarkers in AD patients, but adversely affect cognitively normal subjects.
This abstract and the presentation materials are available to members only; a login is required.