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Diagnostic accuracy of markers for prodromal Alzheimer's disease in independent clinical series
Author(s) -
Prestia Annapaola,
Caroli Anna,
Herholz Karl,
Reiman Eric,
Chen Kewei,
Jagust William J.,
Frisoni Giovanni B.
Publication year - 2013
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2012.09.016
Subject(s) - alzheimer's disease neuroimaging initiative , neuroimaging , medicine , atrophy , biomarker , memory clinic , cerebrospinal fluid , cognitive impairment , dementia , alzheimer's disease , cognitive decline , cohort , pathology , disease , cardiology , psychiatry , biochemistry , chemistry
Objective To 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). Methods Medial 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. Results Sensitivity 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. Conclusions Current findings suggest that Aβ42 concentrations and hippocampal volumes may be used in combination to best identify pAD.