Journal Article

FZJ-2016-07773

http://join2-wiki.gsi.de/foswiki/pub/Main/Artwork/join2_logo100x88.png In vivo Patterns of Tau Pathology, Amyloid-β Burden, and Neuronal Dysfunction in Clinical Variants of Alzheimer’s Disease

Dronse, J. (Corresponding author)FZJ* ; Fliessbach, K. ; Bischof, G. N.FZJ* ; von Reutern, B. ; Faber, J. ; Hammes, J. ; Kuhnert, G. ; Neumaier, B.FZJ* ; Onur, O. A. ; Kukolja, J.FZJ* ; van Eimeren, T.FZJ* ; Jessen, F. ; Fink, G. R.FZJ* ; Klockgether, T. ; Drzezga, A.

2017
IOS Press Amsterdam

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Please use a persistent id in citations: doi:10.3233/JAD-160316

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.

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Contributing Institute(s):

1. Kognitive Neurowissenschaften (INM-3)
2. Nuklearchemie (INM-5)

Research Program(s):

1. 572 - (Dys-)function and Plasticity (POF3-572) (POF3-572)

Appears in the scientific report 2016

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Database coverage:
; BIOSIS Previews ; Current Contents - Life Sciences ; Ebsco Academic Search ; IF < 5 ; JCR ; NCBI Molecular Biology Database ; No Authors Fulltext ; SCOPUS ; Science Citation Index Expanded ; Thomson Reuters Master Journal List ; Web of Science Core Collection

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