Navigating the Role and Approach of Gut Microbiota in Addressing Alzheimer's Disease Pathogenesis
DOI:
https://doi.org/10.36877/pmmb.a0000454Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by amyloid beta plaques and tau protein neurofibrillary tangles, leading to cognitive decline. The lack of effective treatments compounds the significant human and financial burdens AD poses. Despite extensive research, the exact mechanisms of the disease remain elusive. Recent studies have shown promise in using anti-Aβ antibodies to reduce amyloid accumulation and slow dementia progression. However, diversifying therapeutic strategies is crucial for making meaningful progress. In recent years, research has increasingly focused on the microbiota-gut-brain axis in AD. Mounting evidence suggests that changes in gut microbiota composition are linked to AD progression, implicating various pathways. Dysregulation of microbiota taxa can trigger systemic inflammation by increasing gut permeability, ultimately leading to neural damage and neurodegeneration. Poor dietary habits and aging exacerbate gut dysbiosis, worsening AD pathology. However, investigations in this area are still in their early stages, with many aspects awaiting exploration and understanding. A thorough comprehension of the complex interactions within the microbiota-AD relationship is essential for refining therapeutic approaches. Interventions targeting gut microbiota, such as dietary adjustments, probiotics, and faecal microbiota transplantation, offer potential as therapeutics. This review highlights the detrimental role of gut dysbiosis in AD, offering insights into enhancing therapeutic avenues for the disease.
Graphical abstract: The bidirectional interaction between the brain and the gut through neuroendocrine, immune, and metabolic pathways. Created with BioRender.com
Downloads
Published
How to Cite
Issue
Section
License
Copyright (c) 2024 Imrana Jazuli, Akeela Jazeel, Lakshmi Selvaratnam, Deepa Alex, Yatinesh Kumari
This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.
Author(s) shall retain the copyright of their work and grant the Journal/Publisher right for the first publication with the work simultaneously licensed under:
Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). This license allows for the copying, distribution and transmission of the work, provided the correct attribution of the original creator is stated. Adaptation and remixing are also permitted.
This broad license intends to facilitate free access to, as well as the unrestricted reuse of, original works of all types for non-commercial purposes.
The author(s) permits HH Publisher to publish this article that has not been submitted elsewhere.