In vivo Patterns of Tau Pathology, Amyloid-β Burden, and Neuronal Dysfunction in Clinical Variants of Alzheimer's Disease

J Alzheimers Dis. 2017;55(2):465-471. doi: 10.3233/JAD-160316.


The clinical heterogeneity of Alzheimer's disease is not reflected in the rather diffuse cortical deposition of amyloid-β. We assessed the relationship between clinical symptoms, in vivo tau pathology, amyloid distribution, and hypometabolism in variants of Alzheimer's disease using novel multimodal PET imaging techniques. Tau pathology was primarily observed in brain regions related to clinical symptoms and overlapped with areas of hypometabolism. In contrast, amyloid-β deposition was diffusely distributed over the entire cortex. Tau PET imaging may thus serve as a valuable biomarker for the localization of neuronal injury in vivo and may help to validate atypical subtypes of Alzheimer's disease.

Keywords: 18F-AV-1451; 18F-FDG; Alzheimer’s disease; Pittsburghcompound B; T-807; amyloid; molecular imaging; multimodal imaging; positron-emission tomography; tau protein.

MeSH terms

  • Alzheimer Disease / complications
  • Alzheimer Disease / diagnostic imaging
  • Alzheimer Disease / pathology*
  • Amyloid beta-Peptides / metabolism*
  • Atrophy / etiology
  • Brain / diagnostic imaging
  • Brain / metabolism*
  • Brain / pathology*
  • Carbolines / metabolism
  • Cognition Disorders / diagnostic imaging
  • Cognition Disorders / etiology
  • Corticomedial Nuclear Complex / pathology
  • Executive Function
  • Female
  • Fluorodeoxyglucose F18 / metabolism
  • Humans
  • Language Disorders / etiology
  • Male
  • Neuropsychological Tests
  • Positron-Emission Tomography
  • tau Proteins / metabolism*


  • Amyloid beta-Peptides
  • Carbolines
  • tau Proteins
  • Fluorodeoxyglucose F18
  • 7-(6-fluoropyridin-3-yl)-5H-pyrido(4,3-b)indole