Dual-phase amyloid PET: hitting two birds with one stone

One of the major breakthroughs in Alzheimer's disease (AD) clinical research over the past two decades has been the validation of diagnostic biomarkers able to demonstrate the presence of pathological mechanisms of AD and to predict further cognitive decline and dementia onset in mild cognitive impairment (MCI) patients by identifying the prodromal stage of AD [1, 2]. Among AD biomarkers, two main categories exist: (1) amyloidosis biomarkers, able to identify a molecular feature typical of AD: these include cerebrospinal fluid (CSF) amyloid-?42 reduction and PET imaging using radiotracers selectively binding to the fibrillar aggregates of amyloid-? plaques; (2) neurodegeneration biomarkers reflecting neuronal injury, such as the increase of tau and phosphorylated-tau levels in the CSF, regional atrophy as measured by MRI and demonstration of synaptic dysfunction/degeneration by means of 18F-fluorodeoxyglucose (FDG) PET. Neurodegeneration biomarkers are useful tools for further differential diagnosis among amyloid positive and amyloid negative forms of dementia, and also a prognostic tool in the MCI population.