Accelerated age-related cortical thinning in healthy carriers of apolipoprotein E 4

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 4− (no 4 allele) and 37 were 4+ (1 or 2 4 alleles). The genotype groups had similar age, sex and IQ. Two T1-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. 4 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 4-specific age-related thinning with previously published patterns of thinning in normal aging and Alzheimerʹs disease (AD), we conclude that APOE 4 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-β aggregation (occipitotemporal and basal temporal cortex).