PET Imaging of Amyloid and Tau in Alzheimer’s Disease

Abstract

Alzheimer’s disease (AD)Alzheimer’s disease (AD) is characterized by the extracellular deposition of amyloid-β (Aβ)Amyloid-β (Aβ) plaques, intracellular accumulation of hyperphosphorylated tauTau protein, and neuronal loss. Recent advances in the development of positron emission tomography (PET)Positron emission tomography (PET) radiotracers have clarified the neuropathological changes in the living brain. Amyloid PETAmyloid PET tracers such as [11C]PiBPiB, [18F]flutemetamolFlutemetamol, [18F]florbetapirFlorbetapir, [18F]florbetabenFlorbetaben, and [18F]NAV4694 are able to detect the presence or absence of AβAβ pathologies in the early stage of ADAD. Recent amyloid PETAmyloid PET studies have demonstrated that AβAβ accumulation is one of the earliest events in AD that precedes cognitive declineCognitive decline and that the amount of Aβ reaches a plateau upon the onset of dementiaDementia. Amyloid PETAmyloid PET is essential for the development of new therapeutic strategies aimed at reducing AβAβ burden and preventing the onset of dementiaDementia. After successful clinical application of amyloid PETAmyloid PET tracers, several tau PETTau PET tracers, including [18F]flortaucipirFlortaucipir and [18F]MK-6240, have been developed and introduced in clinical research. These tracers are highly sensitive to paired helical filaments of tauTau but are less sensitive to non-AD tau deposits. As expected from postmortem studies, the amount and spatial extent of tau tracer retention are strongly associated with the clinical severity and phenotype of dementia. Tau PETTau PET could thus provide spatiotemporal information on the progression of tauTau pathology and facilitate accurate diagnosis and severity assessment of dementia when used in conjunction with amyloid PETAmyloid PET.