La Fata, G., van Vliet, N., Barnhoorn, S., Brandt, R. M. C., Etheve, S., Chenal, E., Grunenwald, C., Seifert, N., Weber, P., Hoeijmakers, J. H. J., Mohajeri, M. H. and Vermeij, W. P. (2017). Vitamin E Supplementation Reduces Cellular Loss in the Brain of a Premature Aging Mouse Model. JPAD-J. Prev. Alzheimers Dis., 4 (4). S. 226 - 236. PARIS: EDITIONS SERDI. ISSN 2426-0266

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Abstract

BACKGROUND: Aging is a highly complex biological process driven by multiple factors. Its progression can partially be influenced by nutritional interventions. Vitamin E is a lipid-soluble anti-oxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies, including neurodegenerative disorders. PURPOSE: We aimed here to investigate the effect of vitamin E during aging progression in a well characterized mouse model for premature aging. METHOD: Xpg-/- animals received diets with low (similar to 2.5 mg/kg feed), medium (75 mg/kg feed) or high (375 mg/kg feed) vitamin E concentration and their phenotype was monitored during aging progression. Vitamin E content was analyzed in the feed, for stability reasons, and in mouse plasma, brain, and liver, for effectiveness of the treatment. Subsequent age-related changes were monitored for improvement by increased vitamin E or worsening by depletion in both liver and nervous system, organs sensitive to oxidative stress. RESULTS: Mice supplemented with high levels of vitamin E showed a delayed onset of age-related body weight decline and appearance of tremors when compared to mice with a low dietary vitamin E intake. DNA damage resulting in liver abnormalities such as changes in polyploidy, was considerably prevented by elevated amounts of vitamin E. Additionally, immunohistochemical analyses revealed that high intake of vitamin E, when compared with low and medium levels of vitamin E in the diet, reduces the number of p53-positive cells throughout the brain, indicative of a lower number of cells dying due to DNA damage accumulated over time. CONCLUSIONS: Our data underline a neuroprotective role of vitamin E in the premature aging animal model used in this study, likely via a reduction of oxidative stress, and implies the importance of improved nutrition to sustain health.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
La Fata, G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
van Vliet, N.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Barnhoorn, S.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Brandt, R. M. C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Etheve, S.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Chenal, E.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Grunenwald, C.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Seifert, N.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Weber, P.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Hoeijmakers, J. H. J.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mohajeri, M. H.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Vermeij, W. P.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-248421
DOI: 10.14283/jpad.2017.30
Journal or Publication Title: JPAD-J. Prev. Alzheimers Dis.
Volume: 4
Number: 4
Page Range: S. 226 - 236
Date: 2017
Publisher: EDITIONS SERDI
Place of Publication: PARIS
ISSN: 2426-0266
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
Clinical NeurologyMultiple languages
Refereed: Yes
URI: http://kups.ub.uni-koeln.de/id/eprint/24842

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