Vitamin E and Alzheimer's disease in subjects with Down's syndrome

Jackson, Coleen; Holland, Anthony; Williams, Celia A.; Dickerson, J. W. T.

doi:10.1111/j.1365-2788.1988.tb01439.x

Cited by 10 publications

(2 citation statements)

References 14 publications

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“…The levels of glutathione are decreased in these individuals [38][39][40] and increased oxidized glutathione/glutathione ratio has been found in fibroblasts from DS fetuses [36]. Additionally, lower blood and/or plasma levels of other antioxidant molecules such as vitamin E, vitamin C, selenium, and zinc have been found in children and adult DS individuals [38,[41][42][43]. Furthermore, fetal DS brains show reduced levels of taurine in the frontal cortex [44].…”

Section: Mechanisms Of Os Involved In Dsmentioning

confidence: 99%

Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials

Revilla

Martı́nez-Cué

2020

Antioxidants

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There is currently no effective pharmacological therapy to improve the cognitive dysfunction of individuals with Down syndrome (DS). Due to the overexpression of several chromosome 21 genes, cellular and systemic oxidative stress (OS) is one of the most important neuropathological processes that contributes to the cognitive deficits and multiple neuronal alterations in DS. In this condition, OS is an early event that negatively affects brain development, which is also aggravated in later life stages, contributing to neurodegeneration, accelerated aging, and the development of Alzheimer’s disease neuropathology. Thus, therapeutic interventions that reduce OS have been proposed as a promising strategy to avoid neurodegeneration and to improve cognition in DS patients. Several antioxidant molecules have been proven to be effective in preclinical studies; however, clinical trials have failed to show evidence of the efficacy of different antioxidants to improve cognitive deficits in individuals with DS. In this review we summarize preclinical studies of cell cultures and mouse models, as well as clinical studies in which the effect of therapies which reduce oxidative stress and mitochondrial alterations on the cognitive dysfunction associated with DS have been assessed.

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Section: Mechanisms Of Os Involved In Dsmentioning

confidence: 99%

Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials

Revilla

Martı́nez-Cué

2020

Antioxidants

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“…Studies have shown that vitamin E deficiency impairs cognitive performance in mice subjected to oxidative stress [ 2 ]. Meanwhile, one study found that Down syndrome (DS) children have significantly less vitamin E levels than normal children [ 3 ]; while another study showed that DS patients with dementia have lower plasma levels of vitamin E than controls without DS [ 4 ]. These results suggest that intake of essential nutrients such as folate, vitamin B6, vitamin E, selenium, α-lipoic acid might be important in preventing cognitive deterioration in DS and Alzheimer disease (AD) [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

γ-Tocotrienol does not substantially protect DS neurons from hydrogen peroxide-induced oxidative injury

et al. 2012

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BackgroundDown syndrome (DS) neurons are more susceptible to oxidative stress and previous studies have shown that vitamin E was able to reduce oxidative stress and improve DS neurons' viability. Therefore, this study was done to investigate the protective role of γ-tocotrienol (γT3) in DS neurons from hydrogen peroxide (H2O2) -induced oxidative stress. The pro-apoptosis tendency of γT3 was compared to α-tocopherol (αT) in non-stress condition as well.MethodsPrimary culture of DS and euploid neurons were divided into six groups of treatment: control, H2O2, γT3 pre-treatment with H2O2, γT3 only, αT pre-treatment with H2O2 and αT only. The treatments were assessed by MTS assay and apoptosis assay by single-stranded DNA (ssDNA) apoptosis ELISA assay, Hoechst and Neu-N immunofluorescence staining. The cellular uptake of γT3 and αT was determined by HPLC while protein expressions were determined by Western blot. Comparison between groups was made by the Student's t test, one-way ANOVA and Bonferroni adjustment as well as two-way ANOVA for multiple comparisons.ResultsOne day incubation of γT3 was able to reduced apoptosis of DS neurons by 10%, however γT3 was cytotoxic at longer incubation period (14 days) and at concentrations ≥ 100 μM. Pre-treatment of αT and γT3 only attenuate apoptosis and increase cell viability in H2O2-treated DS and euploid neurons by 10% in which the effects were minimal to maintain most of the DS cells' morphology. γT3 act as a free radical scavenger by reducing ROS generated by H2O2. In untreated controls, DS neurons showed lower Bcl-2/Bax ratio and p53 expression compared to normal neurons, while cPKC and PKC-δ expressions were higher in DS neurons. On the other hand, pre-treatment of γT3 in H2O2-treated DS neurons have reduced Bcl-2/Bax ratio, which was not shown in euploid neurons. This suggests that pre-treatment of γT3 did not promote DS cell survival. Meanwhile γT3 and αT treatments without H2O2 as well as pre-treatment of γT3 and αT induced changes in cPKC and PKC-δ expression in DS neurons suggesting interaction of γT3 and αT with PKC activity.ConclusionOur study suggests that γT3 pre-treatment are not sufficient to protect DS neurons from H2O2-induced oxidative assault, instead induced the apoptosis process.

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PASSCLAIM1—Mental state and performance

et al. 2004

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From this review it is concluded that, in principle, the phenomena in these fields are no different to those in other fields of life science. The scientific methods and protocols described in this report can positively demonstrate the effects of foods on mental state and performance in a scientifically valid way. A claim on mental state and performance like other claims must be based on scientific evidence. This report confirms that methodologies do exist to generate sound scientific evidence in this area. Therefore, claims on the enhancement of specific mental functions can and should be substantiated and validated using the methodologies described in this review.

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Vitamin E and Alzheimer's disease in subjects with Down's syndrome

Cited by 10 publications

References 14 publications

Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials

Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials

γ-Tocotrienol does not substantially protect DS neurons from hydrogen peroxide-induced oxidative injury

PASSCLAIM1—Mental state and performance

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