title: Imaging amyloid deposition in Lewy body diseases.
abstract: BACKGROUND
  Extrapyramidal motor symptoms precede dementia in Parkinson disease (PDD) by many years, whereas dementia occurs early in dementia with Lewy bodies (DLB). Despite this clinical distinction, the neuropsychological and neuropathologic features of these conditions overlap. In addition to widespread distribution of Lewy bodies, both diseases have variable burdens of neuritic plaques and neurofibrillary tangles characteristic of Alzheimer disease (AD).
  
  
  OBJECTIVE
  To determine whether amyloid deposition, as assessed by PET imaging with the beta-amyloid-binding compound Pittsburgh Compound B (PiB), can distinguish DLB from PDD, and to assess whether regional patterns of amyloid deposition correlate with specific motor or cognitive features.
  
  
  METHODS
  Eight DLB, 7 PDD, 11 Parkinson disease (PD), 15 AD, and 37 normal control (NC) subjects underwent PiB-PET imaging and neuropsychological assessment. Amyloid burden was quantified using the PiB distribution volume ratio.
  
  
  RESULTS
  Cortical amyloid burden was higher in the DLB group than in the PDD group, comparable to the AD group. Amyloid deposition in the PDD group was low, comparable to the PD and NC groups. Relative to global cortical retention, occipital PiB retention was lower in the AD group than in the other groups. For the DLB, PDD, and PD groups, amyloid deposition in the parietal (lateral and precuneus)/posterior cingulate region was related to visuospatial impairment. Striatal PiB retention in the DLB and PDD groups was associated with less impaired motor function.
  
  
  CONCLUSIONS
  Global cortical amyloid burden is high in dementia with Lewy bodies (DLB) but low in Parkinson disease dementia. These data suggest that beta-amyloid may contribute selectively to the cognitive impairment of DLB and may contribute to the timing of dementia relative to the motor signs of parkinsonism.
authors.affiliation: Massachusetts General Hospital, Boston, MA 02114, USA.
authors.forename: S N
authors.initials: SN
authors.lastname: Gomperts
authors.forename: D M
authors.initials: DM
authors.lastname: Rentz
authors.forename: E
authors.initials: E
authors.lastname: Moran
authors.forename: J A
authors.initials: JA
authors.lastname: Becker
authors.forename: J J
authors.initials: JJ
authors.lastname: Locascio
authors.forename: W E
authors.initials: WE
authors.lastname: Klunk
authors.forename: C A
authors.initials: CA
authors.lastname: Mathis
authors.forename: D R
authors.initials: DR
authors.lastname: Elmaleh
authors.forename: T
authors.initials: T
authors.lastname: Shoup
authors.forename: A J
authors.initials: AJ
authors.lastname: Fischman
authors.forename: B T
authors.initials: BT
authors.lastname: Hyman
authors.forename: J H
authors.initials: JH
authors.lastname: Growdon
authors.forename: K A
authors.initials: KA
authors.lastname: Johnson
mesh_terms: D000368:Aged; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D000814:Aniline Compounds; D001921:Brain / Q000000981:diagnostic imaging / Q000378:metabolism*; D003071:Cognition; D003704:Dementia / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000209:etiology / Q000378:metabolism*; D003937:Diagnosis, Differential; D005260:Female; D006801:Humans; D020961:Lewy Body Disease / Q000503:physiopathology / Q000523:psychology*; D008297:Male; D008875:Middle Aged; D009068:Movement; D009483:Neuropsychological Tests; D010300:Parkinson Disease / Q000503:physiopathology / Q000523:psychology*; D049268:Positron-Emission Tomography; D013844:Thiazoles; D014018:Tissue Distribution
chemical_list: C475519:2-(4'-(methylamino)phenyl)-6-hydroxybenzothiazole; D016229:Amyloid beta-Peptides; D000814:Aniline Compounds; D013844:Thiazoles
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