Evidence map›Paper›PMID 33276671›Full record

ArticleInternational journal of molecular sciences2020

Liver Growth Factor "LGF" as a Therapeutic Agent for Alzheimer's Disease.

Rafael Gonzalo-Gobernado, Juan Perucho, Manuela Vallejo-Muñoz, Maria José Casarejos, Diana Reimers, Adriano Jiménez-Escrig, Ana Gómez, Gonzalo M Ulzurrun de Asanza, Eulalia Bazán

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

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  8. Review
  9. Neuroprotection: Rescue from Neuronal Death in the Brain.International journal of molecular sciences · 2021
    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

9 authors at 2 institutions in 1 country.

Rafael Gonzalo-GobernadoServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-6357-105X
Juan PeruchoServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Manuela Vallejo-MuñozServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Maria José CasarejosServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Diana ReimersServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Adriano Jiménez-EscrigServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Ana GómezServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Gonzalo M Ulzurrun de AsanzaServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.
Eulalia BazánServicio de Neurobiología, Instituto Ramón y Cajal de Investigación Sanitaria (IRYCIS), 28034 Madrid, Spain.ORCID 0000-0002-0126-250X
Instituto Ramón y Cajal de Investigación Sanitaria · ESCentro Nacional de Biotecnología · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a progressive degenerative disorder and the most common cause of dementia in aging populations. Although the pathological hallmarks of AD are well defined, currently no effective therapy exists. Liver growth factor (LGF) is a hepatic albumin-bilirubin complex with activity as a tissue regenerating factor in several neurodegenerative disorders such as Parkinson's disease and Friedreich's ataxia. Our aim here was to analyze the potential therapeutic effect of LGF on the APPswe mouse model of AD. Twenty-month-old mice received intraperitoneal (i.p.) injections of 1.6 µg LGF or saline, twice a week during three weeks. Mice were sacrificed one week later, and the hippocampus and dorsal cortex were prepared for immunohistochemical and biochemical studies. LGF treatment reduced amyloid-β (Aβ) content, phospho-Tau/Tau ratio and the number of Aβ plaques with diameter larger than 25 µm. LGF administration also modulated protein ubiquitination and HSP70 protein levels, reduced glial reactivity and inflammation, and the expression of the pro-apoptotic protein Bax. Because the administration of this factor also restored cognitive damage in APPswe mice, we propose LGF as a novel therapeutic tool that may be useful for the treatment of AD.

Indexed as

Disease SusceptibilityAlzheimer DiseaseAmyloid beta-PeptidesAnimalsBehavior, AnimalBilirubinCerebral CortexDisease Models, AnimalGene ExpressionHippocampusHumansMemory, Short-TermMiceMice, TransgenicMicrogliaPhosphorylationalbumin-bilirubin complexAmyloid beta-PeptidesBilirubinSerum Albumin, Humantau ProteinsAlzheimer’s diseaseamyloid-betainflammationliver growth factormicroglianeuroprotectionTg2576 transgenic mice

Identifiers

PMID33276671
PMCPMC7730107
OpenAlexW3109976220

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.