EDITORIAL article

Front. Neurosci.

Sec. Gut-Brain Axis

Volume 19 - 2025 | doi: 10.3389/fnins.2025.1618286

This article is part of the Research TopicNeuroinflammation and Gut-Brain Axis: Role of Glia CellsView all 5 articles

Editorial: Neuroinflammation and Gut-Brain Axis: Role of Glia Cells

Provisionally accepted
  • 1Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, United States
  • 2Federal University of Ceara, Department of Physiology and Pharmacology, Fortaleza, Ceará, Brazil

The final, formatted version of the article will be published soon.

Gut inflammation has been associated to neurological and psychiatric conditions in humans in a bidirectional manner, which supports a potential role of gut-brain axis [1][2][3][4] . Cognitive impairment, anxiety and depression-like behaviors phenotypes were also reported to occur post-gut inflammation recovers in mouse preclinical model 5,6 , which allows mechanistic studies and development of potential therapeutics.In dementia patients, increased microbe-derived molecules such as p-cresol, iso-butyric acid and iso-valeric acid were detected in fecal samples 7 , which supports the contribution of gut-derived molecules on this neurological condition.Dementia is a general term for loss of memory and other thinking abilities severe enough to affect with daily life. Stroke, Alzheimer's diseases (AD) and Parkinson's diseases (PD) are common cause for dementia 8 . The four papers collected for our special issues, which included three reviews and one original article, discussed about how gut microbiota and/or enteric glia contributes to acute ischemic stroke (AIS), AD and PD.Deng et al performed an epidemiological study of 499 acute ischemic stroke (AIS) patients in combination with preclinical model studies in Bama miniature (BM) pig model to investigate the contribution of gut microbiota derived metabolites in AIS. A phenomenon of delayed bowel movements was observed in large hemispheric infaction (LHI) patients, which may be induced by a strike to the gut-brain axis. 1 H NMR-based metabolomics was also employed to reveal global metabolic profiling in the plasma of AIS patients. Subsequently, a Bama miniature (BM) pig model with LHI was successfully established and employed to investigate the alterations of intestinal barrier integrity, the gut microbial community, and microbiota-derived metabolites. These findings highlight that microbiome-gut-brain axis contributes to both clinical AIS patients and LHI BM pigs.the potential of Drosophila as a robust model for investigating the associations between the flies' gut microbiota and the human microbiota, a connection that helps uncover the mechanisms linking bacterial balance to AD progression and inform future therapeutics. Yan et al reviews recent evidence on the role of acupuncture to modulate gut microbiota as a therapy for AD and found that the evidence suggested that acupuncture combined with modulation of the gut microbiota can be beneficial in the treatment of AD in the future.Lastly, Thomasi et al, by performing an elegant review, showed the potential roles of enteric glia in PD. Thomasi and colleagues focused on generates potential hypothesis on how enteric glia dysfunction can be connected to the development and/or progression of PD. Based on clinical data and animal models of PD in combination of other gut inflammation models, she explained how enteric glia and microbial molecules can affect each other, as well as how this interaction can impact gut dynamics, and the role of enteric glia in enteric neurotransmission, dysmotility, and visceral hypersensitivity. All these aspects, at different stages of the disease, can be related to PD.All these studies provided insights on potential mechanisms related to gut-derived molecules, specifically microbiota and/or enteric glia, to be targeted to prevent progression of brain neuroinflammationassociated to AD, PD and stroke.

Keywords: gut-brain axis, microbiota, glia, Dementia, neurogegeneration

Received: 25 Apr 2025; Accepted: 05 May 2025.

Copyright: © 2025 Costa, Macedo and De Carvalho Lima. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence:
Deiziane Viana da Silva Costa, Division of Infectious Diseases and International Health, University of Virginia, Charlottesville, Virginia, United States
Camila Nayane De Carvalho Lima, Federal University of Ceara, Department of Physiology and Pharmacology, Fortaleza, Ceará, Brazil

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