Evidence map›Paper›PMID 37287396›Full record

ArticleCNS neuroscience & therapeutics2023

Microbial lipopolysaccharide-induced inflammation contributes to cognitive impairment and white matter lesion progression in diet-induced obese mice with chronic cerebral hypoperfusion.

Toshiki Inaba, Kazuo Yamashiro, Naohide Kurita, Yuji Ueno, Nobukazu Miyamoto, Kenichiro Hira, Sho Nakajima, Chikage Kijima, Ryohei Nakaguro, Takao Urabe and 1 more

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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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 at 4 institutions in 1 country.

Toshiki InabaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Kazuo YamashiroDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Naohide KuritaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Yuji UenoDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Nobukazu MiyamotoDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Kenichiro HiraDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Sho NakajimaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Chikage KijimaDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Ryohei NakaguroMetagen Inc., Yamagata, Japan.
Takao UrabeDepartment of Neurology, Juntendo University Urayasu Hospital, Chiba, Japan.
Nobutaka HattoriDepartment of Neurology, Juntendo University School of Medicine, Tokyo, Japan.
Juntendo University · JPUniversity of Yamanashi · JPJuntendo University Urayasu Hospital · JPYamagata Research Institute Of Technology · JP

Funding

JSPS KAKENHI JP17K09763
6 · The paper itself

Abstract

aimsWhite matter lesions (WMLs) are involved in the pathological processes leading to cognitive decline and dementia. We examined the mechanisms underlying the exacerbation of ischemia-induced cognitive impairment and WMLs by diet-induced obesity, including lipopolysaccharide (LPS)-triggered neuroinflammation via toll-like receptor (TLR) 4.

methodsWild-type (WT) and TLR4-knockout (KO) C57BL/6 mice were fed a high-fat diet (HFD) or low-fat diet (LFD), and subjected to bilateral carotid artery stenosis (BCAS). Diet groups were compared for changes in gut microbiota, intestinal permeability, systemic inflammation, neuroinflammation, WML severity, and cognitive dysfunction.

resultsIn WT mice, HFD induced obesity and increased cognitive impairment and WML severity compared with LFD-fed mice following BCAS. HFD caused gut dysbiosis and increased intestinal permeability, and plasma LPS and pro-inflammatory cytokine concentrations. Furthermore, HFD-fed mice had higher LPS levels and higher neuroinflammatory status, including increased TLR4 expression, in WMLs. In TLR4-KO mice, HFD also caused obesity and gut dysbiosis but did not increase cognitive impairment or WML severity after BCAS. No difference was found between HFD- and LFD-fed KO mice for LPS levels or inflammatory status in either plasma or WMLs.

conclusionInflammation triggered by LPS-TLR4 signaling may mediate obesity-associated exacerbation of cognitive impairment and WMLs from brain ischemia.

Indexed as

Brain IschemiaCarotid StenosisCognitive DysfunctionWhite MatterAnimalsDiet, High-FatDysbiosisInflammationLipopolysaccharidesMiceMice, Inbred C57BLMice, ObeseNeuroinflammatory DiseasesObesityToll-Like Receptor 4LipopolysaccharidesToll-Like Receptor 4cognitive impairmentgut microbiotalipopolysaccharideneuroinflammationwhite matter lesion

Identifiers

PMID37287396
PMCPMC10314110
OpenAlexW4379768728

What OpenQuestion holds

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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.