Evidence map›Paper›PMID 24590859›Full record

ReviewNeurochemical research2014

Chronic functional bowel syndrome enhances gut-brain axis dysfunction, neuroinflammation, cognitive impairment, and vulnerability to dementia.

Mak Adam Daulatzai

Registry-linked trialAbstract readReview
PubMed Publisher
In one paragraph

Review in Neurochemical research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03494725 (Proof-of-Concept "Stress & Anxiety Dampening Effects of Lpc-37"), which is not on this map. Cited by 75 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed, 3 pooled it
6.7field-weighted citation impact, top 3% of its field
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.

NCT03494725 nacompletednot on this mapstarted 2018, after this paper: background citation

Proof-of-Concept "Stress & Anxiety Dampening Effects of Lpc-37"

TypeinterventionalSponsorDaacroRan2018 to 2018Enrolled120ConditionsHealthy, Stress, PsychologicalArmsLpc-37, Placebo
3 · Its place in the literature

Who cites it

75 citing papers in PubMed, 3 syntheses or guidelines pooled it, 134 citations in OpenAlex.

  1. Pooled it
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  8. Intestinal Clock Promotes Cognitive Memory Through Adenosine Signaling.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
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15 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Mak Adam DaulatzaiSleep Disorders Group, EEE Department, Melbourne School of Engineering, The University of Melbourne, Grattan Street, 3rd Floor, Room No. 344, Parkville, VIC, 3010, Australia, mak@drmakdaulatzai.us.
University of Melbourne · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The irritable bowel syndrome (IBS) is a common chronic functional gastrointestinal disorder world wide that lasts for decades. The human gut harbors a diverse population of microbial organisms which is symbiotic and important for well being. However, studies on conventional, germ-free, and obese animals have shown that alteration in normal commensal gut microbiota and an increase in pathogenic microbiota-termed "dysbiosis", impact gut function, homeostasis, and health. Diarrhea, constipation, visceral hypersensitivity, and abdominal pain arise in IBS from the gut-induced dysfunctional metabolic, immune, and neuro-immune communication. Dysbiosis in IBS is associated with gut inflammation. Gut-related inflammation is pivotal in promoting endotoxemia, systemic inflammation, and neuroinflammation. A significant proportion of IBS patients chronically consume alcohol, non-steroidal anti-inflammatories, and fatty diet; they may also suffer from co-morbid respiratory, neuromuscular, psychological, sleep, and neurological disorders. The above pathophysiological substrate is underpinned by dysbiosis, and dysfunctional bidirectional "Gut-Brain Axis" pathways. Pathogenic gut microbiota-related systemic inflammation (due to increased lipopolysaccharide and pro-inflammatory cytokines, and barrier dysfunction), may trigger neuroinflammation enhancing dysfunctional brain regions including hippocampus and cerebellum. These as well as dysfunctional vago-vagal gut-brain axis may promote cognitive impairment. Indeed, inflammation is characteristic of a broad spectrum of neurodegenerative diseases that manifest demntia. It is argued that an awareness of pathophysiological impact of IBS and implementation of appropriate therapeutic measures may prevent cognitive impairment and minimize vulnerability to dementia.

Indexed as

AnimalsBrainCognition DisordersDementiaGastrointestinal TractHumansInflammationInflammation MediatorsIrritable Bowel SyndromeInflammation Mediators

Identifiers

PMID24590859
OpenAlexW1971668970

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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 OpenQuestion graph.