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PET Imaging of Amyloid and Tau in Alzheimer’s Disease

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Abstract

Alzheimer’s disease (AD) is characterized by the extracellular deposition of amyloid-β (Aβ) plaques, intracellular accumulation of hyperphosphorylated tau protein, and neuronal loss. Recent advances in the development of positron emission tomography (PET) radiotracers have clarified the neuropathological changes in the living brain. Amyloid PET tracers such as [11C]PiB, [18F]flutemetamol, [18F]florbetapir, [18F]florbetaben, and [18F]NAV4694 are able to detect the presence or absence of Aβ pathologies in the early stage of AD. Recent amyloid PET studies have demonstrated that Aβ accumulation is one of the earliest events in AD that precedes cognitive decline and that the amount of Aβ reaches a plateau upon the onset of dementia. Amyloid PET is essential for the development of new therapeutic strategies aimed at reducing Aβ burden and preventing the onset of dementia. After successful clinical application of amyloid PET tracers, several tau PET tracers, including [18F]flortaucipir and [18F]MK-6240, have been developed and introduced in clinical research. These tracers are highly sensitive to paired helical filaments of tau 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 PET could thus provide spatiotemporal information on the progression of tau pathology and facilitate accurate diagnosis and severity assessment of dementia when used in conjunction with amyloid PET.

Keywords

  • Alzheimer’s disease
  • Amyloid-β
  • Imaging
  • Positron emission tomography (PET)
  • Tau

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Okamura, N., Harada, R. (2022). PET Imaging of Amyloid and Tau in Alzheimer’s Disease. In: Mori, N. (eds) Aging Mechanisms II . Springer, Singapore. https://doi.org/10.1007/978-981-16-7977-3_19

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