. Arctic APP Mutation Carriers Show Low PIB PET Retention in the Presence of Pathological CSF Biomarkers and Reduced FDG Uptake. Human Amyloid Imaging Abstract. 2012 Jan 1;


Background: The dominantly inherited early-onset familial AD (eoFAD) has been proposed as a model to study early disease mechanism of Alzheimer´s disease (AD). Positron emission tomography (PET) using1C-PIB and8F-Flouro-deoxyglucose (18F-FDG) were used to characterize the pathological changes of Arctic APP(APParc) early-onset familial AD in comparison to other AD mutations and sporadic AD disease (sAD) and healthy controls (HCs). All subjects underwent neuropsychology tests as well as magnet resonance imaging (MRI) and cerebrospinal fluid (CSF) sampling. Seven member of the APParc family (two carriers and five non-carriers), seven sAD patients, one carrier of presenilin (PSEN1) mutation, one carrier of Swedish APP(APPswe) mutation and seven healthy controls (HCs) were examined. Low cortical PIB retention was observed in APParc mutation carriers which was in contrast to the high PIB retention measured in PSEN1 ,and APPswe carriers and sAD patients. Pathological CSF biomarkers (including low Aß42) and decreased cerebral glucose metabolism were observed in carriers of APParc as well as in other eo FAD mutation carriers. The lack of fibrillar amyloid, measured by1C-PIB in brain of APParc mutation carriers, combined with reduced Aß42 in CSF and decreased glucose metabolism underline the importance of non-fibrillar forms of Aß (oligomers, protofibrils) for the pathological processes leading to clinical AD.


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