ACE Alzheimer’s: The Role of Vitamin A, C and E (ACE) in Oxidative Stress induced Alzheimer’s Disease

Abstract

Alzheimer's disease (AD), a chronic neurodegenerative disease which is known to progress gradually and has now become a substantial health concern through-out the world. Clinically, cognitive declination and progressive dementia are the main characteristics of AD while pathologically; Aß plaques and tau-neurofibrils are the hallmarks. The present literature search has suggested that oxidative stress is one of the most vital risk factor which can potentially lead to the development of AD.
 Oxidative stress is known to produce the Reactive Oxygen Species (ROS) which has a potential to increase in the structural and functional abnormalities in the glial cells of the brain and which could further lead to a cognitive decline and subsequently, dementia. Hence, in order to curb this oxidative stress in the glial cells, antioxidants have been proved to be of great help according to the literature search done in PubMed, Google Scholar and Scopus. We included Meta-Analysis, Systemic Reviews and Original studies. Vitamins A, C, and E are an example of antioxidants that can be used as adjuvants in the treatment of AD.
 This article focuses on the contemporary literature search and presents forward the evidence-based banes of using Vitamin A, C, and E as an adjuvant therapy for preventing and treating AD.
 Keywords: Vitamin A, Vitamin C, Vitamin E, Antioxidants, Alzheimers disease, Adjuvant therapy

Role of Lipid Peroxidation Process in Neurodegenerative Disorders

“…(2) elimination of LPO products [108,109]. Prevention of LPO products formation is a primary successful method with anti-oxidants such as vitamin C and vitamin E are inhibits the LPO [110]. The alternative method of LPO inhibition is deuteration of PUFA at double bond of methylene bridges (bis-allylic sites) leads to reduce the chain reaction process [111].…”

Protection from the Pathogenesis of Neurodegenerative Disorders, including Alzheimer’s Disease, Amyotrophic Lateral Sclerosis, Huntington’s Disease, and Parkinson’s Diseases, through the Mitigation of Reactive Oxygen Species

“…OS can also lead to alterations in the structure of proteins, and impaired protein structures can further exacerbate oxidative damage [9]. Indeed, ROS causes protein oxidization and modi ied protein structures that easily aggregate and dimerize [30]. These functionally and structurally abnormal oxidized proteins then accumulate within the cytoplasm of neurons in the form of Aß plaques and tau neural ibrillary tangles (NFT) [31].…”

“…These functionally and structurally abnormal oxidized proteins then accumulate within the cytoplasm of neurons in the form of Aß plaques and tau neural ibrillary tangles (NFT) [31]. Aß plaques themselves are also known to be responsible for the formation of ROS, resulting in a continuous cycle of OS [30]. In addition, a growing body of evidence has demonstrated that ROS causes oxidative damage to lipids and DNA, which leads to various cellular dysfunctions [4,32,33].…”

“…A growing body of evidence indicates that a wholesome dietary plan consisting of ish, fruit, and vegetables is important for optimizing cognition and reducing the risk of AD [73]. In particular, reduced levels of fat-soluble vitamins, such as vitamins A, D, E, and K, may be responsible for causing a cognitive decline among AD patients [30,[74][75][76]. Antioxidants that may help treat AD as adjuvants to traditional therapies include vitamins A, C, and E [16,30,75,77].…”

Anti-Oxidant Nutrition: An Adjuvant With a Balance Diet

“…Recently, vitamin A and C and E have been shown to reduce the risk of many diseases including Alzheimer's diseases [11]. Dietary polyunsaturated fatty acids have also known to have immunomodulatory and other beneficial health-promoting effects [12].…”