Evidence map›Paper›PMID 26720273›Full record

ArticlePloS one2015

Role of Liver X Receptor in AD Pathophysiology.

Adrián G Sandoval-Hernández, Luna Buitrago, Herman Moreno, Gloria Patricia Cardona-Gómez, Gonzalo Arboleda

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 49 citations in OpenAlex.

  1. Pooled it
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  19. Genome-wide significant, replicated and functional risk variants for Alzheimer's disease.Journal of neural transmission (Vienna, Austria : 1996) · 2017
    Review
  20. Nuclear receptors in neural stem/progenitor cell homeostasis.Cellular and molecular life sciences : CMLS · 2017
    Review
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 2 countries.

Adrián G Sandoval-HernándezGrupo de Muerte Celular, Instituto de Genética Universidad Nacional de Colombia, Bogotá, Colombia.
Luna BuitragoDepartments of Neurology and Physiology/Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, SUNY Downstate Medical Center, Brooklyn, New York, United States of America.
Herman MorenoDepartments of Neurology and Physiology/Pharmacology, The Robert F. Furchgott Center for Neural and Behavioral Science, SUNY Downstate Medical Center, Brooklyn, New York, United States of America.
Gloria Patricia Cardona-GómezÁrea de Neurobiología Celular y Molecular, Grupo de Neurociencias de Antioquia, Universidad de Antioquia, Calle 70, No. 52-21, Medellín, Colombia.
Gonzalo ArboledaGrupo de Muerte Celular, Instituto de Genética Universidad Nacional de Colombia, Bogotá, Colombia.
SUNY Downstate Health Sciences University · USUniversidad Nacional de Colombia · COUniversidad de Antioquia · CO

Funding

Mouse fMRI and Calcium Dynamics in Alzheimer's PathophysiologyK08AG027476 · NIA · SUNY DOWNSTATE MEDICAL CENTER · PI MORENO, HERMAN · 2006 to 2010
$684k
Development of RNAi as Treatment for NeurodegenerationR01AG029802 · NIA · UNIVERSITY OF CALIFORNIA SANTA BARBARA · PI KOSIK, KENNETH STEPHEN · 2007 to 2011
$674k
NIA NIH HHS AG027476NIA NIH HHS K08 AG027476NIA NIH HHS R01 AG029802NIA NIH HHS R01 AG029802-01
6 · The paper itself

Abstract

Alzheimer's disease (AD) is the major cause of dementia worldwide. The pharmacological activation of nuclear receptors (Liver X receptors: LXRs or Retinoid X receptors: RXR) has been shown to induce overexpression of the ATP-Binding Cassette A1 (ABCA1) and Apolipoprotein E (ApoE), changes that are associated with improvement in cognition and reduction of amyloid beta pathology in amyloidogenic AD mouse models (i.e. APP, PS1: 2tg-AD). Here we investigated whether treatment with a specific LXR agonist has a measurable impact on the cognitive impairment in an amyloid and Tau AD mouse model (3xTg-AD: 12-months-old; three months treatment). The data suggests that the LXR agonist GW3965 is associated with increased expression of ApoE and ABCA1 in the hippocampus and cerebral cortex without a detectable reduction of the amyloid load. We also report that most cells overexpressing ApoE (86±12%) are neurons localized in the granular cell layer of the hippocampus and entorhinal cortex. In the GW3965 treated 3xTg-AD mice we also observed reduction in astrogliosis and increased number of stem and proliferating cells in the subgranular zone of the dentate gyrus. Additionally, we show that GW3965 rescued hippocampus long term synaptic plasticity, which had been disrupted by oligomeric amyloid beta peptides. The effect of GW3965 on synaptic function was protein synthesis dependent. Our findings identify alternative functional/molecular mechanisms by which LXR agonists may exert their potential benefits as a therapeutic strategy against AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsApolipoproteins EATP Binding Cassette Transporter 1BenzoatesBenzylaminesBiomarkersCell ProliferationCerebral CortexCognition DisordersDentate GyrusDNA-Binding ProteinsExcitatory Postsynaptic PotentialsFemaleFluorescent Antibody TechniqueAmyloid beta-PeptidesApolipoproteins EATP Binding Cassette Transporter 1BenzoatesBenzylaminesBiomarkersDNA-Binding ProteinsGW 3965Liver X ReceptorsNerve Tissue ProteinsNestinNeuN protein, mouseNuclear ProteinsOrphan Nuclear Receptorstau Proteins

Identifiers

PMID26720273
PMCPMC4697813
OpenAlexW2207735435

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.