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Low PiB PET retention in presence of pathologic CSF biomarkers in Arctic APP mutation carriers.

Journal article
Authors Michael Schöll
Anders Wall
Steinunn Thordardottir
Daniel Ferreira
Nenad Bogdanovic
Bengt Långström
Ove Almkvist
Caroline Graff
Agneta Nordberg
Published in Neurology
Volume 79
Issue 3
Pages 229-36
ISSN 1526-632X
Publication year 2012
Published at
Pages 229-36
Language en
Links dx.doi.org/10.1212/WNL.0b013e31825f...
www.ncbi.nlm.nih.gov/entrez/query.f...
Keywords Adult, Aged, Alzheimer Disease, cerebrospinal fluid, diagnostic imaging, genetics, Amyloid beta-Peptides, cerebrospinal fluid, genetics, Aniline Compounds, Atrophy, Biomarkers, cerebrospinal fluid, Carbon Radioisotopes, Cognition, physiology, Female, Fluorodeoxyglucose F18, Humans, Image Processing, Computer-Assisted, Magnetic Resonance Imaging, Male, Middle Aged, Mutation, genetics, Neuropsychological Tests, Peptide Fragments, cerebrospinal fluid, Presenilin-1, genetics, Radionuclide Imaging, Radiopharmaceuticals, Thiazoles, tau Proteins, cerebrospinal fluid
Subject categories Medical Biotechnology, Clinical Medicine

Abstract

To investigate the particular pathology of the Arctic APP (APParc) early-onset familial Alzheimer disease (eoFAD) mutation for the first time in vivo with PET in comparison with other eoFAD mutations and sporadic Alzheimer disease (sAD).We examined 2 APParc mutation carriers together with 5 noncarrier siblings cross-sectionally with (11)C-labeled Pittsburgh compound B (PiB) and (18)F-fluorodeoxyglucose (FDG) PET, as well as MRI, CSF biomarkers, and neuropsychological tests. Likewise, we examined 7 patients with sAD, 1 carrier of a presenilin 1 (PSEN1) mutation, 1 carrier of the Swedish APP (APPswe) mutation, and 7 healthy controls (HCs).Cortical PiB retention was very low in the APParc mutation carriers while cerebral glucose metabolism and CSF levels of Aβ(1-42), total and phosphorylated tau were clearly pathologic. This was in contrast to the PSEN1 and APPswe mutation carriers revealing high PiB retention in the cortex and the striatum in combination with abnormal glucose metabolism and CSF biomarkers, and the patients with sAD who showed typically high cortical PiB retention and pathologic CSF levels as well as decreased glucose metabolism when compared with HCs.The lack of fibrillar β-amyloid (Aβ) as visualized by PiB PET in APParc mutation carriers suggests, given the reduced glucose metabolism and levels of Aβ(1-42) in CSF, that other forms of Aβ such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease.

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