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Dietary Vitamin E as a protective factor for Parkinson’s Disease: a clinical and experimental study

T. Schirinzi, G. Martella, P. Imbriani, G. Di Lazzaro, M. Alwardat, M. Pierantozzi, N. Mercuri, A. Pisani (Rome, Italy)

Meeting: 2019 International Congress

Abstract Number: 1519

Keywords: Oxidative stress, Vitamin E

Session Information

Date: Tuesday, September 24, 2019

Session Title: Environmental Causes

Session Time: 1:45pm-3:15pm

Location: Agora 2 West, Level 2

Objective: To test if a higher dietary intake of Vitamin E might represent a protective factor in Parkinson’s disease (PD).

Background: Effective disease-modifying treatments are an urgent need for PD. To counteract oxidative stress is a putative successful strategy, not only by using synthetic compounds, but also by natural agents or dietary choices. Vitamin E, in particular, is a powerful antioxidant, commonly found in vegetables and other components of the diet [1].

Method: We conducted a study including: 1) a retrospective assessment of dietary Vitamin E intake (VEI) in 100 PD patients compared to 100 healthy controls, aimed at determining if a different dietary VEI is associated with diverse clinical conditions; 2) an in vitro protocol in brain slices of a PD mouse model, aimed at evaluating the effects of Vitamin E on synaptic plasticity abnormalities, a peculiar endophenotype observed in distinct PD models. Specifically, we used homozygous PTEN-induced kinase 1 (PINK1) knockout mice (PINK1−/−), an established model of subclinical PD, in which we previously demonstrated the loss of both long-term potentiation (LTP) and long-term depression (LTD) at corticostriatal synapses, in the absence of overt neurodegeneration.

Results: The analysis showed that VEI was lower in PD patients and inversely associated with PD occurrence, independently from age and gender (OR = 1.022; 95% CI = 0.999 – 1.045; p<0.05), though unrelated to clinical severity. Moreover, the chronic administration of Vitamin E (alpha-tocopherol and the water-soluble analogue trolox) fully restored corticostriatal synaptic plasticity in PINK1−/− mice, which is suggestive of a specific protective action.

Conclusion: Our study highlighted the protective role of dietary Vitamin E in PD. Additionally, we observed that it might compensate PINK1 haploinsufficiency and mitochondrial impairment, reverting some central steps of the pathogenic process in a mouse model. Altogether, both clinical and experimental findings suggest that Vitamin E could be a potential useful agent for PD patients. These data, although preliminary, may encourage future confirmatory trials.

References: 1. Jiang Q, 2014. Natural forms of vitamin E: metabolism, antioxidant, and anti-inflammatory activities and their role in disease prevention and therapy. Free Radic Biol Med; 72:76–90.

To cite this abstract in AMA style:

T. Schirinzi, G. Martella, P. Imbriani, G. Di Lazzaro, M. Alwardat, M. Pierantozzi, N. Mercuri, A. Pisani. Dietary Vitamin E as a protective factor for Parkinson’s Disease: a clinical and experimental study [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/dietary-vitamin-e-as-a-protective-factor-for-parkinsons-disease-a-clinical-and-experimental-study/. Accessed May 9, 2025.
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