Pre-clinical detection of Alzheimer's disease using FDG-PET, with or without amyloid imaging Article Report uri icon


MeSH Major

  • Alzheimer Disease
  • Amyloid
  • Brain
  • Cognition Disorders
  • Positron-Emission Tomography


  • The development of prevention therapies for Alzheimer's disease (AD) would greatly benefit from biomarkers that are sensitive to subtle brain changes occurring in the preclinical stage of the disease. Early diagnostics is necessary to identify and treat at risk individuals before irreversible neuronal loss occurs. In vivo imaging has long been used to evaluate brain structural and functional abnormalities as predictors of future AD in non-demented persons. Prior to development of amyloid-β (Aβ) tracers for positron emission tomography (PET), the most widely utilized PET tracer in AD was 2-[18F]fluoro-2-Deoxy-D-glucose (FDG) PET. For over 20 years, FDG-PET has been used to measure cerebral metabolic rates of glucose (CMRglc), a proxy for neuronal activity, in AD. Many studies have shown that CMRglc reductions occur early in AD, correlate with disease progression, and predict histopathological diagnosis. This paper reviews reports of clinical and preclinical CMRglc reductions observed in association with genetic and non-genetic risk factors for AD. We then briefly review brain Aβ PET imaging studies in AD and discuss the potential of combining symptoms-sensitive FDG-PET measures with pathology-specific Aβ-PET to improve the early detection of AD. © 2010 - IOS Press and the authors.

publication date

  • January 2010



  • Report


Digital Object Identifier (DOI)

  • 10.3233/JAD-2010-091504

PubMed ID

  • 20182025

Additional Document Info

start page

  • 843

end page

  • 854


  • 20


  • 3