title: Positron emission tomography of brain β-amyloid and τ levels in adults with Down syndrome.
abstract: OBJECTIVE
  To determine the neuropathological load in the living brain of nondemented adults with Down syndrome using positron emission tomography with 2-(1-{6-[(2-fluorine 18-labeled fluoroethyl)methylamino]-2-napthyl}ethylidene) malononitrile ([(18)F]FDDNP) and to assess the influence of age and cognitive and behavioral functioning. For reference, [(18)F]FDDNP binding values and patterns were compared with those from patients with Alzheimer disease and cognitively intact control participants.
  
  
  METHODS
  Cross-sectional clinical study.
  
  
  METHODS
  Volunteer sample of 19 persons with Down syndrome without dementia (mean age, 36.7 years), 10 patients with Alzheimer disease (mean age, 66.5 years), and 10 controls (mean age, 43.8 years).
  
  
  METHODS
  Binding of [(18)F]FDDNP in brain regions of interest, including the parietal, medial temporal, lateral temporal, and frontal lobes and posterior cingulate gyrus, and the average of all regions (global binding).
  
  
  RESULTS
  The [(18)F]FDDNP binding values were higher in all brain regions in the Down syndrome group than in controls. Compared with the Alzheimer disease group, the Down syndrome group had higher [(18)F]FDDNP binding values in the parietal and frontal regions, whereas binding levels in other regions were comparable. Within the Down syndrome group, age correlated with [(18)F]FDDNP binding values in all regions except the posterior cingulate, and several measures of behavioral dysfunction showed positive correlations with global, frontal, parietal, and posterior cingulate [(18)F]FDDNP binding.
  
  
  CONCLUSIONS
  Consistent with neuropathological findings from postmortem studies, [(18)F]FDDNP positron emission tomography shows high binding levels in Down syndrome comparable to Alzheimer disease and greater levels than in members of a control group. The positive associations between [(18)F]FDDNP binding levels and age as well as behavioral dysfunction in Down syndrome are consistent with the age-related progression of Alzheimer-type neuropathological findings in this population.
authors.affiliation: Department of Psychiatry and Biobehavioral Sciences, and Semel Institute for Neuroscience and Human Behavior, University of California, Los Angeles 90024, USA.
authors.forename: Linda D
authors.initials: LD
authors.lastname: Nelson
authors.forename: Prabha
authors.initials: P
authors.lastname: Siddarth
authors.forename: Vladimir
authors.initials: V
authors.lastname: Kepe
authors.forename: Kevin E
authors.initials: KE
authors.lastname: Scheibel
authors.forename: S C
authors.initials: SC
authors.lastname: Huang
authors.forename: Jorge R
authors.initials: JR
authors.lastname: Barrio
authors.forename: Gary W
authors.initials: GW
authors.lastname: Small
mesh_terms: D000328:Adult; D000368:Aged; D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000378:metabolism*; D003430:Cross-Sectional Studies; D004314:Down Syndrome / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000473:pathology*; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D058225:Plaque, Amyloid / Q000000981:diagnostic imaging / Q000378:metabolism / Q000473:pathology; D049268:Positron-Emission Tomography / Q000379:methods; D011485:Protein Binding; D055815:Young Adult; D016875:tau Proteins / Q000378:metabolism*
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins