부산대학교 도서관

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.neurobiolaging.2006.10.030 Byline: Thomas Espeseth (a), Lars T. Westlye (a), Anders M. Fjell (a), Kristine B. Walhovd (a), Helge Rootwelt (b), Ivar Reinvang (a) Keywords: Apolipoprotein E; Cortical morphometry; Brain aging; Individual differences; Alzheimer's disease Abstract: Effects of APOE genotype on age-related slopes of cortical thinning was estimated by measuring the thickness of the cerebral cortex on a point-by-point basis across the cortical mantle in 96 healthy non-demented volunteers aged 48-75 years. Fifty nine were APOE E4- (no E4 allele) and 37 were E4+ (1 or 2 E4 alleles). The genotype groups had similar age, sex and IQ. Two T.sub.1-weighted MP-RAGE sequences were averaged for each participant to yield images with high signal-to-noise ratio, and quantified using semi-automated analysis tools. E4 carriers had thicker cortex than non-carriers in several frontal and temporal areas in both hemispheres, but showed a steeper age-related decline in adjacent areas. Upon comparison of the E4-specific age-related thinning with previously published patterns of thinning in normal aging and Alzheimer's disease (AD), we conclude that APOE E4 may function to accelerate thinning in areas found to decline in aging (medial prefrontal and pericentral cortex), but also to initiate thinning in areas associated with AD and amyloid-[beta] aggregation (occipitotemporal and basal temporal cortex). Author Affiliation: (a) Department of Psychology, University of Oslo, P.O. Box 1094, Blindern, N-0317 Oslo, Norway (b) Department of Medical Biochemistry, Rikshospitalet-Radiumhospitalet Medical Center, Oslo, Norway Article History: Received 19 May 2006; Revised 24 October 2006; Accepted 30 October 2006