Alzheimer's disease (AD) is defined histologically by the presence of extracellular β-
amyloid (Aβ) plaques and intraneuronal neurofibrillary tangles in the cerebral cortex. The diagnosis of
dementia, along with the prediction of who will develop
dementia, has been assisted by magnetic resonance imaging and positron emission tomography (PET) by using [(18)F]fluorodeoxyglucose (FDG). These techniques, however, are not specific for AD. Based on the chemistry of histologic staining
dyes, several Aβ-specific positron-emitting radiotracers have been developed to image neuropathology of AD. Among these, [(
11)C]PiB is the most studied Aβ-binding PET
radiopharmaceutical in the world. The histologic and biochemical specificity of PiB binding across different regions of the AD brain was demonstrated by showing a direct correlation between Aβ-containing
amyloid plaques and in vivo [(
11)C]PiB retention measured by PET imaging. Because (11)C is not ideal for commercialization, several (18)F-labeled tracers have been developed. At this time, [(18)F]3'-F-PiB (
Flutemetamol), (18)F-AV-45 (
Florbetapir), and (18)F-AV-1 (
Florbetaben) are undergoing extensive phase II and III clinical trials. This article provides a brief review of the
amyloid biology and chemistry of Aβ-specific (11)C and (18)F-PET
radiopharmaceuticals. Clinical trials have clearly documented that PET
radiopharmaceuticals capable of assessing Aβ content in vivo in the brains of AD subjects and subjects with
mild cognitive impairment will be important as diagnostic agents to detect in vivo
amyloid brain pathology. In addition, PET
amyloid imaging will also help test the
amyloid cascade hypothesis of AD and as an aid to assess the efficacy of antiamyloid
therapeutics currently under development in clinical trials.