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dc.contributor.authorFarina, N
dc.contributor.authorLlewellyn, DJ
dc.contributor.authorIsaac, MGEKN
dc.contributor.authorTabet, N
dc.date.accessioned2018-04-04T14:11:22Z
dc.date.issued2017-04-18
dc.description.abstractBackground 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 48months (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.en_GB
dc.description.sponsorshipThis update was supported by the National Institute for Health Research (NIHR), via Cochrane Infrastructure funding to the Cochrane Dementia and Cognitive Improvement group.en_GB
dc.identifier.citationNo. 4en_GB
dc.identifier.doi10.1002/14651858.CD002854.pub5
dc.identifier.urihttp://hdl.handle.net/10871/32316
dc.language.isoenen_GB
dc.publisherCochrane Collaboration / Wileyen_GB
dc.rights.embargoreasonUnder embargo until 18 April 2018 in compliance with publisher policyen_GB
dc.rightsCopyright © 2017 The Cochrane Collaboration. Published by John Wiley & Sons, Ltd.en_GB
dc.titleVitamin E for Alzheimer’s dementia and mild cognitive impairment (Review)en_GB
dc.typeArticleen_GB
exeter.article-numberCD002854en_GB
dc.descriptionThis is the final version of the article. Available from the publisher via the DOI in this record.en_GB
dc.identifier.journalCochrane Database of Systematic Reviewsen_GB


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