vitamin e supplementation reduces cellular loss in the brain of a premature aging mouse model 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 lipidsoluble antioxidant that is investigated as nutritional supplement for its ability to prevent or delay the onset of specific aging pathologies including neurodegenerative disorderspurpose we aimed here to investigate the effect of vitamin e during aging progression in a well characterized mouse model for premature agingmethod xpg animals received diets with low 25 mgkg feed medium 75 mgkg feed or high 375 mgkg 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 agerelated changes were monitored for improvement by increased vitamin e or worsening by depletion in both liver and nervous system organs sensitive to oxidative stressresults mice supplemented with high levels of vitamin e showed a delayed onset of agerelated 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 p53positive cells throughout the brain indicative of a lower number of cells dying due to dna damage accumulated over timeconclusions 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