期刊
NEUROLOGY
卷 79, 期 3, 页码 229-236出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1212/WNL.0b013e31825fdf18
关键词
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资金
- Knut and Alice Wallenberg Foundation
- Strategic Research Program in Neuroscience at Karolinska Institutet
- Swedish Research Council [05817, 21738]
- Swedish Brain Power
- Marianne and Marcus Wallenberg Foundation
- King Gustaf V and Queen Victoria's Foundation of Freemasons
- Old Servants Foundation
- Gun and Bertil Stohne's Foundation
- Brain Foundation
- Swedish Alzheimer Foundation
- Stockholm County Council
- Karolinska Institutet
- Sigurd and Elsa Goljes Foundation
- Swedish Brain Foundation
- Novartis
- GE Healthcare
- Johnson Johnson
- GSK
- Bayer
- Schering
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 C-11-labeled Pittsburgh compound B (PiB) and F-18-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 A beta(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. Conclusions: The lack of fibrillar beta-amyloid (A beta) as visualized by PiB PET in APParc mutation carriers suggests, given the reduced glucose metabolism and levels of A beta(1-42) in CSF, that other forms of A beta such as oligomers and protofibrils are important for the pathologic processes leading to clinical Alzheimer disease. Neurology(R) 2012;79:229-236
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