Alzheimer's disease (AD), a progressive neurodegenerative disorder, is characterized by cognitive decline, memory loss, and behavioral disturbances. Its pathogenesis is complex and multifactorial, involving amyloid-β (Aβ) plaque deposition, neurofibrillary tangle formation, oxidative stress, and neuroinflammation. While currently no cure exists, therapeutic strategies aim to mitigate disease progression and improve patient quality of life. Vitamin E, a potent lipid-soluble antioxidant, has emerged as a potential therapeutic agent due to its multifaceted physiological effects relevant to AD pathology. This article explores the potential mechanisms through which vitamin E might contribute to AD management. Its primary role is scavenging free radicals, reducing oxidative stress, a hallmark of AD. Oxidative stress damages neuronal membranes, mitochondria, and proteins, contributing to neuronal dysfunction and death. Vitamin E, specifically α-tocopherol, effectively neutralizes reactive oxygen species (ROS) and lipid peroxides, protecting neuronal structures from oxidative damage. Furthermore, vitamin E's influence extends beyond direct antioxidant activity. It modulates inflammatory pathways by inhibiting the production of pro inflammatory cytokines, thereby reducing neuroinflammation, another key contributor to AD pathogenesis. Studies suggest that vitamin E can also influence Aβ metabolism, potentially reducing its aggregation and plaque formation. This may involve influencing Aβ-related signaling pathways or interacting with Aβ itself, thereby preventing its neurotoxic effects. However, the clinical efficacy of vitamin E in AD remains a subject of ongoing debate. While some clinical trials have demonstrated modest cognitive benefits, particularly in the early stages of the disease, others have yielded inconsistent results. This variability may be attributed to factors such as dosage, disease stage at intervention, and patient heterogeneity. Furthermore, the precise mechanisms through which vitamin E exerts its effects in the complex milieu of the AD brain require further investigation. Future research should focus on elucidating the optimal dosage, treatment duration, and patient selection criteria for maximizing the therapeutic potential of vitamin E. Investigating the synergistic effects of vitamin E with other therapeutic interventions, such as cholinesterase inhibitors or disease modifying therapies, may also prove beneficial. Ultimately, a comprehensive understanding of vitamin E's physiological actions in the context of AD is crucial for developing effective and targeted therapeutic strategies.