A tale of two tracers: Glucose metabolism and amyloid positron emission tomography imaging in Alzheimer's disease Academic Article uri icon


MeSH Major

  • Adenocarcinoma
  • Antineoplastic Agents
  • Drug Resistance, Neoplasm
  • Esophageal Neoplasms
  • Esophagogastric Junction
  • Niacinamide
  • Phenylurea Compounds
  • Stomach Neoplasms


  • The development of prevention therapies for Alzheimer's disease (AD) would greatly benefit from biomarkers that are sensitive to subtle brain changes occurring prior to the onset of clinical symptoms, when the potential for preservation of function is at the greatest. In vivo brain imaging is a promising tool for the early detection of AD through visualization of abnormalities in brain structure, function and histopathology. Currently, Positron Emission Tomography (PET) imaging with amyloid-beta (Aβ) tracers and 2-[18F]fluoro-2-Deoxy-D-glucose (FDG) is largely utilized in the early and differential diagnosis of AD. Aβ PET tracers bind to Aβ plaques in brain, and provide an in vivo estimate of AD pathology. FDG-PET is used to measure glucose metabolism, a marker of brain activity. This paper reviews brain Aβ-and FDG-PET studies in AD patients as well as in non-demented individuals at risk for AD. We then discuss the potential of combining symptoms-sensitive FDG-PET measures with pathology-specific Aβ-PET to improve the early detection of AD. © 2011 The authors and IOS Press. All rights reserved.

publication date

  • December 2011



  • Academic Article


Digital Object Identifier (DOI)

  • 10.3233/978-1-60750-793-2-219

Additional Document Info

start page

  • 219

end page

  • 234


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