Abstract
This review focuses on the role of Aβ in AD pathogenesis in Down syndrome and current approaches for imaging Aβ in vivo. We will describe how Aβ deposits with age, the posttranslational modifications that can occur, and detection in biofluids. Three unique case studies describing partial trisomy 21 cases without APP triplication, and the occurrences of low level mosaic trisomy 21 in an early onset AD patient are presented. Brain imaging for Aβ includes those by positron emission tomography and ligands (Pittsburgh Compound B, Florbetapir, and FDDNP) that bind Aβ have been published and are summarized here. In combination, we have learned a great deal about Aβ in DS in terms of characterizing age of onset of this pathology and it is exciting to note that there is a clinical trial in DS targeting Aβ that may lead to clinical benefits.
Document Type
Article
Publication Date
1-2018
Digital Object Identifier (DOI)
https://doi.org/10.1016/j.freeradbiomed.2017.09.013
Funding Information
This work was supported by the National Institutes of Health through the National Institutes on Child Health and Development (grant #R01HD064993).
Repository Citation
Head, Elizabeth; Helman, Alex M.; Powell, David K.; and Schmitt, Frederick A., "Down Syndrome, Beta-Amyloid and Neuroimaging" (2018). Sanders-Brown Center on Aging Faculty Publications. 120.
https://uknowledge.uky.edu/sbcoa_facpub/120
Notes/Citation Information
Published in Free Radical Biology and Medicine, v. 114, p. 102-109.
© 2017 Elsevier Inc. All rights reserved.
This manuscript version is made available under the CC‐BY‐NC‐ND 4.0 license https://creativecommons.org/licenses/by-nc-nd/4.0/.
The document available for download is the author's post-peer-review final draft of the article.