Plasma β-amyloid and duration of Alzheimer's disease in adults with Down syndrome
✍ Scribed by V. P. Prasher; S. G. Sajith; P. Mehta; W. B. Zigman; N. Schupf
- Publisher
- John Wiley and Sons
- Year
- 2010
- Tongue
- English
- Weight
- 111 KB
- Volume
- 25
- Category
- Article
- ISSN
- 0885-6230
- DOI
- 10.1002/gps.2321
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Objectives
To investigate the relation of plasma levels of A__β__ peptides (A__β__1‐40 and A__β__1‐42) and apolipoprotein E (APOE) genotype to dementia status, and the duration of Alzheimer's disease (AD) in adults with Down syndrome (DS).
Methods
Adults with DS were recruited from community settings and followed up for a mean period of 6.7 years. Plasma levels A__β__1‐40 and A__β__1‐42 and APOE genotype were determined at the last visit.
Results
There were 83 nondemented participants and 44 participants with prevalent AD. Overall, plasma levels of A__β__1‐42, A__β__1‐40 and the ratio A__β__1‐42/A__β__1‐40 did not differ significantly between the adults with DS. Among demented participants, the mean level of A__β__1‐40 was significantly lower (157.0 vs. 195.3) and the ratio of A__β__1‐42/A__β__1‐40 was significantly higher (0.28 vs. 0.16) in those with more than 4 years duration of dementia than in those with 4 or fewer years' duration of dementia. This pattern was generally similar in those with and without an APOE __ε__4 allele.
Conclusions
There is an association between plasma A__β__ peptide levels and the duration of AD in older persons with DS. The predictive and diagnostic roles of A__β__1‐42 and A__β__1‐40 measurements for AD, however, remain controversial. Change in A__β__ peptide levels with onset of AD and with the duration of dementia may account for a lack of difference between prevalent cases and nondemented individuals and for variation in the predictive power of A__β__ peptide levels. Copyright © 2009 John Wiley & Sons, Ltd.
📜 SIMILAR VOLUMES
Plasma amyloid beta42 peptide (Abeta42) levels are significantly elevated in all genetic forms of early-onset Alzheimer's disease caused by familial Alzheimer's disease mutations or Down's syndrome. Moreover, recent studies have determined that both plasma Abeta42 and Abeta40 levels are significantl