title: FDG-PET changes in brain glucose metabolism from normal cognition to pathologically verified Alzheimer's disease.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Psychiatry, New York University School of Medicine, New York, NY 10016, USA. lisa.mosconi@med.nyu.edu
authors.forename: Lisa
authors.initials: L
authors.lastname: Mosconi
authors.forename: Rachel
authors.initials: R
authors.lastname: Mistur
authors.forename: Remigiusz
authors.initials: R
authors.lastname: Switalski
authors.forename: Wai Hon
authors.initials: WH
authors.lastname: Tsui
authors.forename: Lidia
authors.initials: L
authors.lastname: Glodzik
authors.forename: Yi
authors.initials: Y
authors.lastname: Li
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Pirraglia
authors.forename: Susan
authors.initials: S
authors.lastname: De Santi
authors.forename: Barry
authors.initials: B
authors.lastname: Reisberg
authors.forename: Thomas
authors.initials: T
authors.lastname: Wisniewski
authors.forename: Mony J
authors.initials: MJ
authors.lastname: de Leon
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D000544:Alzheimer Disease / Q000175:diagnosis* / Q000000981:diagnostic imaging*; D001344:Autopsy; D001921:Brain / Q000378:metabolism*; D003072:Cognition Disorders / Q000175:diagnosis / Q000000981:diagnostic imaging; D015140:Dementia, Vascular / Q000175:diagnosis / Q000000981:diagnostic imaging; D005260:Female; D019788:Fluorodeoxyglucose F18 / Q000494:pharmacology*; D005947:Glucose / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D020961:Lewy Body Disease / Q000378:metabolism; D008297:Male; D049268:Positron-Emission Tomography / Q000379:methods*
chemical_list: D019788:Fluorodeoxyglucose F18; D005947:Glucose