Original Article

European Journal of Nuclear Medicine and Molecular Imaging

, Volume 36, Issue 5, pp 811-822

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

  • Lisa MosconiAffiliated withDepartment of Psychiatry, New York University School of MedicineCenter for Brain Health, MHL 400, New York University School of Medicine Email author 
  • , Rachel MisturAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Remigiusz SwitalskiAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Wai Hon TsuiAffiliated withDepartment of Psychiatry, New York University School of MedicineNathan Kline Institute
  • , Lidia GlodzikAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Yi LiAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Elizabeth PirragliaAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Susan De SantiAffiliated withDepartment of Psychiatry, New York University School of Medicine
  • , Barry ReisbergAffiliated withDepartment of Psychiatry, New York University School of Medicine
    • , Thomas WisniewskiAffiliated withDepartment of Psychiatry, New York University School of MedicineDepartment of Neurology, New York University School of MedicineDepartment of Pathology, New York University School of Medicine
    • , Mony J. de LeonAffiliated withDepartment of Psychiatry, New York University School of MedicineNathan Kline Institute

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Abstract

Purpose

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.

Methods

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.

Results

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.

Conclusion

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.

Keywords

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