Vitamin E: A Nutritional Supplementation for Curbing Age Related Neurodegenerative Diseases Progression

Review Article

J Pathol & Microbiol. 2016; 1(2): 1009.

Vitamin E: A Nutritional Supplementation for Curbing Age Related Neurodegenerative Diseases Progression

Patel R¹ and Kalani A²*

¹College of Medicine, University of Florida, USA

²School of Medicine, University of Louisville, USA

*Corresponding author: Anuradha Kalani, School of Medicine University of Louisville, USA

Received: November 09, 2016; Accepted: November 22, 2016;Published: November 25, 2016


Background: Oxidative stress has been described as a well-established causative factor to deteriorate neurons and is associated with ageing and age related neurodegenerative disorders. Vitamin E is a lipophilic natural antioxidant and the generic term for tocopherols and tocotrienols. Vitamin E acts as an antioxidant which play a very important role for normal neurological function as well as in neurodegenerative disease that it is being treated. It is most effective in Alzheimer’s Disease (AD) and has been shown to play a central role in neuroprotection and found to be in effective for neuroprotection in Parkinson’s Disease (PD). Vitamin E is a chain breaking antioxidant which acts as a non-specific protective chemical shield for neurons and protects neurons through antioxidant-independent pathways; they are highly effective and further investigations on their activity might lead to an even more effective application of antioxidants. Reactive oxygen species and free radical generation can lead to neuronal damage associated with AD, PD, amyotrophic lateral sclerosis, Huntington Disease (HD) and cerebral ischemic stroke many signs of oxidative damage. From this review, we would like to highlight the importance of vitamin E in neuroprotection. Conclusion: Since, Vitamin E therapy has not proven promising results in clinical trial; it could suggest that if a person uses vitamin irregularly, as a nutritional supplement, they may have less progression of neurodegenerative disease.

Keywords: Vitamin E; Free radicals; Neurodegenerative disease


AD: Alzheimer’s Disease; PD: Parkinson’s Disease; HD: Huntington Disease; ALS: Amyotrophic Lateral Sclerosis; ROS: Reactive Oxygen Species; RNS: Reactive Nitrogen Species; SOD1: Superoxide Dismutase 1


A number of evidence suggests that generation of free radicals, such as Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS), in the human body causes oxidative stress. Oxidative stress has been shown to play a critical role in development of neurodegenerative disease by enhancing the apoptotic cell death, neuroinflammation, mitochondrial dysfunction, synapse damage, neuronal demyelination, neurofibrillary pathology, tau hyperphosphorylation, aggregation of beta-amyloid Superoxide Dismutase 1 (SOD1) and, alpha-synuclein. All these contributory factors can induce oxidative damage and age related neurodegenerative problem and thus induces pathological condition like Alzheimer’s Disease (AD), Parkinson Disease (PD) and, Amyotrophic Lateral Sclerosis (ALS).

Vitamin E was identified as an essential nutrient [1,2]. The term vitamin E refers to a family of tocochromanols, neutral plant lipids that include tocopherols and tocotrienols. Vitamin E is a fat soluble component which is also known as tocopherol. Vitamin E is highly enriched in human body in which α-tocopherol is most abundant from vitamin E family and highly essential component for human health. The major function of α-tocopherol is believed to be an antioxidant that prevents biological and body physiology from oxidative damage. The most important part of this vitamin is that its antioxidant activity is due to its free radical quenching activity. These free radicals mainly damage the lipid bilayer of cellular components which is made up of unsaturated lipids. Free radical causes the damage of lipid bilayer which is known as lipid peroxidation. Vitamin E prevents the lipid peroxidation of biological membrane by inhibiting or by the interfering the chain reaction of oxidative damage.

Chemistry of Vitamin E

Vitamin E is a group of potent, lipid-soluble, chain-breaking antioxidants, consists of a chroman head with two rings (one phenolic acid ring and one heterocyclic ring) linked to an isoprenoid-derived hydrophobic tail. The vitamin can exist as two types of homologous series: the tocopherol and tocotrienol structures. Both structures are similar except the tocotrienol structure has farnesyl rather than a saturated isoprenoid C16 side chain. Tocopherols (Vitamin E) are equipped to perform a unique function; they can interrupt free radical chain reactions by capturing the free radical; this imparts to them their antioxidant properties. The free hydroxyl group on the aromatic ring is responsible for the antioxidant properties. The hydrogen from this group is donated to the free radical, resulting in a relatively stable free radical form of the vitamin.

Antioxidants mechanism of Vitamin E

Vitamin E members possess a common hydroxylated chromanol ring and a hydrophobic 13-carbon phytyl side chain. Tocopherols have a saturatedphytylchain; whereas the side chain of tocotrienols contains three double bonds. The extent and location of chromanol ring methylation distinguish the various vitamin families. One of the striking features of vitamin E biology is that regardless of the tocopherol composition of dietary intake, the α-tocopherol form is selectively enriched in plasma and tissues of most organisms. Hence, it has been recently proposed that other members of the vitamin E family display biological activities. Accordingly, several studies and observations suggested that α-tocopherol as the major lipid soluble antioxidant in humans [3]. Reports also suggested that that α-tocopherol is an essential nutrient whose absence in human or in mammals severely compromises the health. It has also been noted that the α-tocopherol should be maintained and the recommended daily intake is15mg per day for each healthy adult.

Role of Vitamin E in brain and neuronal injury

Vitamin E (α-tocopherol) is expressed in the brain [4]. Additionally, expression levels of α-tocopherol were shown to increase in patients afflicted with oxidative stress–related diseases [5]. Findings specify that vitamin E is maintained in the CNS and that α-tocopherol may serve to maintain and regulate the brain function (Figure 1). Vitamin E deficiency manifests primarily as neurological and neuromuscular disorders [6-9]. Vitamin E deficiency induced axonalpathy affects sensory neurons. Vitamin E deficiency is a likely contributing factor to the associated neurological deficits. An important pathological hallmark of vitamin E deficiency is the presence of axonal swellings, intracellular aggregates of proliferated endoplasmic reticulum, mitochondria and neurofilaments [10]. These physical barriers for axonal transport may involve in the disruption of neuron function. The evidence regarding this loss is also found with attenuated rates of axonal retrograde and anterograde transport and altered respiratory control in mitochondria isolated from brains of vitamin E deficient rats [11]. In axonal dystrophy, deposition of lipid peroxidation products in lipofuscin aggregates is a hallmark of vitamin E which causes severe oxidative stress.

Citation:Patel R and Kalani A. Vitamin E: A Nutritional Supplementation for Curbing Age Related Neurodegenerative Diseases Progression. J Pathol & Microbiol. 2016; 1(2): 1009.