Evidence map›Paper›PMID 29637444›Full record

ReviewMolecular neurobiology2018

Bacteroidetes Neurotoxins and Inflammatory Neurodegeneration.

Yuhai Zhao, Walter J Lukiw

Abstract readReview
PubMed Publisher
In one paragraph

Review in Molecular neurobiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 86 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
86citing papers in PubMed, 3 pooled it
5.6field-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.

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

86 citing papers in PubMed, 3 syntheses or guidelines pooled it, 123 citations in OpenAlex.

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  18. Gut-derived bacterial vesicles carrying lipopolysaccharide promote microglia-mediated synaptic pruning.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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  20. Review

26 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

2 authors at 1 institution in 1 country.

Yuhai ZhaoLSU Neuroscience Center, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite 904, New Orleans, LA, 70112, USA.
Walter J LukiwLSU Neuroscience Center, Louisiana State University Health Sciences Center, 2020 Gravier Street, Suite 904, New Orleans, LA, 70112, USA. wlukiw@lsuhsc.edu.
Louisiana State University Health Sciences Center New Orleans · US

Funding

OCULAR HSV: LATENCY, REACTIVATION, &RECURRENCER01EY006311 · NEI · LSU HEALTH SCIENCES CENTER · PI HILL, JAMES M · 1985 to 2012
$5.3M
microRNA (miRNA) signaling in Alzheimer's disease(AD)R01AG038834 · NIA · LSU HEALTH SCIENCES CENTER · PI BAZAN, NICOLAS G. · 2011 to 2020
$3.3M
Gene Expression in Alzheimer's DiseaseR01AG018031 · NIA · LSU HEALTH SCIENCES CENTER · PI LUKIW, WALTER J · 2001 to 2006
$1.4M
National Eye Institute EY006311National Institute on Aging AG038834National Institute on Aging AG18031
6 · The paper itself

Abstract

The gram-negative facultative anaerobe Bacteroides fragilis (B. fragilis) constitutes an appreciable proportion of the human gastrointestinal (GI)-tract microbiome. As is typical of most gram-negative bacilli, B. fragilis secretes an unusually complex mixture of neurotoxins including the extremely pro-inflammatory lipopolysaccharide BF-LPS. LPS (i) has recently been shown to associate with the periphery of neuronal nuclei in sporadic Alzheimer's disease (AD) brain and (ii) promotes the generation of the inflammatory transcription factor NF-kB (p50/p65 complex) in human neuronal-glial cells in primary-culture. In turn, the NF-kB (p50/p65 complex) strongly induces the transcription of a small family of pro-inflammatory microRNAs (miRNAs) including miRNA-9, miRNA-34a, miRNA-125b, miRNA-146a, and miRNA-155. These ultimately bind with the 3'-untranslated region (3'-UTR) of several target messenger RNAs (mRNAs) and thereby reduce their expression. Down-regulated mRNAs include those encoding complement factor-H (CFH), an SH3-proline-rich multi-domain-scaffolding protein of the postsynaptic density (SHANK3), and the triggering receptor expressed in myeloid/microglial cells (TREM2), as is observed in sporadic AD brain. Hence, a LPS normally confined to the GI tract is capable of driving a NF-kB-miRNA-mediated deficiency in gene expression that contributes to alterations in synaptic-architecture and synaptic-deficits, amyloidogenesis, innate-immune defects, and progressive inflammatory signaling, all of which are characteristics of AD-type neurodegeneration. This article will review the most recent research which supports the idea that bacterial components of the GI tract microbiome such as BF-LPS can transverse biophysical barriers and contribute to AD-type change. For the first-time, these results indicate that specific GI tract microbiome-derived neurotoxins have a strong pathogenic role in eliciting alterations in NF-kB-miRNA-directed gene expression that drives the AD process.

Indexed as

AnimalsBacteroidetesHumansInflammationMicroRNAsNerve DegenerationNeuronsNeurotoxinsMicroRNAsNeurotoxinsAlzheimer’s diseaseAmyloidogenesisBacteroides fragilisLipopolysaccharideMessenger RNAMicrobiomemicroRNANeuroinflammationPhagocytosisSynaptogenesis

Identifiers

PMID29637444
OpenAlexW2796859943

What OpenQuestion 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 OpenQuestion graph.