This title appears in the Scientific Report :
2016
Relationship of Tau Deposition and Hypometabolism in Alzheimer’s Disease: A Multimodal Imaging Approach Miami Florida, USA)
Relationship of Tau Deposition and Hypometabolism in Alzheimer’s Disease: A Multimodal Imaging Approach Miami Florida, USA)
Relationship of Tau Deposition and Hypometabolism in Alzheimer’s Disease: A Multimodal Imaging ApproachGérard N. Bischof 1,2, Jochen Hammes1, Julian Dronse2,3 ,Klaus Fliessbach4,5, Frank Jessen5,6, Bernd Neumaier7, Özgür Onur3, Juraj Kukolja3, Alexander Drzezga1,5 & Thilo van Eimeren1,2,31Multim...
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Personal Name(s): | Bischof, Gerard Nisal (Corresponding author) |
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Hammes, J. / Dronse, Julian / Fliessbach, K. / Jessen, F. / Neumaier, Bernd / Onur, Özgür / Kukolja, Juraj / Drzezga, A. / van Eimeren, Thilo | |
Contributing Institute: |
Nuklearchemie; INM-5 Kognitive Neurowissenschaften; INM-3 |
Imprint: |
2016
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Conference: | Human Amyloid Imaging Meeting, Miami, FL (United States), 2016-01-13 - 2016-01-15 |
Document Type: |
Abstract |
Research Program: |
(Dys-)function and Plasticity |
Publikationsportal JuSER |
Relationship of Tau Deposition and Hypometabolism in Alzheimer’s Disease: A Multimodal Imaging ApproachGérard N. Bischof 1,2, Jochen Hammes1, Julian Dronse2,3 ,Klaus Fliessbach4,5, Frank Jessen5,6, Bernd Neumaier7, Özgür Onur3, Juraj Kukolja3, Alexander Drzezga1,5 & Thilo van Eimeren1,2,31Multimodal Neuroimaging Group, Department of Nuclear Medicine, University Hospital Cologne, Cologne, Germany 2Cognitive Neuroscience, Institute of Neuroscience and Medicine (INM-3), Research Center Jülich, Jülich, Germany 3Department of Neurology, University Hospital Cologne, Cologne, Germany 4Department of Psychiatry and Psychotherapy, University Hospital Bonn, Bonn, Germany5 German Center for Neurodegenerative Diseases (DZNE)6Department of Psychiatry, University Hospital Cologne, Cologne, Germany 7Institute of Radiochemistry and Experimental Molecular Imaging, University of CologneIn Alzheimer’s Disease (AD), brain atrophy is preceded by gradual metabolic decline, as measured by [18F]FDG PET. Neuropathological hallmarks of the disease are beta-amyloid plaques (Aβ) and tau-based neurofibrillary tangles (Tau). While specific for AD, Aβ burden, as quantified by in vivo PET ligands, is largely unrelated to magnitude and topology of metabolic decline. The very recent development of [18F]AV-1451 (T807) for the in vivo quantification of Tau, allows us to test if tau pathology is more intimately linked to metabolic decline than Aβ. To this end, we adopted a multimodal imaging approach to investigate the relationship of regional glucose hypometabolism (assessed by [18F]FDG PET) with regional measures of Tau ([18F]AV-1451 PET), and Aβ ([11C]PiB PET) in six AD patients. We created z-score deviation images of [18F]AV-1451 and [18F]FDG PET using healthy controls as reference samples (significance threshold: z-score >2). Regional cortical deviation of [18F]AV-1451 uptake correlated strongly with regional glucose hypometabolism (r =.77, p <.001), whereas PiB uptake did not (r = -.01, n.s.) (see Figure, panel A). Deviation of tangle pathology and hypometabolism was most pronounced in brain regions known to be affected by hypometabolism consistently in AD, even in early stages (i.e., parietal cortex, posterior cingulate and temporal cortex). Consistent with the notion that regional tau deposition may precede regional glucose hypometabolism, we found more regions exhibiting exclusive tau deviations (Tau+), than regions with isolated hypometabolism (FDG+; see Figure, panel B). Overall, our results indicate a linear relationship of regional tau deposition and metabolic decline in AD and provide evidence for tau as a potential instigator of neurodegeneration in AD. |