ReviewNaunyn-Schmiedeberg's archives of pharmacology2022
Lipopolysaccharide induced altered signaling pathways in various neurological disorders.
Review in Naunyn-Schmiedeberg's archives of pharmacology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Ficus virens in neurotherapeutics: bridging ethnomedicinal evidence with Nrf2/Keap1 and neuroinflammatory mechanisms.Molecular biology reports · 2026Review
- Proof-of-concept study: APOE4 brain endothelial cells as a phenotypic compound screen.Alzheimer's research & therapy · 2026Article
- TUDCA Ameliorates Cognitive Impairment in APP/PS1 Mice by Modulating the Microbiota-Gut-Brain Axis.Current issues in molecular biology · 2026Article
- Structure matters: commensalFrontiers in cellular neuroscience · 2026Article
- Microbiota and lipid mediators: from molecular crosstalk to therapeutic opportunities.Frontiers in pharmacology · 2026Review
- A modified hot phenol-based protocol for high-purity Escherichia coli lipopolysaccharide extraction: Biochemical validation, stem cell cytotoxicity, and dose dependent multi-organ inflammation in a rat model.Biotechnology reports (Amsterdam, Netherlands) · 2025Article
- The Role of Probiotics in Modulating the Gut Microbiome in Alzheimer's Disease: A Review.Foods (Basel, Switzerland) · 2025Review
- Gut-Spinal Cord Axis in Spinal Cord Injury: Bidirectional Inflammatory Mechanisms and Microbiota-Targeted Therapeutic Strategies.Journal of inflammation research · 2025Review
- Article
- Study on the Influence and Mechanism of Resveratrol on Cognitive Impairment in Chronic Kidney Disease Rats Through Regulating Gut Microbiota and the TLR4/NFκB Pathway.Journal of inflammation research · 2025Article
- Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis.Advances in neurobiology · 2025Review
- Exploring the diversity of biological processes regulated by glial cell line-derived neurotrophic factor, a pleiotropic molecule with therapeutic potential.Frontiers in physiology · 2025Review
- Gut dysbiosis as a potential driver of Parkinson's and Alzheimer's disease pathogenesis.Frontiers in neuroscience · 2025Review
- Irisin Attenuates Neuroinflammation Targeting the NLRP3 Inflammasome.Molecules (Basel, Switzerland) · 2024Article
- Nebulized Lipopolysaccharide Causes Delayed Cortical Neuroinflammation in a Murine Model of Acute Lung Injury.International journal of molecular sciences · 2024Article
- Microbial Heterogeneity Identification of Cerebral Thrombi Via Metagenomic Next-Generation Sequencing-Based Strategy.Journal of the American Heart Association · 2024Article
- In Vitro Astroglial Dysfunction Induced by Neurotoxins: Mimicking Astrocytic Metabolic Alterations of Alzheimer's Disease.Metabolites · 2024Article
- The role of molecular chaperones in the mechanisms of epileptogenesis.Cell stress & chaperones · 2023Review
- Nimbolide Targets Multiple Signalling Pathways to Reduce Neuroinflammation in BV-2 Microglia.Molecular neurobiology · 2023Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Neuroinflammation is defined as an inflammatory response within the brain or spinal cord, whereas the brain's innate immune system is triggered by various inflammatory challenges such as injury, infection, exposure to toxin (LPS) and ageing, which result in cognitive impairment and neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS). Lipopolysaccharide (LPS) is a main structural component of the outer membrane of gram-negative bacteria, widely used systematically to stimulate the immune system and to generate profound physiological and behavioural changes. It consists of three parts: lipid A, a core oligosaccharide and an O side chain. It is reported by several scientists that, besides the systemic alteration, LPS also induces neurodegeneration by promoting neuroinflammation upon binding with the stimulation of Toll-like receptor-4 (TLR4) receptors present on glial cells. The mammalian Toll-like receptor (TLR) family consists of 13 membranes and TLR was discovered as a crucial pattern recognition receptor (PPR) involved in the recognition of pathogen-associated molecular patterns (PAMPs). Future studies will show that damage/danger-associated molecular patterns (DAMPs) are recognised by the involvement of PPRs, generated by the host itself. The stimulation of TLR4 by lipopolysaccharide phosphorylates two signalling pathways, namely the MyD88-dependent pathway and the MyD88-independent pathway. This activation subsequently triggers the release of various pro-inflammatory cytokines that are necessary to activate innate immune responses, and then promotes neuroinflammation. In this review, we critically demonstrated the epidemiology of neuroinflammation, types of TLRs, the molecular mechanism of TLR4 and management of neuroinflammation.
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Registered trials
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.