Evidence map›Paper›PMID 35715821›Full record

ReviewMolecular neurodegeneration2022

Microbial-derived metabolites as a risk factor of age-related cognitive decline and dementia.

Emily Connell, Gwenaelle Le Gall, Matthew G Pontifex, Saber Sami, John F Cryan, Gerard Clarke, Michael Müller, David Vauzour

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed, 4 pooled it
15.8field-weighted citation impact, top 1% 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.

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

124 citing papers in PubMed, 4 syntheses or guidelines pooled it, 197 citations in OpenAlex.

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  18. Metabolomic signaling in sarcoidosis pathogenesis.Current opinion in immunology · 2026
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64 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

8 authors at 2 institutions in 2 countries.

Emily ConnellFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK.
Gwenaelle Le GallFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK.
Matthew G PontifexFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK.
Saber SamiFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK.
John F CryanAPC Microbiome Ireland, University College Cork, Cork, Ireland.
Gerard ClarkeAPC Microbiome Ireland, University College Cork, Cork, Ireland.
Michael MüllerFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK.
David VauzourFaculty of Medicine and Health Sciences, Norwich Medical School, University of East Anglia, Norwich, NR4 7TJ, UK. D.Vauzour@uea.ac.uk.ORCID 0000-0001-5952-8756
University of East Anglia · GBUniversity College Cork · IE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A consequence of our progressively ageing global population is the increasing prevalence of worldwide age-related cognitive decline and dementia. In the absence of effective therapeutic interventions, identifying risk factors associated with cognitive decline becomes increasingly vital. Novel perspectives suggest that a dynamic bidirectional communication system between the gut, its microbiome, and the central nervous system, commonly referred to as the microbiota-gut-brain axis, may be a contributing factor for cognitive health and disease. However, the exact mechanisms remain undefined. Microbial-derived metabolites produced in the gut can cross the intestinal epithelial barrier, enter systemic circulation and trigger physiological responses both directly and indirectly affecting the central nervous system and its functions. Dysregulation of this system (i.e., dysbiosis) can modulate cytotoxic metabolite production, promote neuroinflammation and negatively impact cognition. In this review, we explore critical connections between microbial-derived metabolites (secondary bile acids, trimethylamine-N-oxide (TMAO), tryptophan derivatives and others) and their influence upon cognitive function and neurodegenerative disorders, with a particular interest in their less-explored role as risk factors of cognitive decline.

Indexed as

Cognitive DysfunctionDementiaGastrointestinal MicrobiomeAgingHumansRisk FactorsAlzheimer’s diseaseBile acidsBrainCresolsIndolesMicrobiota-gut-brain axisTMAOTryptophan

Identifiers

PMID35715821
PMCPMC9204954
OpenAlexW4283020259

What Socratic holds

Textmetadata
LicenceCC BY
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.