Plasma Concentrations of Vitamins A and E and Carotenoids in Alzheimer's Disease

Zaman, Zahur; Roche, Steven; Fielden, Peter R.; Fröst, Peter; Niriella, D. C.; Cayley, A. C. D.

doi:10.1093/ageing/21.2.91

Cited by 191 publications

(106 citation statements)

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“…Both vascular dementia and AD were variably associated with reduced serum or plasma levels of vitamins A, C, and E, even when controlled for nutritional status. [83][84][85][86][87] Although vitamin E delayed progression of AD in one clinical study, 88 antioxidant vitamin supplementation did not affect incident cognitive impairment over 5 years, as a secondary outcome of a large placebo-controlled cardiac study involving 20,536 individuals. 89 …”

Section: Antioxidant Levelsmentioning

confidence: 96%

Biomarkers of Alzheimer disease in plasma

Irizarry

2004

Neurotherapeutics

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Summary: Plasma and serum biochemical markers proposed for Alzheimer disease (AD) are based on pathophysiologic processes such as amyloid plaque formation [amyloid ␤-protein (A␤), A␤ autoantibodies, platelet amyloid precursor protein (APP) isoforms], inflammation (cytokines), oxidative stress (vitamin E, isoprostanes), lipid metabolism (apolipoprotein E, 24S-hydroxycholesterol), and vascular disease [homocysteine, lipoprotein (a)]. Most proteins or metabolites evaluated in plasma or serum thus far are, at best, biological correlates of AD: levels are statistically different in AD versus controls in some cohorts, but they lack sensitivity or specificity for diagnosis or for tracking response to therapy. Approaches combining panels of existing biomarkers or surveying the range of proteins in plasma (proteomics) show promise for discovering biomarker profiles that are characteristic of AD, yet distinct from nondemented patients or patients with other forms of dementia.

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Section: Antioxidant Levelsmentioning

confidence: 96%

Biomarkers of Alzheimer disease in plasma

Irizarry

2004

Neurotherapeutics

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“…This observation brings to mind the associations previously noted between oxidative stress, metal ions, and the toxicity of A␤ or APP (26,27), and indirect measures of lipid peroxidation that have more recently showed that oxidative stress correlates with amyloid plaque formation in animal models (28), and with disease severity in humans (29). It is also noteworthy that vitamin E, a lipophilic antioxidant, is relatively deficient in the post-mortem brain tissue of patients of Alzheimer's disease (30), and its administration in pharmacological doses appears to slow the clinical progression of disease (31).…”

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confidence: 99%

Early Synergy between Aβ42 and Oxidatively Damaged Membranes in Promoting Amyloid Fibril Formation by Aβ40

Koppaka

Paul

Murray³

et al. 2003

Journal of Biological Chemistry

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Oxidative lipid membrane damage is known to promote the misfolding of A␤42 into pathological ␤ structure. In fully developed senile plaques of Alzheimer's disease, however, it is the shorter and more soluble amyloid ␤ protein, A␤40, that predominates. To investigate the role of oxidative membrane damage in the misfolding of A␤40, we have examined its interaction with supported lipid monolayer membranes using internal reflection infrared spectroscopy. Oxidatively damaged lipids modestly increased A␤40 accumulation, with adsorption kinetics and a conformation that are distinct from that of A␤42. In stark contrast, pretreatment of oxidatively damaged monolayer membranes with A␤42 vigorously promoted A␤40 accumulation and misfolding. Pretreatment of saturated or undamaged membranes with A␤42 had no such effect. Parallel studies of lipid bilayer vesicles using a dye binding assay to detect fibril formation and electron microscopy to examine morphology demonstrated that A␤42 pretreatment of oxidatively damaged membranes promoted the formation of mature A␤40 amyloid fibrils. We conclude that oxidative membrane damage and A␤42 act synergistically at an early stage to promote fibril formation by A␤40. This synergy could be detected within minutes using internal reflection spectroscopy, whereas a dyebinding assay required several days and much higher protein concentrations to demonstrate this synergy.

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“…A greater mean value (30 mmol/l) was reported by Zaman et al (1992) among control subjects, but in a small sample of 20 subjects with large standard deviation. Only three subjects in our sample (two cases and one control) could be considered as deficient in vitamin E, when considering the cut-off of 11.6 mmol/l proposed by Meydani.…”

Section: Discussionmentioning

confidence: 59%

“…In these studies, higher cognitive performances have been correlated with both high intake of carotenoids (Jama et al, 1996) and high plasmatic concentrations in carotenoids (Haller et al, 1996), in vitamin C (Perrig et al, 1997), or in vitamin E (Schmidt et al, 1998, Perkins et al, 1999. Concerning dementia, plasma antioxidant vitamin concentrations have been found to be lower in AD subjects compared with controls (Zaman et al, 1992;Riviere et al, 1998;Bourdel-Marchasson et al, 2001). However, these studies did not adjust for potential confounders, particularly educational level, which is implicated in both an increased risk of AD (Letenneur et al, 1999) and feeding behaviour (Kilander & Ö hrvall, 1997).…”

Section: Discussionmentioning

confidence: 98%

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Association between antioxidant nutritional indicators and the incidence of dementia: results from the PAQUID prospective cohort study

et al. 2003

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Objective: To analyse the relation between antioxidant vitamins A, E, and malondialdehyde (MDA) lipoperoxidation product plasma concentrations with incident dementia. Design: A nested case-control within the PAQUID (Personnes Agées QUID) cohort. Setting: The PAQUID population-based prospective cohort in southwestern France. Subjects: Among 626 subjects with blood collection at baseline, 46 developed a dementia during the follow-up and were considered to be cases. Each case was matched (on age and sex) to three controls. Results: Plasma vitamin E concentrations were lower among cases (mean value at 22.62 mmol/l (s.d.: 7.38) vs 24.99 (s.d.: 6.73 among controls). The same trend was observed for vitamin A concentrations, but the difference was not significant. On the contrary, MDA concentrations tended to be higher (mean value 1.35 mmol/l (s.d.: 0.53) vs 1.23 (s.d.: 0.44)) among cases. In logistic regression models, plasma values were split into tertiles. Adjusted for confounders, the risk of dementia was significantly increased in the lowest vitamin E tertile (r21.0 mmol/l) (OR ¼ 3.12, P ¼ 0.033) compared to the highest one (Z25.5 mmol/l). The risk of Alzheimer's disease was also increased, with borderline significance (OR ¼ 3.06, P ¼ 0.053). Risks associated with vitamin A were nonsignificant. Similarly, there was a trend to an increased risk of dementia in the highest tertile of MDA (OR ¼ 1.67, P ¼ 0.31). Conclusions: These results suggest that subjects with low plasma vitamin E concentrations are at a higher risk of developing a dementia in subsequent years.

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Plasma Concentrations of Vitamins A and E and Carotenoids in Alzheimer's Disease

Cited by 191 publications

References 0 publications

Biomarkers of Alzheimer disease in plasma

Biomarkers of Alzheimer disease in plasma

Early Synergy between Aβ42 and Oxidatively Damaged Membranes in Promoting Amyloid Fibril Formation by Aβ40

Association between antioxidant nutritional indicators and the incidence of dementia: results from the PAQUID prospective cohort study

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