Amyloid positron emission tomography (PET) has recently emerged as a non-invasive neuroimaging technique for visualizing the accumulation of fibrillar
amyloid-beta in the living human brain. Among several proposed radioligand tracers,
Pittsburgh compound-B (PiB) has gained worldwide acceptance as a standard
amyloid PET probe in a very short period because of its strong impact. Several lines of evidences from PiB-PET studies have suggested that the accumulation of
amyloid-beta starts during the preclinical stage of
Alzheimer disease (AD) and reaches the plateau phase before or during the
mild cognitive impairment (MCI) stage. Therefore,
amyloid-beta may be useful as a
biomarker of AD, not only for the very early diagnosis but also for monitoring the
therapeutic effect of disease-modifying agents that may reduce the amount of deposited
amyloid-beta in the brains of patients with AD. Positive findings on
amyloid PET along with amnestic MCI has been shown to be a strong predictor of AD conversion. The
amyloid imaging technique is also useful to differentiate non-AD type degenerative disorders such as argyrophilic grain
dementia and neurofibrillary tangle-dominant
dementia, which are cumulatively called as
tauopathies. Recently, many
amyloid PET-positive and cognitively normal subjects were found in PiB-PET studies. PiB-PET studies on healthy subjects have also shown that
apolipoprotein (
APO) E4 boosts the accumulation of
amyloid-beta and may consequently accelerate the pathogenesis of AD. In order to evaluate the clinical significance of positive and negative findings on
amyloid PET, further prospective studies and comparison studies on PET pathology are essential.