Gut Microbiota and Neurological Disorders: Unraveling the GutBrain Axis The Gut-Brain Axis in Neurological Disorders
Recent scientific advancements have improved our understanding of health and disease, yet some neurological disorders remain poorly understood. Gut microbiota is a diverse community of bacteria residing in the gut, and they play a role in digestion, metabolism, the immune system, and neuronal functions. There is a bidirectional communication system known as the gut-brain axis (GBA) between the central nervous system and the gut microbiota by neural, endocrine, and immunological mechanisms. Gut microbiota produces metabolites such as short-chain fatty acids (SCFAs), neurotransmitters, and hormones that regulate brain function and behavior. Alteration of gut microbiota or dysbiosis is associated with neurological disorders such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, and depression. Changes in microbiota composition can cause systemic inflammation, regulate the concentrations of neurotransmitters, and affect the integrity of the blood-brain barrier, resulting in neurodegeneration. New therapeutic modalities, including probiotics, prebiotics, nutritional intervention, and fecal microbiota transplantation, have been developed to re-establish homeostasis within the gut and halt disease progression. Metagenomics and artificial intelligence are transforming microbiome research, enabling targeted treatment based on the individualized microbiota signature. Information on the gut-brain axis offers promising directions for the development of novel therapies in psychiatric and neurodegenerative disorders
Authors
- Neha Mishra (ORCID: https://orcid.org/0000-0003-0310-1811)
- Manoj K. Mishra (ORCID: https://orcid.org/0000-0002-3402-388X)
- Vishal Patil
Publication Details
- Journal
- International Journal of Pharmaceutical Research and Applications
- Published
- 2025-03-01
- DOI
- https://doi.org/10.35629/4494-100318581869
- Primary Topic
- Diet and metabolism studies
- Type
- article
- Field-Weighted Citation Impact
- 0.00