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Glucose metabolism and PIB binding in carriers of a His163Tyr presenilin 1 mutation
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2011 (English)In: Neurobiology of Aging, ISSN 0197-4580, E-ISSN 1558-1497, Vol. 32, no 8, 1388-1399 p.Article in journal (Refereed) Published
Abstract [en]

Six young related pre-symptomatic carriers of a His163Tyr mutation in the presenilin 1 gene who will develop early onset familial Alzheimer's disease (eoFAD), and a control group of 23 non-carriers underwent (18)F-fluorodeoxyglucose positron emission tomography (FDG PET). The mutation carriers were followed-up after 2 years. Multivariate analysis showed clear separation of carriers from non-carriers on both occasions, with the right thalamus being the region contributing most to group differentiation. Statistical parametric mapping (SPM) revealed in the carriers non-significantly lower thalamic cerebral glucose metabolism (CMRglc) at baseline and significantly decreased CMRglc in the right thalamus at follow-up. One mutation carrier was followed-up with FDG PET 10 years after baseline and showed reductions in cognition and CMRglc in the posterior cingulate and the frontal cortex. This subject was diagnosed with AD 1 year later and assessed with an additional FDG as well as an (11)C-PIB PET scan 12 years after baseline. Global cortical CMRglc and cognition were distinctly decreased. PIB binding was comparable with sporadic AD patterns but showing slightly higher striatal levels.

Place, publisher, year, edition, pages
2011. Vol. 32, no 8, 1388-1399 p.
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Medical and Health Sciences
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URN: urn:nbn:se:uu:diva-123413DOI: 10.1016/j.neurobiolaging.2009.08.016ISI: 000293028500004PubMedID: 19796846OAI: oai:DiVA.org:uu-123413DiVA: diva2:313918
Available from: 2010-04-27 Created: 2010-04-27 Last updated: 2017-12-12Bibliographically approved

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Wall, AndersLångström, BengtLannfelt, Lars

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Section of Nuclear Medicine and PETDepartment of Biochemistry and Organic ChemistryGeriatrics
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