Evidence map›Paper›PMID 28928740›Full record

ArticleFrontiers in immunology2017

Microbiome-Derived Lipopolysaccharide Enriched in the Perinuclear Region of Alzheimer's Disease Brain.

Yuhai Zhao, Lin Cong, Vivian Jaber, Walter J Lukiw

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 112 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
112citing papers in PubMed, 2 pooled it
6.2field-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

112 citing papers in PubMed, 2 syntheses or guidelines pooled it, 166 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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52 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

4 authors at 2 institutions in 2 countries.

Yuhai ZhaoNeuroscience Center, Louisiana State University School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, United States.
Lin CongNeuroscience Center, Louisiana State University School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, United States.
Vivian JaberNeuroscience Center, Louisiana State University School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, United States.
Walter J LukiwNeuroscience Center, Louisiana State University School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, United States.
Louisiana State University Health Sciences Center New Orleans · USChina Medical University · CN

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
NEI NIH HHS R01 EY006311NIA NIH HHS R01 AG018031NIA NIH HHS R01 AG038834
6 · The paper itself

Abstract

Abundant clinical, epidemiological, imaging, genetic, molecular, and pathophysiological data together indicate that there occur an unusual inflammatory reaction and a disruption of the innate-immune signaling system in Alzheimer's disease (AD) brain. Despite many years of intense study, the origin and molecular mechanics of these AD-relevant pathogenic signals are still not well understood. Here, we provide evidence that an intensely pro-inflammatory bacterial lipopolysaccharide (LPS), part of a complex mixture of pro-inflammatory neurotoxins arising from abundant Gram-negative bacilli of the human gastrointestinal (GI) tract, are abundant in AD-affected brain neocortex and hippocampus. For the first time, we provide evidence that LPS immunohistochemical signals appear to aggregate in clumps in the parenchyma in control brains, and in AD, about 75% of anti-LPS signals were clustered around the periphery of DAPI-stained nuclei. As LPS is an abundant secretory product of Gram-negative bacilli resident in the human GI-tract, these observations suggest (i) that a major source of pro-inflammatory signals in AD brain may originate from internally derived noxious exudates of the GI-tract microbiome; (ii) that due to aging, vascular deficits or degenerative disease these neurotoxic molecules may "leak" into the systemic circulation, cerebral vasculature, and on into the brain; and (iii) that this internal source of microbiome-derived neurotoxins may play a particularly strong role in shaping the human immune system and contributing to neural degeneration, particularly in the aging CNS. This "

Indexed as

Alzheimer’s diseaseinflammatory degenerationlipopolysaccharidemicrobiomemicroRNAsmall non-coding RNAs

Identifiers

PMID28928740
PMCPMC5591429
OpenAlexW2747787638

What OpenQuestion 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 OpenQuestion graph.