Cerebrospinal fluid levels of alpha-tocopherol (vitamin E) in Alzheimer's disease

Jiménez‐Jiménez, Félix Javier; Bustos, F. de; Molina, José Antonio; Benito‐León, Julián; Tallón-Barranco, A.; Gasalla, Teresa; Ortı́-Pareja, M; Guillamón, F.; Rubio, Juan Carlos Colomer; Arenas, Joaquı́n; Enríquez-de-Salamanca, Rafael

doi:10.1007/bf01291887

Cited by 89 publications

(52 citation statements)

References 37 publications

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“…In another study, damage induced by 3,4-methylene dioxy-methamphetmaine (MDMA) (20) and 1-methyl-4-phenyl-1,2,3,6-tetra hy dropyridine (21) to the serotoninergic and dopaminer gic nerve systems was prevented by vitamin C supple mentation. Besides these findings, vitamins E and C levels in the plasma (22) and cerebrospinal fluid of Alzheimer's pa tients (23) were lower than those in normal subjects.…”

mentioning

confidence: 78%

Effect of Supplementation of Vitamin E and Vitamin C on Brain Acetylcholinesterase Activity and Neurotransmitter Levels in Rats Treated with Scopolamine, an Inducer of Dementia.

Lee¹,

Kang

Lee

et al. 2001

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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Summary In the present study, the effects of vitamins E and C on the levels of neuro transmitters and acetylcholinesterase activity in the brains of rats treated with scopo lamine, an inducer of dementia, were examined. Fifty male Sprague-Dawley rats at the age of 5 wk were divided into five groups after 1 wk of adaptation and fed five different diets for 6 wk: a no-scopolamine group, which was a scopolamine-untreated group fed only a basal diet; a scopolamine-treated group fed a basal diet; a vitamin E-supplemented scopolamine treated group; a vitamin C-supplemented scopolamine-treated group; and a vitamins E and C-supplemented scopolamine-treated group. Scopolamine was twice administered by in traperitoneal injection (300mg/kg, body weight), 3 d and 20min prior to sacrifice. Brain acetylcholinesterase activity was markedly reduced by scopolamine injection. However, the supplementation of vitamins E and C in the diet significantly increased the reduced brain acetylcholinesterase activity up to the level of the scopolamine-untreated group. Brain sero tonin concentration in the vitamin C-supplemented scopolamine-treated group was signifi cantly higher than that in the scopolamine-treated group. However, there were no signifi cant differences in brain dopamine and norepinephrine concentrations among all groups. In conclusion, supplementation with vitamin E and/or vitamin C might be useful in main taining brain acetylcholinesterase activity at the normal level and serotonin concentration for some extent under the condition to induce dementia by scopolamine administration.

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confidence: 78%

Effect of Supplementation of Vitamin E and Vitamin C on Brain Acetylcholinesterase Activity and Neurotransmitter Levels in Rats Treated with Scopolamine, an Inducer of Dementia.

Lee¹,

Kang

Lee

et al. 2001

Journal of Nutritional Science and Vitaminology, J Nutr Sci Vit

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“…For vitamin A, 5 [4][5][6][7][8] out of 6 [4][5][6][7][8]14] previous studies showed significantly higher prevalence of AD with lower levels. However, the studies on vitamin A and E and AD either did not adjust for confounders [5,6,9,12,14] or only adjusted for age and gender [4,7,8,10,11] or lipid levels [13] . Therefore, results of these studies are diffi cult to interpret since we showed that the association between vitamin A and E and prevalence of AD disappeared when adjustments were simultaneously made for age, gender and total cholesterol.…”

Section: Discussionmentioning

confidence: 99%

“…However, all these studies were performed in hospital-based populations. Furthermore, many studies did not adjust for confounders [5,6,9,12,14] , whereas those that did make adjustments [4,7,8,10,11,13] only corrected for either age, gender or cholesterol. However, these covariates as well as education and smoking may be important confounders.…”

Section: Introductionmentioning

confidence: 99%

Plasma Levels of Antioxidants Are Not Associated with Alzheimer’s Disease or Cognitive Decline

Engelhart

Ruitenberg²,

Meijer³

et al. 2005

Dement Geriatr Cogn Disord

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Antioxidants prevent oxidative stress that possibly causes neuronal loss in Alzheimer’s disease (AD). We examined whether high plasma levels of the antioxidant vitamins A and E were associated with lower prevalence of AD or cognitive decline (CD). We performed a cross-sectional study within the Rotterdam Study. In an univariate model, higher levels of vitamins A and E were significantly associated with lower prevalence of AD. However, when additional adjustments were made for important confounders, such as age, gender and total cholesterol, the relation substantially weakened – odds ratios per standard deviation increase were 0.87 (95% CI 0.64–1.19) for vitamin A and 0.94 (95% CI 0.60–1.48) for vitamin E. Antioxidants were not related to CD in non-demented subjects. Our findings suggest no association between plasma levels of vitamin A and E and AD or CD.

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“…Jeandel et al (1989) found that serum vitamin A concentrations were decreased in patients with AD. Similarly, other researchers have reported lower serum vitamin A concentrations in patients with AD (Zaman et al 1992;Jimenez-Jimenez et al 1997;Foy et al 1999;Bourdel-Marchasson et al 2001). Schippling et al (2000) reported lower plasma a-carotene levels but normal (3-carotene concentrations.…”

Section: Vitamin Amentioning

confidence: 99%

Antioxidant strategies for Alzheimer's disease

2002

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Oxidative damage is present within the brains of patients with Alzheimer's disease (AD), and is observed within every class of biomolecule, including nucleic acids, proteins, lipids and carbohydrates. Oxidative injury may develop secondary to excessive oxidative stress resulting from β-amyloid-induced free radicals, mitochondrial abnormalities, inadequate energy supply, inflammation or altered antioxidant defences. Treatment with antioxidants is a promising approach for slowing disease progression to the extent that oxidative damage may be responsible for the cognitive and functional decline observed in AD. Although not a uniformly consistent observation, a number of epidemiological studies have found a link between antioxidant intake and a reduced incidence of dementia, AD and cognitive decline in elderly populations. In AD clinical trials molecules with antioxidant properties such as vitamin E andGinkgo bilobaextract have shown modest benefit. A clinical trial with vitamin E is currently ongoing to determine if it can delay progression to AD in individuals with mild cognitive impairment. Combinations of antioxidants might be of even greater potential benefit for AD, especially if the agents worked in different cellular compartments or had complementary activity (e.g. vitamins E, C and ubiquinone). Naturally-occurring compounds with antioxidant capacity are available and widely marketed (e.g. vitamin C, ubiquinone, lipoic acid, β-carotene, creatine, melatonin, curcumin) and synthetic compounds are under development by industry. Nevertheless, the clinical value of these agents for AD prevention and treatment is ambiguous, and will remain so until properly designed human trials have been performed.

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Cerebrospinal fluid levels of alpha-tocopherol (vitamin E) in Alzheimer's disease

Cited by 89 publications

References 37 publications

Effect of Supplementation of Vitamin E and Vitamin C on Brain Acetylcholinesterase Activity and Neurotransmitter Levels in Rats Treated with Scopolamine, an Inducer of Dementia.

Effect of Supplementation of Vitamin E and Vitamin C on Brain Acetylcholinesterase Activity and Neurotransmitter Levels in Rats Treated with Scopolamine, an Inducer of Dementia.

Plasma Levels of Antioxidants Are Not Associated with Alzheimer’s Disease or Cognitive Decline

Antioxidant strategies for Alzheimer's disease

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