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P1‐312: Cortical thickness comparison between PiB‐positive and PiB‐negative healthy control patients
Author(s) -
Dore Vincent,
Bourgeat Pierrick,
Fripp Jurgen,
Acosta Oscar,
Chetelat Gael,
Szoeke Cassandra,
Ellis Kathryn,
Martins Ralph,
Villemagne Victor,
Masters Colin,
Ames David,
Rowe Christopher,
Salvado Olivier
Publication year - 2011
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2011.05.591
Subject(s) - pittsburgh compound b , biomarker , psychology , medicine , nuclear medicine , pathology , alzheimer's disease , disease , chemistry , biochemistry
International audienceBackground: Studies have showed that B-amyloid plaques are likely to only exhibit local affects on the cortex at early stages of the disease before or when early cognition impairments occur. Understanding when and where neurodegeneration starts in the cortex may provide insights into the pathogenesis of AD. In this study, we focus on elderly Healthy Control (HC). While the majority of subjects in this group have low neocortical PiB retention (PiB SURV<1.5), some present high PiB retention (PiB SURV>¼1.5), which is often seen as prodromal AD. In this abstract, we first identify discriminating regions using AD/PiB-negative HC analysis to then find difference between PiB-positive HC and PiB-negative HC. Methods: 119 subjects underwent a MRI scan and a 11C-PIB PET scans as part of the Australian Imaging, Biomarker and Lifestyle study. PiB scans were normalized using the standardized uptake value ratio (SUVR) method. In the subject cohort, 29 patients were AD, while the other 90 were HC; 33 of whom were PiB-positive and 57 were PiB-negative. We used a surface based approach to identify the regions where the cortical thickness in AD patients was significantly lower than PiB-negative HC. Individual mean cortical thicknesses were calculated in the significant patch of each AAL region. T-test analysis was performed between the 3 groups (AD, PiB-negative HC, PiB-positive HC) in each tessellated region while controlling for age. Results: In the discriminating regions of AD/PiB-negative (Figure 1), we showed that PiB-positive HC had significantly lower cortical thickness than PiB-negative HC in the hippocampus and amygdala region, in the precuneus and in the superior temporal gyrus in the left hemisphere Table 1). The regions in the right hemisphere showed the same patterns but were not significant. Conclusions: The results showed that atrophy patterns in PiB-positive HC group were similar to AD group but to a lesser extent, suggesting an effect of amyloid plaques early on in asymptomatic individuals