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Cited by 104Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsAntioxidant Activity and Oxidative Stress

The DOI matches its Crossref record; 150 of the 154 references it cites were found in a registry or an index, and 1 are not checked yet.

Vitamin E for Alzheimer's dementia and mild cognitive impairment

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Farina, Nicolas, Llewellyn, David, Isaac, Mokhtar Gad El Kareem Nasr, Tabet, Naji·2017·Cochrane Database of Systematic Reviews
DOI 10.1002/14651858.cd002854.pub4PMC PMC6464807
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Abstract

BACKGROUND: Vitamin E occurs naturally in the diet. It has several biological activities, including functioning as an antioxidant to scavenge toxic free radicals. Evidence that free radicals may contribute to the pathological processes behind cognitive impairment has led to interest in the use of vitamin E supplements to treat mild cognitive impairment (MCI) and Alzheimer's disease (AD). This is an update of a Cochrane Review first published in 2000, and previously updated in 2006 and 2012. OBJECTIVES: To assess the efficacy of vitamin E in the treatment of MCI and dementia due to AD. SEARCH METHODS: We searched the Specialized Register of the Cochrane Dementia and Cognitive Improvement Group (ALOIS), the Cochrane Library, MEDLINE, Embase, PsycINFO, CINAHL, LILACS as well as many trials databases and grey literature sources on 22 April 2016 using the terms: "Vitamin E", vitamin-E, alpha-tocopherol. SELECTION CRITERIA: We included all double-blind, randomised trials in which treatment with any dose of vitamin E was compared with placebo in people with AD or MCI. DATA COLLECTION AND ANALYSIS: We used standard methodological procedures according to the Cochrane Handbook for Systematic Reviews of Interventions. We rated the quality of the evidence using the GRADE approach. Where appropriate we attempted to contact authors to obtain missing information. MAIN RESULTS: Four trials met the inclusion criteria, but we could only extract outcome data in accordance with our protocol from two trials, one in an AD population (n = 304) and one in an MCI population (n = 516). Both trials had an overall low to unclear risk of bias. It was not possible to pool data across studies owing to a lack of comparable outcome measures.In people with AD, we found no evidence of any clinically important effect of vitamin E on cognition, measured with change from baseline in the Alzheimer's Disease Assessment Scale - Cognitive subscale (ADAS-Cog) over six to 48 months (mean difference (MD) -1.81, 95% confidence interval (CI) -3.75 to 0.13, P = 0.07, 1 study, n = 272; moderate quality evidence). There was no evidence of a difference between vitamin E and placebo groups in the risk of experiencing at least one serious adverse event over six to 48 months (risk ratio (RR) 0.86, 95% CI 0.71 to 1.05, P = 0.13, 1 study, n = 304; moderate quality evidence), or in the risk of death (RR 0.84, 95% CI 0.52 to 1.34, P = 0.46, 1 study, n = 304; moderate quality evidence). People with AD receiving vitamin E showed less functional decline on the Alzheimer's Disease Cooperative Study/Activities of Daily Living Inventory than people receiving placebo at six to 48 months (mean difference (MD) 3.15, 95% CI 0.07 to 6.23, P = 0.04, 1 study, n = 280; moderate quality evidence). There was no evidence of any clinically important effect on neuropsychiatric symptoms measured with the Neuropsychiatric Inventory (MD -1.47, 95% CI -4.26 to 1.32, P = 0.30, 1 study, n = 280; moderate quality evidence).We found no evidence that vitamin E affected the probability of progression from MCI to probable dementia due to AD over 36 months (RR 1.03, 95% CI 0.79 to 1.35, P = 0.81, 1 study, n = 516; moderate quality evidence). Five deaths occurred in each of the vitamin E and placebo groups over the 36 months (RR 1.01, 95% CI 0.30 to 3.44, P = 0.99, 1 study, n = 516; moderate quality evidence). We were unable to extract data in accordance with the review protocol for other outcomes. However, the study authors found no evidence that vitamin E differed from placebo in its effect on cognitive function, global severity or activities of daily living . There was also no evidence of a difference between groups in the more commonly reported adverse events. AUTHORS' CONCLUSIONS: We found no evidence that the alpha-tocopherol form of vitamin E given to people with MCI prevents progression to dementia, or that it improves cognitive function in people with MCI or dementia due to AD. However, there is moderate quality evidence from a single study that it may slow functional decline in AD. Vitamin E was not associated with an increased risk of serious adverse events or mortality in the trials in this review. These conclusions have changed since the previous update, however they are still based on small numbers of trials and participants and further research is quite likely to affect the results.

