title: Cognitively normal individuals with AD parents may be at risk for developing aging-related cortical thinning patterns characteristic of AD.
abstract: Children of Alzheimer's disease (AD) patients are at heightened risk of developing AD due to genetic influences, including the apolipoprotein E4 (ApoE4) allele. In this study, we assessed the earliest cortical changes associated with AD in 71 cognitively healthy, adult children of AD patients (AD offspring) as compared with 69 with no family history of AD (non-AD offspring). Cortical thickness measures were obtained using FreeSurfer from 1.5T magnetic resonance (MR) scans. ApoE genotyping was obtained. Primary analyses examined family history and ApoeE4 effects on cortical thickness. Secondary analyses examined age effects within groups. All comparisons were adjusted using False Discovery Rate at a significance threshold of p<0.05. There were no statistically significant differences between family history and ApoE4 groups. Within AD offspring, increasing age was related to reduced cortical thickness (atrophy) over large areas of the precuneus, superior frontal and superior temporal gyri, starting at around age 60. Further, these patterns existed within female and maternal AD offspring, but were absent in male and paternal AD offspring. Within non-AD offspring, negative correlations existed over small regions of the superior temporal, insula and lingual cortices. These results suggest that as AD offspring age, cortical atrophy is more prominent, particularly if the parent with AD is mother or if the AD offspring is female.
authors.affiliation: Department of Psychiatry and Behavioral Sciences, Northwestern University, Feinberg School of Medicine, Chicago, IL 60614, USA.
authors.forename: Katherine
authors.initials: K
authors.lastname: Reiter
authors.forename: Kathryn I
authors.initials: KI
authors.lastname: Alpert
authors.forename: Derin J
authors.initials: DJ
authors.lastname: Cobia
authors.forename: Mary J
authors.initials: MJ
authors.lastname: Kwasny
authors.forename: John C
authors.initials: JC
authors.lastname: Morris
authors.forename: John C
authors.initials: JC
authors.lastname: Csernansky
authors.forename: Lei
authors.initials: L
authors.lastname: Wang
mesh_terms: D000368:Aged; D000375:Aging / Q000502:physiology*; D000483:Alleles; D000544:Alzheimer Disease / Q000235:genetics / Q000473:pathology* / Q000523:psychology; D053327:Apolipoprotein E4 / Q000235:genetics; D002540:Cerebral Cortex / Q000473:pathology*; D005190:Family; D005260:Female; D007839:Functional Laterality / Q000502:physiology; D006801:Humans; D007091:Image Processing, Computer-Assisted; D016014:Linear Models; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D010290:Parents; D012306:Risk
chemical_list: D053327:Apolipoprotein E4