Early striatal amyloid deposition distinguishes Down syndrome and autosomal dominant Alzheimer's disease from late-onset amyloid deposition

Ann D. Cohen, Eric McDade, Brad Christian, Julie Price, Chester Mathis, William Klunk, Benjamin L. Handen

Research output: Contribution to journalArticle

12 Scopus citations

Abstract

Introduction: The objective of this study was to evaluate amyloid β (Aβ) deposition patterns in different groups of cerebral β amyloidosis: (1) nondemented with amyloid precursor protein overproduction (Down syndrome); (2) nondemented with abnormal processing of amyloid precursor protein (preclinical autosomal dominant Alzheimer disease); (3) presumed alteration in Aβ clearance with clinical symptoms (late-onset AD); and (4) presumed alterations in Aβ clearance (preclinical AD). Methods: We performed whole-brain voxelwise comparison of cerebral Aβ between 23 Down syndrome, 10 preclinical autosomal dominant Alzheimer disease, 17 late-onset AD, and 16 preclinical AD subjects, using Pittsburgh Compound B–positron emission tomography. Results: We found both Down syndrome and preclinical autosomal dominant Alzheimer disease shared a distinct pattern of increased bilateral striatal and thalamic Aβ deposition compared to late-onset AD and preclinical AD. Conclusion: Disorders associated with early-life alterations in amyloid precursor protein production or processing are associated with a distinct pattern of early striatal fibrillary Aβ deposition before significant cognitive impairment. A better understanding of this unique pattern could identify important mechanisms of Aβ deposition and possibly important targets for early intervention.

Original languageEnglish
Pages (from-to)743-750
Number of pages8
JournalAlzheimer's and Dementia
Volume14
Issue number6
DOIs
StatePublished - Jun 2018

Keywords

  • Autosomal dominant Alzheimer dementia
  • Aβ42
  • Diffuse plaque
  • Down syndrome
  • Pittsburgh compound B
  • Striatum

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