Abstract

Amyloid positron emission tomography (PET) imaging with [11C]-PIB, which has high affinity for fibrillar Aβ, detects Aβ deposition in the brain and is a distinctive and reliable biomarker of Alzheimer's disease (AD) [18F]-labeled amyloid PET imaging, including [18F]-florbetapir, [18F]-flutemetamol, and [18F]-florbetaben, has recently been approved and replaces [11C]-PIB PET imaging in clinical practice. The procedures of amyloid PET imaging are performed according to protocol. In postmortem histopathology, these amyloid tracers have been shown to bind to Aβ plaques. Amyloid PET imaging can distinguish individuals with no or sparse amyloid plaques from those with moderate to frequent plaques. The diagnostic accuracy has been evaluated with visual and quantitative analysis. Amyloid PET imaging differentiated AD patients from healthy control subjects with a high degree of sensitivity and specificity. In addition, subjects with cognitively normal or mild cognitive impairment (MCI) progressed to MCI or AD dementia, respectively, when Aβ deposition was identified by amyloid PET imaging. Amyloid PET imaging can identify the status of the Aβ deposition of the underlying AD pathophysiology, increase diagnostic certainty, and alter management. In the predementia phase of AD, amyloid PET imaging can predict progression to AD dementia.

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