Abstract
PurposeCerebral beta-amyloid and regional glucose metabolism assessed by positron emission tomography (PET) are used as diagnostic biomarkers for Alzheimer’s disease (AD). The present study validates the incremental diagnostic value of amyloid PET in addition to clinical diagnosis and [18F]FDG PET in a real-life memory clinic population.MethodsOf 138 consecutive patients with cognitive impairment who received combined [18F]FDG and [11C]PIB PET, 84 were diagnosed with major neurocognitive disorder (DSM-5) and included. Baseline clinical and [18F]FDG PET diagnoses were independently established with and without access to amyloid PET results and were dichotomized into AD or non-AD disorders. The incremental value of amyloid PET was evaluated in terms of: (1) the change in clinical and [18F]FDG PET diagnoses, (2) the change in agreement between clinical and [18F]FDG PET diagnoses, and (3) diagnostic accuracy using an interdisciplinary consensus diagnosis after an extended follow-up (2.4 ± 1.3 years after PET) as the reference.ResultsAfter disclosure of the amyloid PET results, clinical and [18F]FDG PET diagnoses changed in 23% and 18% of patients, respectively, and agreement between both ratings increased from 62% to 86% (p < 0.001). The accuracy of clinical and [18F]FDG PET diagnoses improved from 71% to 89% (p < 0.01) and from 76% to 94% (p < 0.001), respectively. The additional value of amyloid PET was rather uniform in relation to age at onset and consistency with appropriate use criteria.ConclusionAmyloid PET provides significant incremental diagnostic value beyond clinical and [18F]FDG PET diagnoses of AD. Given the high diagnostic accuracy of combined clinical and amyloid PET assessment, further studies are needed to clarify the role of an additional [18F]FDG PET scan in these patients.
Highlights
And correct differential diagnosis of dementia is of therapeutic and prognostic importance
All relevant medical charts were thoroughly reviewed by a board-certified dementia specialist (S.H.) in each patient and all relevant clinical information, including neuropsychological assessment, magnetic resonance imaging (MRI), computed tomography (CT), dopamine transporter single-photon emission CT (DAT SPECT), cerebrospinal fluid (CSF) biomarker and genetic testing, was incorporated into a clinical vignette, which had been developed based on current consensus criteria [3, 19,20,21,22,23,24,25]
According to the baseline clinical diagnosis on positron emission tomography (PET), 41 and 43 patients were classified as having Alzheimer’s disease (AD) and non-AD, respectively
Summary
And correct differential diagnosis of dementia is of therapeutic and prognostic importance. A multicentre post-mortem study [1] yielded a sensitivity and specificity of only 71% each for a clinical diagnosis of ‘probable Alzheimer’s disease (AD)’ and of 83% and 55% for ‘possible AD’, respectively, when the clinical diagnosis was based on the 1984 criteria of McKhann et al [2]. According to the revised criteria [3], imaging of regional cerebral glucose metabolism (with [18F]FDG) and of cerebral beta-amyloid deposits with positron emission tomography (PET) may be employed to enhance diagnostic certainty. In the differential diagnostics of AD, the two approaches are complementary: [18F]FDG PET detects neurodegeneration and amyloid imaging detects underlying AD pathology. A combined assessment of neurodegeneration and amyloid pathology is proposed in the guidelines of McKhann et al [3] and is often performed in
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