Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β plaques and neurofibrillary tangles. Despite extensive research, the exact pathophysiology remains unclear. Recent studies highlight the role of the gut microbiota-gut-brain axis in AD, with altered gut microbiota composition linked to disease progression. The microbiota influences AD through mechanisms such as neuroinflammation, immune modulation, and amyloid clearance. While studies show changes in gut microbiota in AD patients and animal models, results are inconsistent due to factors like study design and population differences. Animal studies support a link between gut microbiota and AD pathologies, but causality remains unclear. The microbiota may regulate AD via direct infection or indirect pathways involving immune and metabolic systems. Key mechanisms include neuroinflammation, immune modulation, and the production of metabolites like short-chain fatty acids (SCFAs), which can influence brain function. SCFAs have complex roles in AD, with some studies showing neuroprotective effects and others indicating pro-inflammatory effects. Host genetic factors, such as APOE alleles, and sex differences also influence microbiota composition and AD pathology. Therapeutic strategies targeting the gut microbiota include antibiotics, fecal microbiota transplantation (FMT), prebiotics, probiotics, and postbiotics. These approaches aim to restore microbial balance and alleviate AD symptoms. While promising, further research is needed to understand the mechanisms and ensure the safety and efficacy of microbiota-based therapies in AD.Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-β plaques and neurofibrillary tangles. Despite extensive research, the exact pathophysiology remains unclear. Recent studies highlight the role of the gut microbiota-gut-brain axis in AD, with altered gut microbiota composition linked to disease progression. The microbiota influences AD through mechanisms such as neuroinflammation, immune modulation, and amyloid clearance. While studies show changes in gut microbiota in AD patients and animal models, results are inconsistent due to factors like study design and population differences. Animal studies support a link between gut microbiota and AD pathologies, but causality remains unclear. The microbiota may regulate AD via direct infection or indirect pathways involving immune and metabolic systems. Key mechanisms include neuroinflammation, immune modulation, and the production of metabolites like short-chain fatty acids (SCFAs), which can influence brain function. SCFAs have complex roles in AD, with some studies showing neuroprotective effects and others indicating pro-inflammatory effects. Host genetic factors, such as APOE alleles, and sex differences also influence microbiota composition and AD pathology. Therapeutic strategies targeting the gut microbiota include antibiotics, fecal microbiota transplantation (FMT), prebiotics, probiotics, and postbiotics. These approaches aim to restore microbial balance and alleviate AD symptoms. While promising, further research is needed to understand the mechanisms and ensure the safety and efficacy of microbiota-based therapies in AD.