FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer’s disease

  • Lisa Mosconi
  • Rachel Mistur
  • Remigiusz Switalski
  • Wai Hon Tsui
  • Lidia Glodzik
  • Yi Li
  • Elizabeth Pirraglia
  • Susan De Santi
  • Barry Reisberg
  • Thomas Wisniewski
  • Mony J. de Leon
Original Article



We report the first clinicopathological series of longitudinal FDG-PET scans in post-mortem (PM) verified cognitively normal elderly (NL) followed to the onset of Alzheimer’s-type dementia (DAT), and in patients with mild DAT with progressive cognitive deterioration.


Four NL subjects and three patients with mild DAT received longitudinal clinical, neuropsychological and dynamic FDG-PET examinations with arterial input functions. NL subjects were followed for 13 ± 5 years, received FDG-PET examinations over 7 ± 2 years, and autopsy 6 ± 3 years after the last FDG-PET. Two NL declined to mild cognitive impairment (MCI), and two developed probable DAT before death. DAT patients were followed for 9 ± 3 years, received FDG-PET examinations over 3 ± 2 years, and autopsy 7 ± 1 years after the last FDG-PET. Two DAT patients progressed to moderate-to-severe dementia and one developed vascular dementia.


The two NL subjects who declined to DAT received a PM diagnosis of definite AD. Their FDG-PET scans indicated a progression of deficits in the cerebral metabolic rate for glucose (CMRglc) from the hippocampus to the parietotemporal and posterior cingulate cortices. One DAT patient showed AD with diffuse Lewy body disease (LBD) at PM, and her last in vivo PET was indicative of possible LBD for the presence of occipital as well as parietotemporal hypometabolism.


Progressive CMRglc reductions on FDG-PET occur years in advance of clinical DAT symptoms in patients with pathologically verified disease. The FDG-PET profiles in life were consistent with the PM diagnosis.


Dementia Alzheimer’s disease FDG-PET Positron emission tomography Early detection 

Supplementary material

259_2008_1039_MOESM1_ESM.doc (150 kb)
Supplementary File 1Diagram illustrating the first and last clinical examination, all PET scans, time of clinical change, and post-mortem examinations for every patient over time (years 1979–2004) (DOC 149 KB).
259_2008_1039_MOESM2_ESM.doc (402 kb)
Supplementary File 2FDG-PET scans showing medial temporal lobe (MTL) hypometabolism for each subject at the last PET scan, as compared to a healthy control with normal MTL CMRglc. The scans are reformatted to a plane parallel to the plane of the temporal lobe, a plane that runs approximately parallel to the long axis of the hippocampus at an infraorbital angulation of 20° to 25° negative to the canthomeatal plane. This axial orientation enables examination of the full anterior–posterior extent of the hippocampal region and most of the parahippocampal gyrus (Mosconi et al; Eur J Nucl Med Mol Imaging 2006; 33:210–21). CMRglc values are represented on a color-coded scale ranging from 0 to 50 μmol/100 g per minute (DOC 551 KB).


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Copyright information

© Springer-Verlag 2009

Authors and Affiliations

  • Lisa Mosconi
    • 1
    • 5
  • Rachel Mistur
    • 1
  • Remigiusz Switalski
    • 1
  • Wai Hon Tsui
    • 1
    • 4
  • Lidia Glodzik
    • 1
  • Yi Li
    • 1
  • Elizabeth Pirraglia
    • 1
  • Susan De Santi
    • 1
  • Barry Reisberg
    • 1
  • Thomas Wisniewski
    • 1
    • 2
    • 3
  • Mony J. de Leon
    • 1
    • 4
  1. 1.Department of PsychiatryNew York University School of MedicineNew YorkUSA
  2. 2.Department of NeurologyNew York University School of MedicineNew YorkUSA
  3. 3.Department of PathologyNew York University School of MedicineNew YorkUSA
  4. 4.Nathan Kline InstituteOrangeburgUSA
  5. 5.Center for Brain Health, MHL 400New York University School of MedicineNew YorkUSA

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