The only definitive method for diagnosing Alzheimer disease (AD) has been a combination of clinical diagnosis and findings of pathognomonic amyloid-β (Aβ) plaques and neurofibrillary tangles of hyperphosphorylated forms of the protein tau on examination of the brain at autopsy. In April 2012, however, the Food and Drug Administration approved Aβ positron emission tomography (PET) with florbetapir F-18 (Amyvid; Lilly USA) to identify areas of accumulation of Aβ plaques.1 The label for florbetapir F-18 states that a negative scan result indicates a reduced likelihood that any cognitive impairment is due to AD, but that a positive scan result does not establish a diagnosis of Alzheimer or any other neurodegenerative disease because excess Aβ is also found in adults with normal cognition. Although this review assessed the evidence for all purported diagnostic tests for AD, it focused on the evidence related to Aβ PET scans.
Pearson SD, Ollendorf DA, Colby JA. Amyloid-β Positron Emission Tomography in the Diagnostic Evaluation of Alzheimer Disease: Summary of Primary Findings and Conclusions. JAMA Intern Med. 2014;174(1):133–134. doi:10.1001/jamainternmed.2013.11711
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