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Early striatal amyloid deposition distinguishes Down syndrome and autosomal dominant Alzheimer's disease from late‐onset amyloid deposition
Author(s) -
Cohen Ann D.,
McDade Eric,
Christian Brad,
Price Julie,
Mathis Chester,
Klunk William,
Handen Benjamin L.
Publication year - 2018
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2018.01.002
Subject(s) - amyloid (mycology) , pittsburgh compound b , pathology , alzheimer's disease , glial fibrillary acidic protein , amyloidosis , medicine , disease , neuroscience , psychology , immunohistochemistry
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.