A recent update on involvement of gut microbiota alterations in alzheimer’s disease pathogenesis

Changes in gut microbiota (GMB) composition, referred to as dysbiosis, are progressively associated with the onset and advancement of Alzheimer’s disease (AD). The gut-brain axis, a bidirectional communication pathway, is implicated, with the GMB influencing the central nervous system (CNS) through various immunological pathways. Research has found changes in the kinds and quantities of bacteria in the intestines of AD patients compared to healthy people. For instance, there’s commonly a reduction in helpful bacteria such as Firmicutes and Bifidobacteria, alongside a rise in potentially harmful bacteria including Bacteroidetes and Proteobacteria. Gut microorganisms can affect the immune system and play a role in neuroinflammation, an essential characteristic of AD. Dysbiosis may compromise the integrity of the gut and blood-brain barriers, facilitating the entry of harmful substances, such as inflammatory molecules and bacterial byproducts, into the brain. GMB can generate amyloid-like proteins and lipopolysaccharides (LPS), which might play a role in the buildup of amyloid plaques in the brain, a characteristic of AD. Further investigation is required to completely comprehend the exact processes through which changes in GMB influence AD. AD still has very limited options when it comes to pharmacological treatment. The disruption of the brain-gut-microbiota link may contribute to the onset of AD and provide new insights into its pathology and treatment. In this review, we explore alterations in the GMB that are linked to the pathophysiology of AD disorder.