Literature DB >> 30359879

Comparison of longitudinal Aβ in nondemented elderly and Down syndrome.

Dana L Tudorascu1, Stewart J Anderson2, Davneet S Minhas3, Zheming Yu3, Diane Comer4, Patrick Lao5, Sigan Hartley6, Charles M Laymon7, Beth E Snitz3, Brian J Lopresti3, Sterling Johnson8, Julie C Price9, Chester A Mathis3, Howard J Aizenstein10, William E Klunk10, Benjamin L Handen10, Brad T Christian5, Ann D Cohen11.   

Abstract

Down syndrome (DS) predisposes individuals to early Alzheimer's disease (AD). Using Pittsburgh Compound B ([11C]PiB), a pattern of striatal amyloid beta (Aβ) that is elevated relative to neocortical binding has been reported, similar to that of nondemented autosomal dominant AD mutation carriers. However, it is not known whether changes in striatal and neocortical [11C]PiB retention differ over time in a nondemented DS population when compared to changes in a nondemented elderly (NDE) population. The purpose of this work was to assess longitudinal changes in trajectories of Aβ in a nondemented DS compared to an NDE cohort. The regional trajectories for anterior ventral striatum (AVS), frontal cortex, and precuneus [11C]PiB retention were explored over time using linear mixed effects models with fixed effects of time, cohort, and time-by-cohort interactions and subject as random effects. Significant differences between DS and NDE cohort trajectories for all 3 region of interests were observed (p < 0.05), with the DS cohort showing a faster accumulation in the AVS and slower accumulation in the frontal cortex and precuneus compared to the NDE cohort. These data add to the previously reported distinct pattern of early striatal deposition not commonly seen in sporadic AD by demonstrating that individuals with DS may also accumulate Aβ at a rate faster in the AVS when compared to NDE subjects.
Copyright © 2018 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  Alzheimer's disease; Amyloid; Down syndrome

Mesh:

Substances:

Year:  2018        PMID: 30359879      PMCID: PMC6251757          DOI: 10.1016/j.neurobiolaging.2018.09.030

Source DB:  PubMed          Journal:  Neurobiol Aging        ISSN: 0197-4580            Impact factor:   4.673


  29 in total

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2.  Diffuse plaques in the cerebellum and corpus striatum in Down's syndrome contain amyloid beta protein (A beta) only in the form of A beta 42(43).

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3.  Optimizing PiB-PET SUVR change-over-time measurement by a large-scale analysis of longitudinal reliability, plausibility, separability, and correlation with MMSE.

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Journal:  Neuroimage       Date:  2016-08-27       Impact factor: 6.556

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Authors:  Victor L Villemagne; Rachel S Mulligan; Svetlana Pejoska; Kevin Ong; Gareth Jones; Graeme O'Keefe; J Gordon Chan; Kenneth Young; Henri Tochon-Danguy; Colin L Masters; Christopher C Rowe
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5.  Alzheimer's disease: striatal amyloid deposits and neurofibrillary changes.

Authors:  H Braak; E Braak
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Journal:  Arch Neurol       Date:  2008-11

10.  Relationships between flortaucipir PET tau binding and amyloid burden, clinical diagnosis, age and cognition.

Authors:  Michael J Pontecorvo; Michael D Devous; Michael Navitsky; Ming Lu; Stephen Salloway; Frederick W Schaerf; Danna Jennings; Anupa K Arora; Anne McGeehan; Nathaniel C Lim; Hui Xiong; Abhinay D Joshi; Andrew Siderowf; Mark A Mintun
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Journal:  Neurobiol Aging       Date:  2020-05-31       Impact factor: 4.673

2.  Frontal cortex and striatal cellular and molecular pathobiology in individuals with Down syndrome with and without dementia.

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4.  Postmortem Neocortical 3H-PiB Binding and Levels of Unmodified and Pyroglutamate Aβ in Down Syndrome and Sporadic Alzheimer's Disease.

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5.  PET measurement of longitudinal amyloid load identifies the earliest stages of amyloid-beta accumulation during Alzheimer's disease progression in Down syndrome.

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Review 6.  Basal Forebrain Cholinergic Neurons: Linking Down Syndrome and Alzheimer's Disease.

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7.  Post-mortem analyses of PiB and flutemetamol in diffuse and cored amyloid-β plaques in Alzheimer's disease.

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