Gut Microbiota as a Modulator of Post-Stress Neuroinflammation: Methodological Limitations of Existing Research Practices

According to the current hypothesis, gut microbiota has a significant impact on the central nervous system and behavior through various mechanisms, including modulation of the immune system and the hypothalamic-pituitary-adrenal axis (HPA axis), epigenetic regulation of gene expression, and production of metabolites. The gut-brain axis is one of the key targets for research into the mechanisms of Alzheimer’s disease, pathological anxiety, mood disorders, and autism. It is suggested that post-stress neuroinflammation, which may be related to changes in the microbiota, plays a role in the development of these pathologies. However, the discovered “dysbiotic patterns” in the microbiomes of animal models under different stress models and in patients suffering from psychopathologies are not specific and may be secondary to the disease. The lack of understanding of the mechanisms by which gut microbiota is involved in the pathogenesis of neuro- and psychopathologies hinders the translation of results obtained from animal models. The review discusses the main methodological problems of research on the “gut-brain axis” and explores ways to address them.

Authors

Institutions

Publication Details

Journal
Neurochemical Journal
Published
2024-12-01
DOI
https://doi.org/10.1134/s1819712424700260
Primary Topic
Gut microbiota and health
Type
article
Field-Weighted Citation Impact
0.00
Controls
|||
ALL TIME
JAN
FEB
MAR
APR
MAY
JUN
JUL
AUG
SEP
OCT
article

Gut Microbiota as a Modulator of Post-Stress Neuroinflammation: Methodological Limitations of Existing Research Practices

I. G. Shalaginova, A. E. Vylegzhanina, Dmitriy Katserov, S. P. Luzikova
Neurochemical Journal
Gut microbiota and health
article

Gut Microbiota as a Modulator of Post-Stress Neuroinflammation: Methodological Limitations of Existing Research Practices

I. G. Shalaginova, A. E. Vylegzhanina, Dmitriy Katserov, S. P. Luzikova
article en

Abstract

According to the current hypothesis, gut microbiota has a significant impact on the central nervous system and behavior through various mechanisms, including modulation of the immune system and the hypothalamic-pituitary-adrenal axis (HPA axis), epigenetic regulation of gene expression, and production of metabolites. The gut-brain axis is one of the key targets for research into the mechanisms of Alzheimer’s disease, pathological anxiety, mood disorders, and autism. It is suggested that post-stress neuroinflammation, which may be related to changes in the microbiota, plays a role in the development of these pathologies. However, the discovered “dysbiotic patterns” in the microbiomes of animal models under different stress models and in patients suffering from psychopathologies are not specific and may be secondary to the disease. The lack of understanding of the mechanisms by which gut microbiota is involved in the pathogenesis of neuro- and psychopathologies hinders the translation of results obtained from animal models. The review discusses the main methodological problems of research on the “gut-brain axis” and explores ways to address them.

Neurochemical JournalVol. 18(4)
Immanuel Kant Baltic Federal University (RU), Pavlov Institute of Physiology of the Russian Academy of Sciences (RU)
Zero hunger
Openalex Percentile: Top 77%
Gut microbiota and health
AI Navigator

Ask Laika to Summarize, Analyze, and Connect papers live on the map.

Summarize Papers & Methodologies

Extract key findings, datasets, and comparative methods across publications.

Benchmark Rankings & Visual Analytics

Rank top research institutions, authors, funders, topics, and journals by Field-Weighted Citation Impact (FWCI) and paper volume with instant charts.

Connect Distant Disciplines

Bridge topological clusters on the map to find hidden collaborative intersections.

Gut Microbiota as a Modulator of Post-Stress Neuroinflammation: Methodological Limitations of Existing Research Practices — I. G. Shalaginova, A. E. Vylegzhanina, et al. · Neurochemical Journal (2024) | TGRS Research Map | TGRS