Evidence map›Paper›PMID 29297151›Full record

ArticleNeurotoxicity research2018

Liver X Receptor Agonist GW3965 Regulates Synaptic Function upon Amyloid Beta Exposure in Hippocampal Neurons.

C Báez-Becerra, F Filipello, A Sandoval-Hernández, H Arboleda, G Arboleda

Abstract read
PubMed Publisher
In one paragraph

Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.7field-weighted citation impact, top 5% 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

14 citing papers in PubMed, 31 citations in OpenAlex.

  1. Neuro-HIV-New insights into pathogenesis and emerging therapeutic targets.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2023
    Article
  2. Review
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  4. Review
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  6. Oxysterols Modulate the Acute Effects of Ethanol on HippocampalThe Journal of pharmacology and experimental therapeutics · 2021
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Protective Variants in Alzheimer's Disease.Current genetic medicine reports · 2019
    Article
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 2 institutions in 2 countries.

C Báez-BecerraGrupos de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia.
F FilipelloLaboratory of Pharmacology and Brain Pathology, Humanitas Clinical and Research Center, Milan, Italy.
A Sandoval-HernándezGrupos de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia.
H ArboledaGrupos de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia.
G ArboledaGrupos de Neurociencias y Muerte Celular, Facultad de Medicina e Instituto de Genética, Universidad Nacional de Colombia, Bogotá, Colombia. gharboledab@unal.edu.co.
Universidad Nacional de Colombia · COHumanitas University · IT

Funding

Colciencias 110161538259DIEB 37405
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disease characterized by beta-amyloid (Aβ) accumulation and neurofibrillary tangles formation in the brain which are associated to synaptic deficits and dementia. Liver X receptor (LXR) agonists have been demonstrated to revert of pathologic and cognitive defects in murine models of AD through the regulation of Apolipoprotein E, ATP-Binding Cassette A1 (ABCA1), by dampening neuroinflammation and also by reducing the levels of amyloid-β (Aβ) accumulation in the brain. However, the role of LXR with regard to the regulation of synaptic function remains relatively understudied. In the present paper, we analyzed the in-vitro effect of the LXR agonist GW3965 on synaptic function upon exposure of primary hippocampal cultures to oligomeric amyloid-β (oAβ(1-42)). We showed that oAβ(1-42) exposure significantly decreased the density of mature (mushroom shaped) dendritic spines density and synaptic contacts number. oAβ(1-42) also modulates the expression of pre- (VGlut1, SYT1, SV2A) and post-synaptic (SHANK2, NMDA) proteins, it decreases the expression of PINK1, and increases ROCKII, and activates of caspase-3; these changes were prevented by the pre-treating neuronal cultures with GW3965. These results show further support the role of the LXR agonist GW3965 in synaptic physiology and highlight its potential as an alternative pharmacological strategy for AD.

Indexed as

Amyloid beta-PeptidesAnimalsBenzoatesBenzylaminesCells, CulturedDendritic SpinesEmbryo, MammalianGene Expression RegulationHippocampusLiver X ReceptorsL-Lactate DehydrogenaseMembrane GlycoproteinsMiceMice, Inbred C57BLNerve Tissue ProteinsNeuronsAmyloid beta-Peptidesamyloid beta-protein (1-42)BenzoatesBenzylaminesGW 3965Liver X ReceptorsL-Lactate DehydrogenaseMembrane GlycoproteinsNerve Tissue ProteinsPeptide FragmentsProtein KinasesPTEN-Induced Putative KinaseReceptors, N-Methyl-D-Aspartaterho-Associated KinasesShank2 protein, mouseSv2a protein, mouseSynaptotagmin ISyt1 protein, mouseVesicular Glutamate Transport Protein 1Alzheimer’s diseaseAmyloid-βGW3965Hippocampal neuronsLiver X receptorsSynapsis

Identifiers

PMID29297151
OpenAlexW2782055390

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.