Faculty of Computing, Health and Science
School of Medical Sciences
β-amyloid has been shown to play a crucial role in Alzheimer's disease (AD). In vivo β-amyloid imaging using [11C] Pittsburgh compound B (PiB) positron emission tomography has made it possible to analyze the relationship between β-amyloid deposition and different pathological markers involved in AD. PiB allows us to stratify the population between subjects which are likely to have prodromal AD, and those who don't. The comparison of the cortical thickness in these different groups is important to better understanding and detect the first symptoms of the disease which may lead to an earlier therapeutic care to reduce neurone loss. Several techniques have been developed to compare the cortical volume and/or thickness between AD and HC groups. However due to the noise introduced by the cortical thickness estimation and by the registration, these methods do not allow to unveil any major different when comparing prodromal AD groups with healthy control subjects group. To improve our understanding of where initial Alzheimer neurodegeneration occurs in the cortex we have developed a surface based technique, and have applied it to the discrimination between PIB-positive and PiB-negative HCs. We first identify the regions where AD patients show high cortical atrophy by using an AD/PiB-HC vertex-wise T-test. In each of these discriminating regions, comparison between PiB+ HC, PiB-HC and AD are performed. We found some significant differences between the two HC groups in the hippocampus and in the temporal lobe for both hemisphere and in the precuneus and occipital regions only for the left hemisphere.