Unraveling the molecular mechanisms of vitamin deficiency in Alzheimer's disease pathophysiology

Abstract

Alzheimer's disease (AD) is the most prevalent progressive neurodegenerative disease often characterized by memory loss, cognitive decline, and behavioral changes. The actual pathophysiology of AD remains unclear, but several factors including genetic, environmental, and lifestyle contribute significantly to the pathogenesis of AD. Even after over two decades of combined efforts to create novel interventions that can retard the progress of the disease, researchers still only have a small number of alternate medicines with poor efficacy. There is a recent growth of interest in the role of nutrients in brain health as we learn more about what nutrients are and how they impact hormonal and neurological processes that can result in a variety of neurological and psychiatric conditions. Additionally, deficiency of vitamins also gained attention for their pivotal roles in cognitive health. Vitamins, a crucial dietary supplement, regulate various physiological functions and maintain neuronal health, energy metabolism, and antioxidant defence. Vitamin B, such as B1, B6, and B12, are chief constituents for the metabolism of homocysteine and the release of neurotransmitters, a decrease in vitamin E and D may result in increased oxidative damage, which further contributes to neuronal loss. Vitamin deficiencies may make AD degenerative processes more severe as increased amyloid-beta (Aβ) plaque development and tau protein phosphorylation, are two characteristics of AD. This review explores a comprehensive summary of the most widely used vitamins and discusses the findings of recent research on the relationship between these vital micronutrients and AD.