Microbiome is an important component in the neurobiology of neurodegenerative [diseases. This page provides detailed information about its structure, function, and role in disease processes. [1] [1]
The gut microbiome comprises the trillions of microorganisms residing in the gastrointestinal tract, including bacteria, archaea, fungi, and viruses. Emerging research has established bidirectional communication between the gut and brain through the gut-brain-axis, with profound implications for neurodegenerative diseases including alzheimers, parkinsons, als, and huntington-pathway. The gut microbiome has been identified as a fundamental regulator of brain health, with disturbances in microbial composition (dysbiosis) linked to neuroinflammation, protein-aggregation, blood-brain-barrier dysfunction, and cognitive decline (Cryan et al., 2019. [2] [2]
Early microbiome changes have been detected in preclinical alzheimers patients and prodromal parkinsons patients, suggesting that gut dysbiosis may contribute to disease initiation rather than simply being a consequence of neurodegeneration (Zhu et al., 2024. [3] [3]
The human gut contains: [4]
| Bacterial Group | Role | Relevance to Neurodegeneration | [5]
|----------------|------|-------------------------------| [6]
| Lactobacillus | Probiotic; GABA production | Reduced in AD and PD patients | [7]
| Bifidobacterium | SCFA production; immune modulation | Reduced in AD; associated with cognitive function | [8]
| Faecalibacterium prausnitzii | Major butyrate producer; anti-inflammatory | Depleted in PD and multiple-sclerosis | [9]
| Akkermansia muciniphila | Mucin degradation; barrier integrity | Altered in PD; emerging therapeutic target | [10]
| Prevotella | Fiber degradation | Dramatically reduced in PD | [11]
| Enterobacteriaceae | Pro-inflammatory; LPS production | Elevated in AD and PD dysbiosis |
| Desulfovibrio | Hydrogen sulfide production | Elevated in PD; may promote alpha-synuclein aggregation | [5]
The gut and brain communicate through multiple interconnected pathways, collectively termed the gut-brain-axis (Cryan et al., 2019: [6]
Constipation and other GI symptoms precede PD motor symptoms by 10-20 years and correlate with ENS alpha, supporting the gut-origin hypothesis. [10]
als patients show gut dysbiosis with reduced Ruminococcaceae and Faecalibacterium, and increased Enterobacteriaceae. In SOD1-mutant mice, protective gut bacteria (Akkermansia muciniphila) produce nicotinamide that delays disease progression. [1]
huntington-pathway patients show altered gut microbiome composition with increased intestinal permeability. Mutant huntingtin expression in the ENS may contribute to GI dysfunction. [2]
MS patients consistently show reduced Prevotella and Clostridia, with increased Methanobrevibacter. FMT from MS patients to germ-free mice induces autoimmune CNS pathology. [3]
Clinical trials of probiotic formulations in AD and PD patients have shown:
FMT is being investigated as a therapeutic approach:
The study of Microbiome has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying [mechanisms of neurodegeneration and continues to drive therapeutic development. [10]
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions. [1]
Cryan JF, et al. The microbiota-. gut-brain-axis. Physiol Rev. 2019;99(4):1877-2013. DOI. 2019. ↩︎
Zhu S, et al. Microbiota-. Gut-Brain Axis and its therapeutic applications in neurodegenerative diseases. Signal Transduct Target Ther. 2024;9(1):37. DOI. 2024. ↩︎
Qin J, et al. A human gut microbial gene catalogue established by metagenomic sequencing. Nature. 2010;464(7285):59-65. DOI. 2010. ↩︎
Vogt NM, et al. Gut microbiome alterations in. alzheimers. Sci Rep. 2017;7(1):13537. DOI. 2017. ↩︎
Scheperjans F, et al. Gut microbiota are related to. parkinsons and clinical phenotype. Mov Disord. 2015;30(3):350-358. DOI. 2015. ↩︎
Sampson TR, et al. Gut microbiota regulate motor deficits and neuroinflammation in a model of. parkinsons. Cell. 2016;167(6):1469-1480.e12. DOI. 2016. ↩︎
Minter MR, et al. Antibiotic-induced perturbations in gut microbial diversity influences neuro-inflammation and amyloidosis in a murine model of. alzheimers. Sci Rep. 2016;6:30028. DOI. 2016. ↩︎
[Braak H, et al. [Staging of brain pathology related to sporadic Parkinson's Disease](https://doi.org/10.1016/S0197-4580(02). Neurobiol Aging. 2003. ↩︎
Cattaneo A, et al. Association of brain amyloidosis with pro-inflammatory gut bacterial taxa and peripheral inflammation markers in cognitively impaired elderly. Neurobiol Aging. 2017;49:60-68. DOI. 2017. ↩︎
Aho VTE, et al. Gut microbiota in Parkinson''s Disease: temporal stability and relations to disease progression. EBioMedicine. 2019;44:691-707. DOI. 2019. ↩︎
Svensson E, et al. Vagotomy and subsequent risk of Parkinson's Disease. Ann Neurol. 2015;78(4):522-529. DOI. 2015. ↩︎