Mapping biochemistry to metabolism: FDG-PET and amyloid burden in Alzheimer's disease

Neuroreport. 1999 Sep 29;10(14):2911-7. doi: 10.1097/00001756-199909290-00007.


We evaluated the relationship between amyloid-beta protein (A beta) concentration and the metabolic abnormality in an Alzheimer's disease (AD) patient as measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET). Across most regions there were significant inverse correlations among FDG-PET intensity values and both insoluble. The temporal lobe samples showed no significant correlation between FDG-PET values and A beta deposition. Findings support A beta as contributing to the hypometabolism in regions of the AD brain that are still relatively viable metabolically; those regions with chronic pathologic damage, such as temporal cortex, may have other factors that contribute to metabolic deficits.

Publication types

  • Case Reports
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Aged
  • Aged, 80 and over
  • Algorithms
  • Alzheimer Disease / diagnostic imaging*
  • Alzheimer Disease / metabolism*
  • Amyloid beta-Peptides / metabolism*
  • Body Burden
  • Brain Chemistry / physiology
  • Brain Mapping
  • Fluorodeoxyglucose F18
  • Humans
  • Image Processing, Computer-Assisted
  • Male
  • Radiopharmaceuticals
  • Tomography, Emission-Computed


  • Amyloid beta-Peptides
  • Radiopharmaceuticals
  • Fluorodeoxyglucose F18