The Link between Gut Microbiome, Amyloid-Beta Deposition, Brain Inflammation, and Alzheimer’s Disease: A Review of Current Literature

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles, and cognitive decline. AD has gained increasing global attention. As the aging population continues to grow, the economic burden on individuals, families, and healthcare systems rises, emphasizing the urgent need for early detection and natural therapeutic approaches to address these challenges. The gut microbiota regulates essential physiological functions, including digestion, nutrient absorption, and inflammatory signaling. Dysbiosis, or changes in gut microbiome composition, is marked by the overgrowth of pathogenic bacteria and depletion of beneficial species. Gut dysbiosis is also linked to pathological features of AD, such as increased Aβ deposition, compromised intestinal and blood-brain barrier integrity, and neuroinflammation through the brain-gut microbiome axis (BGMA). However, the connection between the gut microbiome and AD pathological hallmarks remains unclear. This narrative review aims to explore current research on the relationship between gut dysbiosis and the pathological features of AD, with the goal of highlighting the role of the gut system in brain function and AD pathogenesis. Vitamin E, due to its antioxidative and anti-inflammatory properties, may serve as a promising natural option for modulating the gut microbiome while potentially delaying AD progression and promoting a balanced microbial composition.