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.
