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July 17, 2012; 79 (3) Articles

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

Michael Schöll, Anders Wall, Steinunn Thordardottir, Daniel Ferreira, Nenad Bogdanovic, Bengt Långström, Ove Almkvist, Caroline Graff, Agneta Nordberg
First published June 13, 2012, DOI: https://doi.org/10.1212/WNL.0b013e31825fdf18
Michael Schöll
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Anders Wall
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Steinunn Thordardottir
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Daniel Ferreira
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Nenad Bogdanovic
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Bengt Långström
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Ove Almkvist
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Caroline Graff
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Agneta Nordberg
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Citation
Low PiB PET retention in presence of pathologic CSF biomarkers in Arctic APP mutation carriers
Michael Schöll, Anders Wall, Steinunn Thordardottir, Daniel Ferreira, Nenad Bogdanovic, Bengt Långström, Ove Almkvist, Caroline Graff, Agneta Nordberg
Neurology Jul 2012, 79 (3) 229-236; DOI: 10.1212/WNL.0b013e31825fdf18

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Abstract

Objective: 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).

Methods: We examined 2 APParc mutation carriers together with 5 noncarrier siblings cross-sectionally with 11C-labeled Pittsburgh compound B (PiB) and 18F-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).

Results: Cortical PiB retention was very low in the APParc mutation carriers while cerebral glucose metabolism and CSF levels of Aβ1-42, 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.

Conclusions: 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 Aβ1-42 in CSF, that other forms of Aβ such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease.

GLOSSARY

Aβ=
β-amyloid;
AD=
Alzheimer disease;
APParc=
Arctic APP;
APPswe=
Swedish APP mutation carrier;
CAA=
cerebral amyloid angiopathy;
eoFAD=
early-onset familial Alzheimer disease;
FDG=
18F-fluorodeoxyglucose;
MCI=
mild cognitive impairment;
MMSE=
Mini-Mental State Examination;
p-tau=
phosphorylated tau;
PiB=
Pittsburgh compound B;
sAD=
sporadic Alzheimer disease;
t-tau=
total tau;
varAD=
variant AD

Footnotes

  • Study funding: Supported by grants from the Knut and Alice Wallenberg Foundation, the Strategic Research Program in Neuroscience at Karolinska Institutet, the Swedish Research Council (project 05817 and 21738), the Swedish Brain Power, the Marianne and Marcus Wallenberg Foundation, the King Gustaf V and Queen Victoria's Foundation of Freemasons, the Old Servants Foundation, the Gun and Bertil Stohne's Foundation, the Brain Foundation, the Swedish Alzheimer Foundation, and the Regional Agreement on Medical Training and Clinical Research (ALF) between Stockholm County Council and the Karolinska Institutet.

  • Editorial, page 206

  • Supplemental data at www.neurology.org

  • Received September 2, 2011.
  • Accepted December 1, 2011.
  • Copyright © 2012 by AAN Enterprises, Inc.
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