Purpose: The proof of concept for in vivo targeting of beta-amyloid plaques (Abeta) in patients with Alzheimer's disease (AD) by means of nuclear imaging methods has been shown in recent clinical studies.
Methods: For positron emission tomography (PET), the five compounds [(11)C]PIB, 3'[(18)F]FPIB, [(18)F]FDDNP, [(11)C]SB-13 and [(18)F]F-SB-13 have been developed by a formal charge neutralisation of agents used for staining of AD brain post mortem.
Results: In AD-patients, these compounds have been shown to possess a selective uptake in the brain regions known to have a high Abeta-load. Progress towards tracers with proportionality between tracer uptake and quantity of Abeta-load, of use for longitudinal studies of AD patients, is addressed in the current development of Abeta-tracers.
Conclusion: Despite the extensive information on the structure-affinity relationship of several Abeta-binding compounds, data on the regional brain binding kinetics-beyond uptake in healthy rodents-have been obtained only for a few compounds. Recent results indicate that PET-imaging of Abeta-deposits in transgenic rodent models of AD is feasible which may be valuable for a more relevant preclinical evaluation of Abeta-tracers.