In vivo Patterns of Tau Pathology, Amyloid-β Burden, and Neuronal Dysfunction in Clinical Variants of Alzheimer’s Disease

Article type: Short Communication

Authors: Dronse, Julian^{a; b; 1; *} | Fliessbach, Klaus^{c; d; 1} | Bischof, Gérard N.^{b; e} | von Reutern, Boris^{a; b} | Faber, Jennifer^{d; f} | Hammes, Jochen^e | Kuhnert, Georg^e | Neumaier, Bernd^{g; h} | Onur, Oezguer A.^{a; b} | Kukolja, Juraj^{a; b} | van Eimeren, Thilo^{a; b; d; e} | Jessen, Frank^{d; i} | Fink, Gereon R.^{a; b} | Klockgether, Thomas^{d; f} | Drzezga, Alexander^{d; e}

Affiliations: [a] Department of Neurology, University Hospital Cologne, Cologne, Germany | [b] Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Jülich, Germany | [c] Department of Psychiatry and Psychotherapy, University Hospital Bonn, Bonn, Germany | [d] German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany | [e] Multimodal Neuroimaging Group, Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany | [f] Department of Neurology, University Hospital Bonn, Bonn, Germany | [g] Nuclear Chemistry, Institute of Neuroscience and Medicine (INM-5), Research Center Jülich, Jülich, Germany | [h] Institute of Radiochemistry and Experimental Molecular Imaging, University Hospital Cologne, Cologne, Germany | [i] Department of Psychiatry, University Hospital Cologne, Cologne, Germany

Correspondence: [*] Correspondence to: Julian Dronse, MD, Department of Neurology, University Hospital Cologne, Kerpener Str. 62, 50937 Cologne, Germany. Tel.: +49 221 478 97493; Fax: +49 221 478 86068; E-mail: julian.dronse@uk-koeln.de.

Note: [1] These authors contributed equally to this work.

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.

Keywords: Alzheimer’s disease, amyloid, ¹⁸F-AV-1451, ¹⁸F-FDG, molecular imaging, multimodal imaging, Pittsburghcompound B, positron-emission tomography, T-807, tau protein

DOI: 10.3233/JAD-160316

Journal: Journal of Alzheimer's Disease, vol. 55, no. 2, pp. 465-471, 2017