https://ogma.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:5479 Sat 24 Mar 2018 11:04:12 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:8131 .05, t-test). Diffuse cortical atrophy was detected for both ε4+ (p = .0001, permutation test) and ε4− patients (p = .0001, permutation test) relative to controls, and overall gray matter loss was about 15% in each patients group. Differences in gray matter loss between carriers and non-carriers mapped to the temporal cortex and right occipital pole (20% greater loss in carriers) and to the posterior cingulate, left orbitofrontal and dorsal fronto-parietal cortex (5–15% greater loss in non-carriers). APOE effect in AD was not significant (p > .74, ANOVA), but a significant APOE by region (temporal vs fronto-parietal cortex) interaction was detected (p = .002, ANOVA), in both early and late-onset patients (p < .05, ANOVA). We conclude that the ε4 allele modulates disease phenotype in AD, being associated with a pattern of differential temporal and fronto-parietal vulnerability.]]> Sat 24 Mar 2018 08:40:03 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:17666 Sat 24 Mar 2018 07:57:48 AEDT ]]> https://ogma.newcastle.edu.au/vital/access/ /manager/Repository/uon:24884 Sat 24 Mar 2018 07:14:55 AEDT ]]>