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|Title:||Imaging tau and amyloid-β proteinopathies in Alzheimer disease and other conditions.|
|Authors:||Villemagne, Victor L;Doré, Vincent;Burnham, Samantha C;Masters, Colin L;Rowe, Christopher C|
|Affiliation:||Department of Molecular Imaging and Therapy, Centre for PET, Austin Health, Heidelberg, Victoria, Australia|
Department of Medicine, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia
The Florey Institute of Neuroscience and Mental Health and University of Melbourne, Parkville, Victoria, Australia
CSIRO, Health and Biosecurity Flagship, The Australian eHealth Research Centre, Royal Brisbane and Women's Hospital, Herston, Queensland, Australia
eHealth, CSIRO Health and Biosecurity, Melbourne, Parkville, Victoria, Australia
|Citation:||Nature reviews. Neurology 2018; 14(4): 225-236|
|Abstract:||Most neurodegenerative disorders are associated with aggregated protein deposits. In the case of Alzheimer disease (AD), extracellular amyloid-β (Aβ) aggregates and intracellular tau neurofibrillary tangles are the two neuropathological hallmarks of the disease. Aβ-PET imaging has already been approved for clinical use and is being used in clinical trials of anti-Aβ therapies both for patient recruitment and as an outcome measure. These studies have shown that Aβ accumulation is a protracted process that can extend for more than 2 decades before the onset of clinical AD. This Review describes how in vivo brain imaging of Aβ pathology has revolutionized the evaluation of patients with clinical AD by providing robust and reproducible statements of global or regional brain Aβ burden and enabling the monitoring of disease progression. The role of selective tau imaging is discussed, focusing on how longitudinal tau and Aβ imaging studies might reveal the various effects (sequential and/or parallel, independent and/or synergistic) of these proteins on progression, cognition and other disease-specific biomarkers of neurodegeneration. Finally, imaging studies are discussed in the context of elucidating the respective roles of Aβ and tau in AD and in advancing our understanding of the relationship and/or interplay between these two proteinopathies.|
|Appears in Collections:||Journal articles|
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