Evidence map›Paper›PMID 32244957›Full record

ReviewInternational journal of molecular sciences2020

Insights into the Therapeutic Potential of Glucocorticoid Receptor Modulators for Neurodegenerative Diseases.

Alejandro F De Nicola, Maria Meyer, Rachida Guennoun, Michael Schumacher, Hazel Hunt, Joseph Belanoff, E Ronald de Kloet, Maria Claudia Gonzalez Deniselle

Open access · goldAbstract readReview
In one paragraph

Review 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 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

11 citing papers in PubMed, 38 citations in OpenAlex.

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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

8 authors at 4 institutions in 4 countries.

Alejandro F De NicolaLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Obligado 2490, 1428 Buenos Aires, Argentina.
Maria MeyerLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Obligado 2490, 1428 Buenos Aires, Argentina.
Rachida GuennounU1195 Inserm and University Paris-Sud and University Paris Saclay 80 rue du Général Leclerc, 94276 Kremlin-Bicêtre, France.
Michael SchumacherU1195 Inserm and University Paris-Sud and University Paris Saclay 80 rue du Général Leclerc, 94276 Kremlin-Bicêtre, France.
Hazel HuntCORCEPT Therapeutics, 149 Commonwealth Dr, Menlo Park, CA 94025, USA.
Joseph BelanoffCORCEPT Therapeutics, 149 Commonwealth Dr, Menlo Park, CA 94025, USA.
E Ronald de KloetDivision of Endocrinology, Dept. of Internal Medicine, Leiden University Medical Center, Albinusdreef 2, 2333 ZA Leiden, The Netherlands.ORCID 0000-0001-9176-1830
Maria Claudia Gonzalez DeniselleLaboratory of Neuroendocrine Biochemistry, Instituto de Biologia y Medicina Experimental-CONICET, Obligado 2490, 1428 Buenos Aires, Argentina.
Consejo Nacional de Investigaciones Científicas y Técnicas · ARCorcept Therapeutics (United States) · USInserm · FRLeiden University Medical Center · NL

Funding

Consejo Nacional de Investigaciones Científicas y Técnicas Salaries for argentine researchersCorcept Therapeutics, California, USA purchase of reagentsUniversidad de Buenos Aires Ubacyt # 20020170100224BA
6 · The paper itself

Abstract

Glucocorticoids are crucial for stress-coping, resilience, and adaptation. However, if the stress hormones become dysregulated, the vulnerability to stress-related diseases is enhanced. In this brief review, we discuss the role of glucocorticoids in the pathogenesis of neurodegenerative disorders in both human and animal models, and focus in particular on amyotrophic lateral sclerosis (ALS). For this purpose, we used the Wobbler animal model, which mimics much of the pathology of ALS including a dysfunctional hypothalamic-pituitary-adrenal axis. We discuss recent studies that demonstrated that the pathological cascade characteristic for motoneuron degeneration of ALS is mimicked in the genetically selected Wobbler mouse and can be attenuated by treatment with the selective glucocorticoid receptor antagonist (GRA) CORT113176. In long-term treatment (3 weeks) GRA attenuated progression of the behavioral, inflammatory, excitatory, and cell-death-signaling pathways while increasing the survival signal of serine-threonine kinase (pAkt). The action mechanism of the GRA may be either by interfering with GR deactivation or by restoring the balance between pro- and anti-inflammatory signaling pathways driven by the complementary mineralocorticoid receptor (MR)- and GR-mediated actions of corticosterone. Accordingly, GR antagonism may have clinical relevance for the treatment of neurodegenerative diseases.

Indexed as

AnimalsCorticosteroneDisease Models, AnimalHumansInflammationModels, BiologicalNeurodegenerative DiseasesReceptors, GlucocorticoidCorticosteroneReceptors, Glucocorticoidamyotrophic lateral sclerosisglucocorticoid receptor antagonistneurodegenerationneuroinflammationWobbler mouse

Identifiers

PMID32244957
PMCPMC7139912
OpenAlexW3011345425

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.