Evidence map›Paper›PMID 41017678›Full record

ArticleNeural regeneration research2026

Immune dysregulation and gut microbiota: Connection to health and disease development.

Ana Paula de Araújo Boleti, Pedro Henrique de Oliveira Cardoso, Breno Emanuel Farias Frihling, Luiz Filipe Ramalho Nunes de Moraes, Ellynes Amancio Correia Nunes, Lincoln Takashi Hota Mukoyama, Maria Eduarda Freitas Biembengute, Vívia Cleisla Bezerra de Melo, Marcos Fernandes Morales, Alinne Pereira de Castro and 1 more

Abstract read
In one paragraph

Article in Neural regeneration research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. The Role of ProbioticsInternational journal of molecular sciences · 2026
    Review
  4. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors.

Ana Paula de Araújo BoletiS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Pedro Henrique de Oliveira CardosoS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Breno Emanuel Farias FrihlingS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Luiz Filipe Ramalho Nunes de MoraesS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Ellynes Amancio Correia NunesS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Lincoln Takashi Hota MukoyamaS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Maria Eduarda Freitas BiembenguteS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Vívia Cleisla Bezerra de MeloS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Marcos Fernandes MoralesS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Alinne Pereira de CastroS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.
Ludovico MiglioloS-Inova Biotech, Programa de Pós-Graduação em Biotecnologia, Universidade Católica Dom Bosco, Campo Grande, MS, Brazil.ORCID 0000-0002-6606-2189

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neuroinflammation is a key pathophysiological mechanism in various neurological diseases, such as Alzheimer's disease and neuropsychiatric disorders. This review article analyzes the role of inflammatory mediators and their signaling pathways in the pathogenesis of neurodegenerative diseases, focusing on the molecular mechanisms that promote neurodegeneration and hinder neural regeneration. Recent evidence suggests that alterations in inflammatory processes in the brain are associated with cognitive impairment, progressive neurodegeneration, and impaired synaptic plasticity. Activation of Toll-like receptors triggers an inflammatory cascade involving pro-inflammatory cytokines such as interleukins and tumor necrosis factor alpha, which significantly contributes to neuronal dysfunction and cell death. Furthermore, we are investigating how these neuroinflammatory processes interfere with neural regeneration mechanisms and the maintenance of central nervous system homeostasis. Neural biomarkers associated with inflammation are emerging as potential diagnostic tools and therapeutic targets for neurological diseases, particularly anxiety disorders and Alzheimer's disease. Both experimental and clinical studies suggest that interventions aimed at modulating neuroinflammation could be a promising therapeutic approach to promoting neuroprotection and stimulating neural regeneration. This review summarizes the latest research on the molecular mechanisms of neuroinflammation and its effect on brain function. It also highlights potential neuroprotective and regenerative strategies for treating neurological diseases.

Indexed as

dysbiosisgastrointestinal disordersimmune responseinflammationmicrobiotanerve regenerationneurological diseases

Identifiers

PMID41017678
PMCPMC13557694

What Socratic holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.