Abstract

In the past 10 years, the development and evaluation of PET tracers for imaging fibrillar amyloid in the human brain in patients with Alzheimer’s disease (AD) has been very successful. Brain β-amyloid plaque load is one of the “neuropathological hallmarks” of AD and has been implicated in the pathogenesis and therapy of AD. The recent approval of [F]florbetapir by the Food and Drug Administration (FDA) and the European Medicines Agency (EMA) in April and January 2013, respectively, for PET imaging of cerebral amyloid underlines the achievement of an important goal of molecular imaging, and emphasizes the potential role of this tool in the early diagnosis and management of patients with dementia. There are, however, some cautions concerning the use of brain amyloid radiotracers in clinical practice that have to be addressed. Therefore, the Alzheimer’s Association and the Society of Nuclear Medicine and Molecular Imaging (SNMMI) convened the Amyloid Imaging Taskforce (AIT). The AIT recently published their guidance report in which they describe “specific use criteria” which underlines their vision of the clinical utility of amyloid PET [1]. Since we believe that amyloid imaging will be an important new tool for routine clinical studies in the near future, we resolved to provide a brief description and evaluation of this new technique and the most important topics described in the report. In addition we provide some comments on the report [1]. A hallmark study by Klunk and coworkers, published in 2004, was the first study showing that the [C]-labelled tracer termed Pittsburgh Compound-B (PiB) is able to detect amyloid deposits in patients suffering from AD [2]. Subsequently many studies have replicated this finding [3–7]. Also, a substantial number of papers on [C]PiB PET have been published in the European Journal of Nuclear Medicine and

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