Abstract

Recent development in molecular imaging enables measurement of fibrillar amyloid plaque in Alzheimer (AD) brain using positron emission tomography (PET). Three tracers (florbetapir, flutemetamol, florbetaben) have been approved by FDA and EMA for use in clinical assessment of memory impairment to exclude AD. The use of amyloid PET imaging is considered to be appropriate in patients with persistent and progressive unexplained mild cognitive impairment (MCI), in patients with established dementia with atypical clinical course or aetiology and in young patients with atypical-onset dementia. The focus of amyloid PET has so far been to understand the time course of amyloid plaque levels in AD and to use amyloid PET to discriminate between AD and patient with mild cognitive impairment (MCI) who will most likely or less likely convert to AD, respectively, at clinical follow-up. Very few studies have so far directly tested the added value of amyloid imaging as biomarker in diagnostic procedure and patient management in a clinical context. The present study reviews studies describing the possible role of PET amyloid imaging in excluding AD as well as strengthen the diagnosis of AD and detecting prodromal AD. Some studies report as a change in diagnosis following amyloid PET imaging and in therapeutic management and planning for the future for the patient and their family. Future clinical studies are needed to evaluate the appropriate clinical use of amyloid PET imaging in relation to cerebral glucose PET imaging, and CSF biomarkers.

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