title: Tau-PET Binding Distinguishes Patients With Early-stage Posterior Cortical Atrophy From Amnestic Alzheimer Disease Dementia.
abstract: BACKGROUND
  Flortaucipir (tau) positron emission tomography (PET) binding distinguishes individuals with clinically well-established posterior cortical atrophy (PCA) due to Alzheimer disease (AD) from cognitively normal (CN) controls. However, it is not known whether tau-PET binding patterns differentiate individuals with PCA from those with amnestic AD, particularly early in the symptomatic stages of disease.
  
  
  METHODS
  Flortaucipir and florbetapir (β-amyloid) PET imaging were performed in individuals with early-stage PCA (N=5), amnestic AD dementia (N=22), and CN controls (N=47). Average tau and β-amyloid deposition were quantified using standard uptake value ratios and compared at a voxelwise level, controlling for age.
  
  
  RESULTS
  PCA patients [median age-at-onset, 59 (51 to 61) years] were younger at symptom onset than similarly staged individuals with amnestic AD [75 (60 to 85) years] or CN controls [73 (61 to 90) years; P=0.002]. Flortaucipir uptake was higher in individuals with early-stage symptomatic PCA versus those with early-stage amnestic AD or CN controls, and greatest in posterior regions. Regional elevations in florbetapir were observed in areas of greatest tau deposition in PCA patients.
  
  
  CONCLUSIONS
  Flortaucipir uptake distinguished individuals with PCA and amnestic AD dementia early in the symptomatic course. The posterior brain regions appear to be uniquely vulnerable to tau deposition in PCA, aligning with clinical deficits that define this disease subtype.
authors.affiliation: *The Charles F and Joanne Knight Alzheimer Disease Research Center †Department of Neurology ‡Mallinckrodt Institute of Radiology §Department of Neurological Surgery, Washington University School of Medicine, St. Louis, MO.
authors.forename: Gregory S
authors.initials: GS
authors.lastname: Day
authors.forename: Brian A
authors.initials: BA
authors.lastname: Gordon
authors.forename: Kelley
authors.initials: K
authors.lastname: Jackson
authors.forename: Jon J
authors.initials: JJ
authors.lastname: Christensen
authors.forename: Maria
authors.initials: M
authors.lastname: Rosana Ponisio
authors.forename: Yi
authors.initials: Y
authors.lastname: Su
authors.forename: Beau M
authors.initials: BM
authors.lastname: Ances
authors.forename: Tammie L S
authors.initials: TLS
authors.lastname: Benzinger
authors.forename: John C
authors.initials: JC
authors.lastname: Morris
mesh_terms: D000367:Age Factors; D017668:Age of Onset; D000368:Aged; D000544:Alzheimer Disease / Q000175:diagnosis / Q000000981:diagnostic imaging / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000814:Aniline Compounds; D001284:Atrophy / Q000473:pathology; D002540:Cerebral Cortex / Q000473:pathology; D005026:Ethylene Glycols; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D049268:Positron-Emission Tomography / Q000379:methods*
chemical_list: D016229:Amyloid beta-Peptides; D000814:Aniline Compounds; D005026:Ethylene Glycols; C545186:florbetapir