Niklas Mattsson1, Philip S Insel2, Michael Donohue3, Jonas Jögi4, Rik Ossenkoppele5, Tomas Olsson6, Michael Schöll7, Ruben Smith8, Oskar Hansson9. 1. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden; Lund University, Skåne University Hospital, Department of Clinical Sciences, Neurology, Lund, Sweden. Electronic address: niklas.mattsson@med.lu.se. 2. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; Center for Imaging of Neurodegenerative Diseases, Department of Veterans Affairs Medical Center, San Francisco, CA, USA; Department of Radiology and Biomedical Imaging, University of California, San Francisco, CA, USA. 3. Department of Neurology, Alzheimer's Therapeutic Research Institute, University of Southern California, San Diego, CA, USA. 4. Department of Clinical Physiology and Nuclear Medicine, Skåne University Hospital, Lund, Sweden. 5. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; VU University Medical Center, Department of Neurology and Alzheimer Center, Amsterdam Neuroscience, Amsterdam, the Netherlands. 6. Department of Radiation Physics, Skåne University Hospital, Lund, Sweden. 7. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; Wallenberg Centre for Molecular and Translational Medicine and the Department of Psychiatry and Neurochemistry, University of Gothenburg, Gothenburg, Sweden. 8. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; Lund University, Skåne University Hospital, Department of Clinical Sciences, Neurology, Lund, Sweden. 9. Clinical Memory Research Unit, Faculty of Medicine, Lund University, Lund, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden.
Abstract
INTRODUCTION: The relative importance of structural magnetic resonance imaging (MRI) and tau positron emission tomography (PET) to predict diagnosis and cognition in Alzheimer's disease (AD) is unclear. METHODS: We tested 56 cognitively unimpaired controls (including 27 preclinical AD), 32 patients with prodromal AD, and 39 patients with AD dementia. Optimal classifiers were constructed using the least absolute shrinkage and selection operator with 18F-AV-1451 (tau) PET and structural MRI data (regional cortical thickness and subcortical volumes). RESULTS: 18F-AV-1451 in the amygdala, entorhinal cortex, parahippocampal gyrus, fusiform, and inferior parietal lobule had 93% diagnostic accuracy for AD (prodromal or dementia). The MRI classifier involved partly the same regions plus the hippocampus, with 83% accuracy, but did not improve upon the tau classifier. 18F-AV-1451 retention and MRI were independently associated with cognition. DISCUSSION: Optimized tau PET classifiers may diagnose AD with high accuracy, but both tau PET and structural brain MRI capture partly unique information relevant for the clinical deterioration in AD.
INTRODUCTION: The relative importance of structural magnetic resonance imaging (MRI) and tau positron emission tomography (PET) to predict diagnosis and cognition in Alzheimer's disease (AD) is unclear. METHODS: We tested 56 cognitively unimpaired controls (including 27 preclinical AD), 32 patients with prodromal AD, and 39 patients with AD dementia. Optimal classifiers were constructed using the least absolute shrinkage and selection operator with 18F-AV-1451 (tau) PET and structural MRI data (regional cortical thickness and subcortical volumes). RESULTS: 18F-AV-1451 in the amygdala, entorhinal cortex, parahippocampal gyrus, fusiform, and inferior parietal lobule had 93% diagnostic accuracy for AD (prodromal or dementia). The MRI classifier involved partly the same regions plus the hippocampus, with 83% accuracy, but did not improve upon the tau classifier. 18F-AV-1451 retention and MRI were independently associated with cognition. DISCUSSION: Optimized tau PET classifiers may diagnose AD with high accuracy, but both tau PET and structural brain MRI capture partly unique information relevant for the clinical deterioration in AD.
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