| Literature DB >> 27802224 |
Julian Dronse1,2, Klaus Fliessbach3,4, Gérard N Bischof2,5, Boris von Reutern1,2, Jennifer Faber4,6, Jochen Hammes5, Georg Kuhnert5, Bernd Neumaier7,8, Oezguer A Onur1,2, Juraj Kukolja1,2, Thilo van Eimeren1,2,4,5, Frank Jessen4,9, Gereon R Fink1,2, Thomas Klockgether4,6, Alexander Drzezga4,5.
Abstract
The clinical heterogeneity of Alzheimer's disease is not reflected in the rather diffuse cortical deposition of amyloid-β. We assessed the relationship between clinical symptoms, in vivo tau pathology, amyloid distribution, and hypometabolism in variants of Alzheimer's disease using novel multimodal PET imaging techniques. Tau pathology was primarily observed in brain regions related to clinical symptoms and overlapped with areas of hypometabolism. In contrast, amyloid-β deposition was diffusely distributed over the entire cortex. Tau PET imaging may thus serve as a valuable biomarker for the localization of neuronal injury in vivo and may help to validate atypical subtypes of Alzheimer's disease.Entities:
Keywords: 18F-AV-1451; 18F-FDG; Alzheimer’s disease; Pittsburghcompound B; T-807; amyloid; molecular imaging; multimodal imaging; positron-emission tomography; tau protein
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Year: 2017 PMID： 27802224 DOI： 10.3233/JAD-160316
Source DB: PubMed Journal: J Alzheimers Dis ISSN： 1387-2877 Impact factor: 4.472