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Alzheimers Dement. 2018 Jun;14(6):743-750. doi: 10.1016/j.jalz.2018.01.002. Epub 2018 Mar 1.

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

Author information

1
Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA. Electronic address: cohenad@upmc.edu.
2
Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Neurology, Washington University School of Medicine, St. Louis, MO, USA.
3
Department of Medical Physics, University of Wisconsin-Madison School of Medicine, Madison, WI, USA.
4
Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; A. A. Martinos Center for Biomedical Imaging, Massachusetts General Hospital, Cambridge, MA, USA.
5
Department of Radiology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
6
Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA; Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.
7
Department of Psychiatry, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

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.

KEYWORDS:

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

PMID:
29477284
PMCID:
PMC5994364
[Available on 2019-06-01]
DOI:
10.1016/j.jalz.2018.01.002

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