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Research works printed but not linked: 14

  1. Dysken, 2014, Effect of vitamin E and memantine on functional decline in Alzheimer, JAMA, 311, 1161
  2. Sano, 1997, Effects of selegiline and alpha-tocopherol on cognitive and functional outcome measures in moderately impaired patients with Alzheimer's disease, Neurology, 48, A377
  3. Sano, 1996, Expanding the severity range of patients in clinical trials for Alzheimer's disease: a multicentre clinical trial of selegiline and a-tocopherol, Neurology, 45 Suppl 4, 289
  4. Alavi Naeini, 2013, Effect of vitamin E and C supplementation on elderly with mild cognitive impairment (MCI) in Isfahan, Iran, Annals of Nutrition & Metabolism, 1145
  5. Anand, 2011, Supplementation of vitamin E improves cognitive status and oxidative stress in type 2 diabetes mellitus, International Research Journal of Pharmacy, 2, 169
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  8. Morris, 2012, Symposium 1: vitamins and cognitive development and performance, Proceedings of the Nutrition Society, 1, 10.1017/S0029665111003296 · DOI
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  10. Srour, 2013, Status of serum 25 (OH)-vitamin d in elderly Iranian subjects after one year supplementation with vitamin E and C, Annals of Nutrition & Metabolism, 1506
  11. Vinyoles-Bargallo, 2010, During the first year of treatment, donepezil delays the incidence of Alzheimer's disease in patients with cognitive deterioration. Vitamin E is not efficient, FMC Formacion Medica Continuada en Atencion Primaria, 12, 715
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  14. Prince, 2015, World Alzheimer Report 2015

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Metadata

Authors
Farina, N., Llewellyn, D., Isaac, M. G. E. K. N., & Tabet, N.
Affiliations
  • Brighton and Sussex Medical School (GB)
  • University of Exeter (GB)
  • Sussex Partnership NHS Foundation Trust (GB)
ORCID
Venue
Cochrane Database of Systematic Reviews
Publisher
John Wiley & Sons, Ltd
Published
2017-01-27
Volume
1
Pages
CD002854-CD002854
ISSN
1361-6137 (ISSN-L)
DOI
10.1002/14651858.cd002854.pub4
PMC
PMC6464807
OpenAlex
W2939258234
Cited by
104
References
154
Citations by year
2026: 8 · 2025: 10 · 2024: 13 · 2023: 14 · 2022: 11 · 2021: 15 · 2020: 10 · 2019: 7 · 2018: 10 · 2017: 6
Type
reference entry
Language
en
Update notices
new_version (2017-04-18)
Open access
Locations
  • Cochrane Database of Systematic Reviews (publishedVersion)
  • Europe PMC (PubMed Central) (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Biochemistry (medical) › Antioxidant Activity and Oxidative Stress
Keywords
vitamin E, alpha-tocopherol, Alzheimer's disease, mild cognitive impairment, dementia, cognitive function, antioxidant supplementation, adverse events, treatment efficacy, placebo comparison, ADAS-Cog, risk of bias, GRADE quality of evidence, publication bias, risk of bias assessment, risk of bias assessment tools
MeSH terms
Alzheimer Disease, Antioxidants, Humans, Vitamin E, Randomized Controlled Trials as Topic, Outcome Assessment, Health Care, Disease Progression, alpha-Tocopherol, Cognitive Dysfunction

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