Evidence map›Paper›PMID 31075861›Full record

ReviewInternational journal of molecular sciences2019

Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration.

Carla Ribeiro Alvares Batista, Giovanni Freitas Gomes, Eduardo Candelario-Jalil, Bernd L Fiebich, Antonio Carlos Pinheiro de Oliveira

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 297 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
297citing papers in PubMed, 2 pooled it
21.5field-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

297 citing papers in PubMed, 2 syntheses or guidelines pooled it, 500 citations in OpenAlex.

  1. Lipopolysaccharide-mediated macrophage polarization, conserved pathogenesis, and implications for peripheral neuropathy: a systematic review.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
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  13. Prolonged systemic inflammation worsens impairments to astrocyte CaAlzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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237 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

5 authors at 3 institutions in 3 countries.

Carla Ribeiro Alvares BatistaDepartment of Pharmacology, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte 31270-901, Brazil. cacaribeiro@gmail.com.ORCID 0000-0001-5826-4330
Giovanni Freitas GomesDepartment of Pharmacology, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte 31270-901, Brazil. gvnngomes@gmail.com.
Eduardo Candelario-JalilDepartment of Neuroscience, University of Florida, Gainesville, FL 32610, USA. ecandelario@ufl.edu.ORCID 0000-0003-3631-1989
Bernd L FiebichNeuroimmunology and Neurochemistry Research Group, Department of Psychiatry and Psychotherapy, Medical Center⁻University of Freiburg, Faculty of Medicine, University of Freiburg, D-79104 Freiburg, Germany. bernd.fiebich@uniklinik-freiburg.de.
Antonio Carlos Pinheiro de OliveiraDepartment of Pharmacology, Universidade Federal de Minas Gerais, Av. Antonio Carlos 6627, Belo Horizonte 31270-901, Brazil. antoniooliveira@icb.ufmg.br.
Universidade Federal de Minas Gerais · BRUniversity of Florida · USUniversity of Freiburg · DE

Funding

Conselho Nacional de Desenvolvimento Científico e Tecnológico CNPq - 309718/2015-5Conselho Nacional de Desenvolvimento Científico e Tecnológico CNPq - 424588/2016-1Fundação de Amparo à Pesquisa do Estado de Minas Gerais CBB-APQ-02044-15
6 · The paper itself

Abstract

A large body of experimental evidence suggests that neuroinflammation is a key pathological event triggering and perpetuating the neurodegenerative process associated with many neurological diseases. Therefore, different stimuli, such as lipopolysaccharide (LPS), are used to model neuroinflammation associated with neurodegeneration. By acting at its receptors, LPS activates various intracellular molecules, which alter the expression of a plethora of inflammatory mediators. These factors, in turn, initiate or contribute to the development of neurodegenerative processes. Therefore, LPS is an important tool for the study of neuroinflammation associated with neurodegenerative diseases. However, the serotype, route of administration, and number of injections of this toxin induce varied pathological responses. Thus, here, we review the use of LPS in various models of neurodegeneration as well as discuss the neuroinflammatory mechanisms induced by this toxin that could underpin the pathological events linked to the neurodegenerative process.

Indexed as

AnimalsDisease Models, AnimalHumansInflammationLipopolysaccharidesNerve DegenerationNervous SystemNeurodegenerative DiseasesLipopolysaccharidesAlzheimer’s diseaseamyotrophic lateral sclerosisHuntington’s diseaseinflammationlipopolysaccharideneurodegenerationParkinson’s disease

Identifiers

PMID31075861
PMCPMC6539529
OpenAlexW2944532057

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.