There is a growing body of evidence linking the intestinal environment and the central nervous system (CNS). The so-called gut-brain (GBA) axis consists of bidirectional communication between the enteric bacteria and the CNS via hormonal, neural, and immune pathways. Changes in the intestinal environment can affect mood, emotion, or cognitive abilities, and in turn, emotional factors can influence gastrointestinal function. Significantly gut microbiota's pathological conditions can evoke impairment of the gastrointestinal mucosal barrier, triggering a systemic inflammatory response in neural cells, and ultimately, neuronal degeneration. The dysbiosis has been demonstrated to be linked to Parkinson's disease, Alzheimer's disease, multiple sclerosis, and amyotrophic lateral sclerosis. Age-related changes in the microbiota, immune system, and gut barrier and blood-brain-barrier functions are also critical for neurodegeneration. Moreover, the hypothesis that the misfolded and aggregated proteins originate in the gut and spread in a prion-like fashion also highlights the role of the GBA in neurodegeneration.
Therefore, contemporary research focuses on compounds that might benefit against neurodegeneration by restoring the gut microbiome's dysbiosis. Of note, the progressive pathological processes start years before the clinical onset of the disease, and at the time of diagnosis, the disease stage is too advanced for successful therapy. Furthermore, diagnostic targeting of new putative early markers of neurodegenerative diseases, including those associated with gut, microbiota, and neuroinflammation, can create an opportunity to develop novel neuroprotective and disease-modifying therapeutic options.
In light of the above, diet is a major etiological factor for the initiation and development of neurodegenerative disorders since it influences the microbiota throughout the whole life. Food constituents play a key role in age-related changes in the elderly microbiota and possibly contribute to the triggering an initial proteinopathy event within the gut at any stage of life. On the other hand, some phytoconstituents are biotransformed by commensal bacteria into metabolites with higher neuroprotective activity than their precursor structures and hence exert a beneficial effect on the brain. Interestingly, the immense metabolic potential of enteric bacteria has given rise to the development of the transplantation of fecal microbiota from healthy individuals as an experimental therapy in the treatment of neurodegenerative diseases.
This Research Topic aims to provide novel insights into the nature of the gut bacteria-neuro-immune crosstalk in neurodegeneration.
Potential topics include but are not limited to the following:
- The regulatory role of microbiota in stress and neuroinflammation
- Pathways involved in intestinal metabolites of microbial origin influencing the central nervous system
- Neurotransmitters in Microbiomes
-The hypothesis of prion-like propagation of misfolded proteins within the GBA
- Putative metabolic markers of neurodegenerative diseases
- GBA as a new therapeutic target in pharmacotherapies restoring microbiota homeostasis towards neuroprotection
-The role of probiotic intervention on possible treatment and prevention of neurodegenerative diseases
- Preventing and treating neurodegenerative diseases by antibiotics
- The endotoxin hypothesis of neurodegeneration
- Polyphenols-gut microbiota interplay against neurodegeneration
- The role of diet in modulating the gut bacteria-neuro-immune crosstalk
- Gut microbiota transplantation in neurodegenerative diseases
- Pros and cons of current in vivo models of neurodegenerative diseases in neglecting the influence of GBA axis on animals phenotype.
We would like to thank Justyna Barut, PhD student at the Maj Institute of Pharmacology for contributing this image.
There is a growing body of evidence linking the intestinal environment and the central nervous system (CNS). The so-called gut-brain (GBA) axis consists of bidirectional communication between the enteric bacteria and the CNS via hormonal, neural, and immune pathways. Changes in the intestinal environment can affect mood, emotion, or cognitive abilities, and in turn, emotional factors can influence gastrointestinal function. Significantly gut microbiota's pathological conditions can evoke impairment of the gastrointestinal mucosal barrier, triggering a systemic inflammatory response in neural cells, and ultimately, neuronal degeneration. The dysbiosis has been demonstrated to be linked to Parkinson's disease, Alzheimer's disease, multiple sclerosis, and amyotrophic lateral sclerosis. Age-related changes in the microbiota, immune system, and gut barrier and blood-brain-barrier functions are also critical for neurodegeneration. Moreover, the hypothesis that the misfolded and aggregated proteins originate in the gut and spread in a prion-like fashion also highlights the role of the GBA in neurodegeneration.
Therefore, contemporary research focuses on compounds that might benefit against neurodegeneration by restoring the gut microbiome's dysbiosis. Of note, the progressive pathological processes start years before the clinical onset of the disease, and at the time of diagnosis, the disease stage is too advanced for successful therapy. Furthermore, diagnostic targeting of new putative early markers of neurodegenerative diseases, including those associated with gut, microbiota, and neuroinflammation, can create an opportunity to develop novel neuroprotective and disease-modifying therapeutic options.
In light of the above, diet is a major etiological factor for the initiation and development of neurodegenerative disorders since it influences the microbiota throughout the whole life. Food constituents play a key role in age-related changes in the elderly microbiota and possibly contribute to the triggering an initial proteinopathy event within the gut at any stage of life. On the other hand, some phytoconstituents are biotransformed by commensal bacteria into metabolites with higher neuroprotective activity than their precursor structures and hence exert a beneficial effect on the brain. Interestingly, the immense metabolic potential of enteric bacteria has given rise to the development of the transplantation of fecal microbiota from healthy individuals as an experimental therapy in the treatment of neurodegenerative diseases.
This Research Topic aims to provide novel insights into the nature of the gut bacteria-neuro-immune crosstalk in neurodegeneration.
Potential topics include but are not limited to the following:
- The regulatory role of microbiota in stress and neuroinflammation
- Pathways involved in intestinal metabolites of microbial origin influencing the central nervous system
- Neurotransmitters in Microbiomes
-The hypothesis of prion-like propagation of misfolded proteins within the GBA
- Putative metabolic markers of neurodegenerative diseases
- GBA as a new therapeutic target in pharmacotherapies restoring microbiota homeostasis towards neuroprotection
-The role of probiotic intervention on possible treatment and prevention of neurodegenerative diseases
- Preventing and treating neurodegenerative diseases by antibiotics
- The endotoxin hypothesis of neurodegeneration
- Polyphenols-gut microbiota interplay against neurodegeneration
- The role of diet in modulating the gut bacteria-neuro-immune crosstalk
- Gut microbiota transplantation in neurodegenerative diseases
- Pros and cons of current in vivo models of neurodegenerative diseases in neglecting the influence of GBA axis on animals phenotype.
We would like to thank Justyna Barut, PhD student at the Maj Institute of Pharmacology for contributing this image.