Diagnostic accuracy of markers for prodromal Alzheimer's disease in independent clinical series |
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| Institution: | 1. Laboratory of Epidemiology Neuroimaging and Telemedicine, and Unit for the Clinical Translation of Research, IRCCS Centro San Giovanni di Dio FBF, Brescia, Italy;2. Medical Imaging Unit, Biomedical Engineering Department, Mario Negri Institute for Pharmacological Research, Bergamo, Italy;3. University of Manchester, Manchester, UK;4. Banner Alzheimer''s Institute, Phoenix, AZ, USA;5. Helen Wills Neuroscience Institute, University of California, Berkeley, CA, USA;1. Ochsner Clinic Foundation, New Orleans, Louisiana;2. Groupe D׳analyse, Ltée, Montreal, Quebec, Canada;3. Janssen Scientific Affairs, LLC, Raritan, New Jersey;1. Department of Food Science and Human Nutrition, Iowa State University, Ames, Iowa, USA;2. Department of Psychology, Iowa State University, Ames, Iowa, USA;3. Department of Neurology, University of Iowa, Iowa City, Iowa, USA;4. Bryan Alzheimer''s Disease Research Center, Duke University, Durham, North Carolina, USA;5. Zinfandel Pharmaceuticals, Chapel Hill, North Carolina, USA;6. Geriatric Research Education and Clinical Center, Wm. S. Middleton Veterans Hospital, Madison, Wisconsin, USA;7. Wisconsin Alzheimer''s Disease Research Center, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA;8. Department of Health Sciences Research, Mayo Clinic (Rochester), Rochester, Minnesota, USA;9. Wisconsin Alzheimer''s Institute, University of Wisconsin School of Medicine and Public Health, Madison, Wisconsin, USA;1. Department of Clinical Radiology and Nuclear Medicine, University Medical Center Mannheim, Mannheim, Germany;2. Department of Radiology, German Cancer Research Center (DKFZ), Germany;3. Institute of Diagnostic and Interventional Radiology, University Hospital Zurich, Zurich, Switzerland;4. Department of Radiation Oncology, University Hospital Zurich, Zurich, Switzerland;5. Department of Surgery and Transplantation, University Hospital Zurich, Zurich, Switzerland;6. Medical Faculty Mannheim, University of Heidelberg, Mannheim, Germany;7. Department of Diagnostic and Interventional Radiology, University Hospital Bonn, Bonn, Germany;1. Cognition and Brain Plasticity Group [Bellvitge Biomedical Research Institute-] IDIBELL, L’Hospitalet de Llobregat, Barcelona 08097, Spain;2. Department of Basic Psychology, Campus Bellvitge, University of Barcelona, Barcelona 08097, Spain;3. Vision & Control of Action (VISCA) Group, Department of Basic Psychology, Campus Mundet, University of Barcelona, Barcelona 08035, Spain;4. Catalan Institution for Research and Advanced Studies, ICREA, Barcelona 08010, Spain |
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| Abstract: | ObjectiveTo capitalize on data from different clinical series to compare sensitivity and specificity of individual biomarkers for predicting mild cognitive impairment (MCI) progression to Alzheimer's disease (AD).MethodsMedial temporal atrophy, cortical hypometabolism, and cerebrospinal fluid biomarkers were assessed in 18 patients with mild cognitive impairment (MCI) with prodromal AD (pAD; conversion time, 26 ± 12 months) and 18 stable MCI (sMCI) patients from the Translational Outpatient Memory Clinic cohort, as well as in 24 pAD patients (conversion time, 36 ± 12 months) and 33 sMCI patients from the Alzheimer's Disease Neuroimaging Initiative cohort. Medial temporal atrophy was measured by manual, semi-automated, and automated hippocampal volumetry; cortical hypometabolism was measured using several indices of AD-related hypometabolism pattern; and cerebrospinal fluid markers were amyloid β (Aβ)42 and total tau protein concentrations. For each biomarker, sensitivity for pAD, specificity for sMCI, and diagnostic accuracy were computed.ResultsSensitivity to predict MCI conversion to AD in the Alzheimer's Disease Neuroimaging Initiative and Translational Outpatient Memory Clinic cohorts was 79% and 94% based on Aβ42, 46% and 28% based on hippocampal volumes, 33% to 66% and 56% to 78% based on different hypometabolism indices, and 46% and 61% based on total tau levels, respectively. Specificity to exclude sMCI was 27% and 50% based on Aβ42, 76% and 94% based on hippocampal volumes, 58% to 67% and 55% to 83% based on different hypometabolism indices, and 61% and 83% based on total tau levels, respectively.ConclusionsCurrent findings suggest that Aβ42 concentrations and hippocampal volumes may be used in combination to best identify pAD. |
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