Abstract
Vitamin E deficiency is associated with many neurological problems. Although the mechanisms of vitamin E action in neurodegenerative diseases are not clear, there are many possible mechanisms. Examples of such mechanisms are the protective effects of vitamin E against oxidative stress damage and its suppressive role in the expression of many genes involved in the development of neurodegeneration. Many studies have evaluated the relationship between vitamin E intake or vitamin E levels in body fluids and neurodegenerative diseases. Some studies concluded that vitamin E can play a protective role in neurodegeneration with respect to diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), stroke and amyotrophic lateral sclerosis (ALS). Vitamin E supplementation was also associated with risk factors for some neurodegenerative diseases. In this review, we discuss the possible effects of vitamin E on the development and course of AD, PD, stroke and ALS, and the potential mechanisms involved. Vitamin E deficiency is associated with many neurological problems. Although the mechanisms of vitamin E action in neurodegenerative diseases are not clear, there are many possible mechanisms. Examples of such mechanisms are the protective effects of vitamin E against oxidative stress damage and its suppressive role in the expression of many genes involved in the development of neurodegeneration. Many studies have evaluated the relationship between vitamin E intake or vitamin E levels in body fluids and neurodegenerative diseases. Some studies concluded that vitamin E can play a protective role in neurodegeneration with respect to diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and amyotrophic lateral sclerosis (ALS). Vitamin E supplementation was also associated with risk factors for some neurodegenerative diseases. In this review, we discuss the possible effects of vitamin E on the development and course of AD, PD, stroke and ALS, and the potential mechanisms involved.
Highlights
Characterized by specific neuronal cell losses, neu‐ rodegenerative diseases are among the leading cause of disabilities in elderly people (Knight, 1997; Floyd and Hensley 2002, Ricciarelli et al, 2007)
This review focuses on the potential effects and mechanisms of vitamin E action in Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and amyotrophic lateral sclerosis (ALS)
Expression levels of mutations in TTPA are marked‐ ly elevated in brain samples from human patients af‐ flicted with oxidative stress‐related neurodegenera‐ tive diseases such as ataxia with vitamin E deficiency (AVED) and AD. These findings demonstrate that vitamin E and TTPA may have critical roles in neurodegenerative diseases (Joshi and Praticò, 2012; Ulatowski and Manor, 2015)
Summary
Characterized by specific neuronal cell losses, neu‐ rodegenerative diseases are among the leading cause of disabilities in elderly people (Knight, 1997; Floyd and Hensley 2002, Ricciarelli et al, 2007). Reactive oxygen species (ROS) cause cell damage by means of lipid peroxidation and oxidation of proteins and DNA (Halliwell, 1999). Cells have devel‐ oped various defense and repair mechanisms in order to cope with oxidative stress. Antioxidants such as vi‐ tamin E play important roles in these defense mech‐ anisms (Halliwell, 1999; Ricciarelli et al, 2007). It is believed that vitamin E, through these mechanisms, may have ther‐ apeutic effects in many neurodegenerative diseases in‐ cluding Alzheimer’s disease (AD), Parkinson’s disease (PD), stroke and amyotrophic lateral sclerosis (ALS) as illustrated in Fig. 1 (Sung et al, 2004; Ascherio et al, 2005; Ricciarelli et al, 2007)
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