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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 41 out of 100. Biomarkers

Topic: Gut, metabolism and diet

Background Neuroinflammation plays an important role in the onset and progression of neurodegenerative diseases such as Alzheimer's disease. Lipopolysaccharide (LPS, endotoxin) levels are higher in the brains of Alzheimer's disease patients and are associated with neuroinflammation and cognitive decline, while neural cholinergic signaling controls inflammation. This study aimed to examine the efficacy of galantamine, a clinically approved cholinergic agent, in alleviating LPS-induced neuroinflammation and cognitive decline as well as the associated mechanism. Methods Mice were treated with galantamine (4 mg/kg, intraperitoneal injection) for 14 days prior to LPS exposure (intracerebroventricular injection). Cognitive tests were performed, including the Morris water maze and step-through tests. mRNA expression of the microglial marker (CD11b), astrocytic marker (GFAP), and pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α) were examined in the hippocampus by quantitative RT-PCR. The inflammatory signaling molecule, nuclear factor-kappa B (NF-κB p65), and synapse-associated proteins (synaptophysin, SYN, and postsynaptic density protein 95, PSD-95) were examined in the hippocampus by western blotting. Furthermore, NF-κB p65 levels in microglial cells and hippocampal neurons were examined in response to LPS and galantamine. Results Galantamine treatment prevented LPS-induced deficits in spatial learning and memory as well as memory acquisition of the passive avoidance response. Galantamine decreased the expression of microglia and astrocyte markers (CD11b and GFAP), pro-inflammatory cytokines (IL-1β, IL-6, and TNF-α), and NF-κB p65 in the hippocampus of LPS-exposed mice. Furthermore, galantamine ameliorated LPS-induced loss of synapse-associated proteins (SYN and PSD-95) in the hippocampus. In the in vitro study, LPS increased NF-κB p65 levels in microglia (BV-2 cells); the supernatant of LPS-stimulated microglia (Mi-sup), but not LPS, decreased the viability of hippocampal neuronal cells (HT-22 cells) and increased NF-κB p65 levels as well as expression of pro-inflammatory cytokines (IL-1β, IL-6) in HT-22 cells. Importantly, galantamine reduced the inflammatory response not only in the BV-2 microglia cell line, but also in the HT-22 hippocampal neuronal cell line. Conclusions These findings indicate that galantamine could be a promising treatment to improve endotoxin-induced cognitive decline and neuroinflammation in neurodegenerative diseases.

Key findings

Study details

How this study scored 41/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record left out, no data; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 2 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited left out, no data; Citations per year left out, no data; Impact for its field and year left out, no data; Cited by studies here left out, no data; Still being cited left out, no data; Senior author's track record left out, no data; Institution's track record left out, no data; Multi-centre collaboration left out, no data; Indexed in PubMed 2 of 2; Free to read 2 of 2. 24 of the 58 points it could be judged on, which is 41 of 100. Total 41 of 100.24 of the 58 points we could judge = 41 of 100

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported and randomised / blinded because the record does not state it. We have no data on journal's citation record, times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record and multi-centre collaboration, so those were left out: it earned 24 of the 58 points we could judge it on, which is 41 out of 100.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Journal of neuroinflammation)
Journal's citation record — / 4 No journal record from OpenAlex — left out of this score
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 2 / 5 2018 — within 10 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Laboratory or animal study (title names “mice”) — scores zero
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited — / 7 No citation count (not found in OpenAlex) — left out of this score
Citations per year — / 5 No citation count or no year — left out of this score
Impact for its field and year — / 6 No field-weighted citation impact (OpenAlex has none yet) — left out of this score
Cited by studies here — / 6 Not yet checked against this library's citation graph — left out of this score
Still being cited — / 4 No yearly citation counts — left out of this score
Senior author's track record — / 4 Senior author's record not available — left out of this score
Institution's track record — / 3 No institution listed in OpenAlex — left out of this score
Multi-centre collaboration — / 3 Institutions not listed — left out of this score
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 29669582)
Free to read 2 / 2 Free to read
Points 24 / 58 Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 24 of the 58 points we could judge it on is 41 out of 100.
Total 41 / 100 —

What each of these 20 components measures, and what this score is not →

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Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.

APA 7th

Liu, Y., Zhang, Y., Zheng, X., Fang, T., Yang, X., Luo, X., et al. (2018). Galantamine improves cognition, hippocampal inflammation, and synaptic plasticity impairments induced by lipopolysaccharide in mice. Journal of neuroinflammation. https://doi.org/10.1186/s12974-018-1141-5

Vancouver

Liu Y, Zhang Y, Zheng X, Fang T, Yang X, Luo X, et al. Galantamine improves cognition, hippocampal inflammation, and synaptic plasticity impairments induced by lipopolysaccharide in mice. Journal of neuroinflammation. 2018. doi:10.1186/s12974-018-1141-5. PMID: 29669582.

BibTeX

@article{liu2018-29669582,
  author  = {Liu, Y. and Zhang, Y. and Zheng, X. and Fang, T. and Yang, X. and Luo, X. and Guo, A. and Newell, K. A. and others},
  title   = {{Galantamine improves cognition, hippocampal inflammation, and synaptic plasticity impairments induced by lipopolysaccharide in mice}},
  journal = {Journal of neuroinflammation},
  year    = {2018},
  doi     = {10.1186/s12974-018-1141-5},
  pmid    = {29669582},
  url     = {https://doi.org/10.1186/s12974-018-1141-5}
}

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