amyloid-beta-peptides has been researched along with astaxanthine* in 2 studies
2 other study(ies) available for amyloid-beta-peptides and astaxanthine
Article | Year |
---|---|
Amyloid β levels in human red blood cells.
Amyloid β-peptide (Aβ) is hypothesized to play a key role by oxidatively impairing the capacity of red blood cells (RBCs) to deliver oxygen to the brain. These processes are implicated in the pathogenesis of Alzheimer's disease (AD). Although plasma Aβ has been investigated thoroughly, the presence and distribution of Aβ in human RBCs are still unclear. In this study, we quantitated Aβ40 and Aβ42 in human RBCs with ELISA assays, and provided evidence that significant amounts of Aβ could be detected in RBCs and that the RBC Aβ levels increased with aging. The RBC Aβ levels increased with aging. On the other hand, providing an antioxidant supplement (astaxanthin, a polar carotenoid) to humans was found to decrease RBC Aβ as well as oxidative stress marker levels. These results suggest that plasma Aβ40 and Aβ42 bind to RBCs (possibly with aging), implying a pathogenic role of RBC Aβ. Moreover, the data indicate that RBC Aβ40 and Aβ42 may constitute biomarkers of AD. As a preventive strategy, therapeutic application of astaxanthin as an Aβ-lowering agent in RBCs could be considered as a possible anti-dementia agent.. Controlled-Trials.com ISRCTN42483402. Topics: Adult; Age Factors; Aged; Alzheimer Disease; Amyloid beta-Peptides; Antioxidants; Dietary Supplements; Erythrocytes; Female; Humans; Male; Middle Aged; Peptide Fragments; Xanthophylls; Young Adult | 2012 |
Amyloid β-induced erythrocytic damage and its attenuation by carotenoids.
The presence of amyloid β-peptide (Aβ) in human blood has recently been established, and it has been hypothesized that Aβ readily contacts red blood cells (RBC) and oxidatively impairs RBC functions. In this study, we conducted in vitro and in vivo studies, which provide evidence that Aβ induces oxidative injury to RBC by binding to them, causing RBC phospholipid peroxidation and diminishing RBC endogenous carotenoids, especially xanthophylls. This type of damage is likely to injure the vasculature, potentially reducing oxygen delivery to the brain and facilitating Alzheimer's disease (AD). As a preventive strategy, because the Aβ-induced RBC damage could be attenuated by treatment of RBC with xanthophylls, we suggest that xanthophylls may contribute to the prevention of AD. Topics: Amyloid beta-Peptides; Animals; Antioxidants; Carotenoids; Erythrocytes; Flow Cytometry; Hemolysis; Humans; Lipid Peroxides; Lutein; Male; Mice; Mice, Inbred C57BL; Oxidation-Reduction; Oxidative Stress; Peptide Fragments; Phospholipids; Protein Binding; Xanthophylls | 2011 |