Gut Dysbiosis and Neurodegeneration: The Expanding Role of the Microbiome in Alzheimer's Disease Pathogenesis and Therapy

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles (tau), and chronic neuroinflammation. Emerging research highlights the gut-brain axi98s (GBA) as a critical mediator in AD pathogenesis, where gut dysbiosis disrupts neural, endocrine, immune, and metabolic signalling. This review synthesizes current evidence on how microbial metabolites (e.g., short-chain fatty acids, tryptophan derivatives), gut barrier dysfunction, and systemic inflammation contribute to Aβ aggregation, tau hyperphosphorylation, and microglial activation. We explore therapeutic interventions including probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary modifications that target the GBA to mitigate AD progression. Clinical and preclinical studies underscore the potential of microbiome-based therapies, though challenges in standardization and causality remain. Future research should integrate multi-omics approaches and personalized medicine to harness the GBA for AD prevention and treatment.

Publication Details

Journal
Zenodo (CERN European Organization for Nuclear Research)
Published
2025-06-24
DOI
https://doi.org/10.5281/zenodo.15730139
Primary Topic
Neuroendocrine regulation and behavior
Type
article
Field-Weighted Citation Impact
0.00
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article

Gut Dysbiosis and Neurodegeneration: The Expanding Role of the Microbiome in Alzheimer's Disease Pathogenesis and Therapy

Zenodo (CERN European Organization for Nuclear Research)
Neuroendocrine regulation and behavior
article

Gut Dysbiosis and Neurodegeneration: The Expanding Role of the Microbiome in Alzheimer's Disease Pathogenesis and Therapy

article en

Abstract

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid-beta (Aβ) plaques, neurofibrillary tangles (tau), and chronic neuroinflammation. Emerging research highlights the gut-brain axi98s (GBA) as a critical mediator in AD pathogenesis, where gut dysbiosis disrupts neural, endocrine, immune, and metabolic signalling. This review synthesizes current evidence on how microbial metabolites (e.g., short-chain fatty acids, tryptophan derivatives), gut barrier dysfunction, and systemic inflammation contribute to Aβ aggregation, tau hyperphosphorylation, and microglial activation. We explore therapeutic interventions including probiotics, prebiotics, fecal microbiota transplantation (FMT), and dietary modifications that target the GBA to mitigate AD progression. Clinical and preclinical studies underscore the potential of microbiome-based therapies, though challenges in standardization and causality remain. Future research should integrate multi-omics approaches and personalized medicine to harness the GBA for AD prevention and treatment.

Zenodo (CERN European Organization for Nuclear Research)
Good health and well-being
Openalex Percentile: Top 48%
Neuroendocrine regulation and behavior
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