Abstract

In Alzheimer’s Disease (AD) dual-tracer positron emission tomography (PET) studies with 2-[18F]-fluoro-2-deoxy-D-glucose (FDG) and 11C-labelled Pittsburgh Compound B (PIB) are used to assess metabolism and cerebral amyloid-β deposition, respectively. Regional cerebral metabolism and blood flow (rCBF) are closely coupled, both providing an index for neuronal function. The present study compared PIB-derived rCBF, estimated by the ratio of tracer influx in target regions relative to reference region (R1) and early-stage PIB uptake (ePIB), to FDG scans. Fifteen PIB positive (+) patients and fifteen PIB negative (-) subjects underwent both FDG and PIB PET scans to assess the use of R1 and ePIB as a surrogate for FDG. First, subjects were classified based on visual inspection of the PIB PET images. Then, discriminative performance (PIB+ versus PIB-) of rCBF methods were compared to normalized regional FDG uptake. Strong positive correlations were found between analyses, suggesting that PIB-derived rCBF provides information that is closely related to what can be seen on FDG scans. Yet group related differences between method’s distributions were seen as well. Also, a better correlation with FDG was found for R1 than for ePIB. Further studies are needed to validate the use of R1 as an alternative for FDG studies in clinical applications.

Highlights

  • Several clinical studies were performed over the last years to validate biomarkers for evaluating the pathological mechanisms of Alzheimer’s disease (AD)

  • Positron emission tomography (PET) is becoming part of the clinical routine in Alzheimer’s Disease (AD), considering its ability to assess a broad range of these biomarkers and, of functional processes related to AD pathophysiology

  • Phamacokinetic analysis of dynamic Pittsburgh Compound B (PIB) positron emission tomography (PET) studies provides high-quality Regional cerebral metabolism and blood flow (rCBF) images comparable with those obtained by FDG standardized uptake value ratios (SUVR)

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Summary

Introduction

Several clinical studies were performed over the last years to validate biomarkers for evaluating the pathological mechanisms of Alzheimer’s disease (AD). The prodromal phase of AD, known as mild cognitive impairment (MCI), which is characterized by the onset of the earliest cognitive symptoms that do not meet dementia criteria, can present abnormal levels of these biomarkers [1]. In this context, positron emission tomography (PET) is becoming part of the clinical routine in AD, considering its ability to assess a broad range of these biomarkers and, of functional processes related to AD pathophysiology. PET imaging allows visual interpretation of the results for direct clinical use but, more importantly, provides quantitative brain data that may be used to further understand the pathophysiology [5]

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