Selenium levels in serum, red blood cells, and cerebrospinal fluid of alzheimer's disease patients: A report from the Australian Imaging, Biomarker & Lifestyle Flagship Study of Ageing (AIBL)
- Author(s)
- Cardoso, BR; Hare, DJ; Bush, AI; Li, QX; Fowler, CJ; Masters, CL; Martins, RN; Ganio, K; Lothian, A; Mukherjee, S; Kapp, EA; Roberts, BR; Aibl research group;
- Details
- Publication Year 2017-02-10,Volume 57,Issue #1,Page 183-193
- Journal Title
- J Alzheimers Dis
- Publication Type
- Journal Article
- Abstract
- Selenium (Se) protects cells against oxidative stress damage through a range of bioactive selenoproteins. Increased oxidative stress is a prominent feature of Alzheimer's disease (AD), and previous studies have shown that Se deficiency is associated with age-related cognitive decline. In this study, we assessed Se status in different biofluids from a subgroup of participants in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing. As Se in humans can either be an active component of selenoproteins or inactive via non-specific incorporation into other proteins, we used both size exclusion chromatography-inductively coupled plasma-mass spectrometry (SEC-ICP-MS) and tandem mass spectrometry to characterize selenoproteins in serum. We observed no differences in total Se concentration in serum or cerebrospinal fluid of AD subjects compared to mildly cognitively impairment patients and healthy controls. However, Se levels in erythrocytes were decreased in AD compared to controls. SEC-ICP-MS analysis revealed a dominant Se-containing fraction. This fraction was subjected to standard protein purification and a bottom-up proteomics approach to confirm that the abundant Se in the Justify fraction was due, in part, to selenoprotein P. Although we observed differences in Se levels in erythrocytes that are consistent with systemic changes in Se status in AD, no significant change in the total serum level was observed. The lack of change in the Se level is at odds with our previous observations in a Brazilian population deficient in Se, and we attribute this to the Australian cohort being Se-replete.
- Publisher
- IOS
- Research Division(s)
- Systems Biology And Personalised Medicine
- PubMed ID
- 28222503
- Publisher's Version
- https://doi.org/10.3233/JAD-160622
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2017-04-06 09:28:06
Last Modified: 2017-04-07 03:28:14