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Vitamin E and Alzheimer's disease: what do we know so far?
Clin Interv Aging. 2019; 14:1303-1317.CI

Abstract

Vitamin E has been proposed as a potential clinical intervention for Alzheimer's disease (AD) given the plausibility of its various biological functions in influencing the neurodegenerative processes associated with the condition. The tocopherol and tocotrienol isoforms of vitamin E have multiple properties including potent antioxidant and anti-inflammatory characteristics, in addition to influences on immune function, cellular signalling and lowering cholesterol. Several of these roles offer a theoretical rationale for providing benefit for the treatment of AD-associated pathology. Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD development while intake, particularly from dietary sources, may limit or reduce the rate of disease progression. This benefit may be linked to synergistic actions between vitamin E isoforms and other micronutrients. Nevertheless, randomised trials have found limited and inconsistent evidence of vitamin E supplementation as an effective clinical intervention. Thus, despite a strong rationale in support of a beneficial role for vitamin E for the treatment of AD, the evidence remains inconclusive. Several factors may partly explain this discrepancy and represent the difficulties of translating complex laboratory evidence and dietary interactions into clinical interventions. Methodological design limitations of existing randomised trials and restrictions to supplementation with a single vitamin E isoform may also limit the influence of effect. Moreover, several factors influence individual responsiveness to vitamin E intake and recent findings suggest variation in the underlying genetic architecture attenuates vitamin E biological availability and activity which likely contributes to the variation in clinical responsiveness and the failure of randomised trials to date. Importantly, the clinical safety of vitamin E remains controversial and warrants further investigation.

Authors+Show Affiliations

Centre for Public Health, Queen's University Belfast, Belfast, UK.Centre for Public Health, Queen's University Belfast, Belfast, UK.Centre for Public Health, Queen's University Belfast, Belfast, UK.Centre for Public Health, Queen's University Belfast, Belfast, UK.

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

31409980

Citation

Browne, Declan, et al. "Vitamin E and Alzheimer's Disease: what Do We Know so Far?" Clinical Interventions in Aging, vol. 14, 2019, pp. 1303-1317.
Browne D, McGuinness B, Woodside JV, et al. Vitamin E and Alzheimer's disease: what do we know so far? Clin Interv Aging. 2019;14:1303-1317.
Browne, D., McGuinness, B., Woodside, J. V., & McKay, G. J. (2019). Vitamin E and Alzheimer's disease: what do we know so far? Clinical Interventions in Aging, 14, 1303-1317. https://doi.org/10.2147/CIA.S186760
Browne D, et al. Vitamin E and Alzheimer's Disease: what Do We Know so Far. Clin Interv Aging. 2019;14:1303-1317. PubMed PMID: 31409980.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vitamin E and Alzheimer's disease: what do we know so far? AU - Browne,Declan, AU - McGuinness,Bernadette, AU - Woodside,Jayne V, AU - McKay,Gareth J, Y1 - 2019/07/18/ PY - 2019/05/10/received PY - 2019/07/04/accepted PY - 2019/8/15/entrez PY - 2019/8/15/pubmed PY - 2019/12/18/medline KW - Alzheimer’s disease KW - antioxidants KW - tocopherols KW - tocotrienols KW - vitamin E SP - 1303 EP - 1317 JF - Clinical interventions in aging JO - Clin Interv Aging VL - 14 N2 - Vitamin E has been proposed as a potential clinical intervention for Alzheimer's disease (AD) given the plausibility of its various biological functions in influencing the neurodegenerative processes associated with the condition. The tocopherol and tocotrienol isoforms of vitamin E have multiple properties including potent antioxidant and anti-inflammatory characteristics, in addition to influences on immune function, cellular signalling and lowering cholesterol. Several of these roles offer a theoretical rationale for providing benefit for the treatment of AD-associated pathology. Diminished circulating concentrations of vitamin E have been demonstrated in individuals with AD. Reduced plasma levels have furthermore been associated with an increased risk of AD development while intake, particularly from dietary sources, may limit or reduce the rate of disease progression. This benefit may be linked to synergistic actions between vitamin E isoforms and other micronutrients. Nevertheless, randomised trials have found limited and inconsistent evidence of vitamin E supplementation as an effective clinical intervention. Thus, despite a strong rationale in support of a beneficial role for vitamin E for the treatment of AD, the evidence remains inconclusive. Several factors may partly explain this discrepancy and represent the difficulties of translating complex laboratory evidence and dietary interactions into clinical interventions. Methodological design limitations of existing randomised trials and restrictions to supplementation with a single vitamin E isoform may also limit the influence of effect. Moreover, several factors influence individual responsiveness to vitamin E intake and recent findings suggest variation in the underlying genetic architecture attenuates vitamin E biological availability and activity which likely contributes to the variation in clinical responsiveness and the failure of randomised trials to date. Importantly, the clinical safety of vitamin E remains controversial and warrants further investigation. SN - 1178-1998 UR - https://www.unboundmedicine.com/medline/citation/31409980/Vitamin_E_and_Alzheimer's_disease:_what_do_we_know_so_far DB - PRIME DP - Unbound Medicine ER -