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Neurosciences: NeurologyNeurology Posters |
1 Centre for PET, Austin Hospital, Melbourne, Victoria, Australia; 2 Neuroscience and Neurology, Osaka City University Medical School, Osaka, Japan; 3 Prince of Wales Medical Research Institute, The University of New South Wales, Sydney, New South Wales, Australia; 4 Molecular Imaging Research Program, RIKEN, Kobe, Japan; 5 The Mental Health Research Institute, University of Melbourne, Melbourne, Victoria, Australia
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Objectives: Supported by compelling genetic data associated with the rare early onset familial Alzheimers disease (FAD), the Aβcentric theory states that Aβ is involved in the presymptomatic stages of sporadic Alzheimers disease (AD). Mutations of the APP, presenilin 1 (PS1), presenilin 2 (PS2) genes, or ApoE polymorphism lead to increased Aβ levels, even before symptoms arise. We evaluated the PiB retention pattern in individuals carrying either PS1 or APP mutations.
Methods: Three PS1 (31 yo male, 39 yo female, and a 52 yo female, respectively) and 1 APP (48 yo male) mutation carriers underwent 11C-PiB PET scans. Aβ burden was quantified using Standardized Uptake Value normalized to whole brain, given the high PiB retention in cerebellum and pons. PiB retention was compared against a well-characterized cohort of healthy controls (HC; n=30) and AD (n=30) patients.
Results: All mutation carriers had very high PiB retention in the striatum, with some presenting PiB retention in posterior cingulate/precuneus, and orbitofrontal cortices. The pattern of PiB retention was similar in the PS1 and APP mutation carriers. Neither striatal nor cortical Aβ burden nor the regional pattern of PiB retention was related to cognitive status.
Conclusions: Consistent with previous reports (Klunk et al., 2007), we found that FAD presents a different pattern of Aβ deposition than AD, with higher striatal and lower cortical PiB retention.
Research Support: Neurosciences Victoria
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