Journal
ALZHEIMERS & DEMENTIA
Volume 14, Issue 6, Pages 743-750Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jalz.2018.01.002
Keywords
Down syndrome; Autosomal dominant Alzheimer dementia; Pittsburgh compound B; Striatum; Diffuse plaque; A beta 42
Categories
Funding
- The National Institutes of Health [P50 AG005133, RF1 AG025516, P01 AG025204, R01AG031110]
- Lilly
- Roche
- NIA
- NICHD
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Introduction: The objective of this study was to evaluate amyloid beta (A beta) deposition patterns in different groups of cerebral beta 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 A beta clearance with clinical symptoms (late-onset AD); and (4) presumed alterations in A beta clearance (preclinical AD). Methods: We performed whole-brain voxelwise comparison of cerebral A beta 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 A beta 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 A beta deposition before significant cognitive impairment. A better understanding of this unique pattern could identify important mechanisms of A beta deposition and possibly important targets for early intervention. (C) 2018 the Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
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