Evidence map›Paper›PMID 40671688›Full record

ArticleACS chemical neuroscience2025

Novel Dual Mechanism GRT-X Agonist Acting on Kv7 Potassium Channel/Translocator Protein Receptor Prevents Motoneuron Degeneration Following Exposure to Mouse and Human Amyotrophic Lateral Sclerosis/Frontotemporal Dementia Astrocyte-Conditioned Media.

Vera M Masegosa, Elsa Fritz, Daniela Corvalan, Fabiola Rojas, Polett Garcés, Xavier Navarro, Petra Bloms-Funke, Brigitte van Zundert, Mireia Herrando-Grabulosa

Abstract read
In one paragraph

Article in ACS chemical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Biochemistry and biophysics reports · 2026
    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

9 authors.

Vera M MasegosaDepartment of Cell Biology, Physiology and Immunology, Institute of Neurosciences, Universitat Autònoma de Barcelona, Bellaterra 08193, Spain.
Elsa FritzInstitute of Biomedical Sciences (ICB), Faculty of Medicine & Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370035, Chile.
Daniela CorvalanInstitute of Biomedical Sciences (ICB), Faculty of Medicine & Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370035, Chile.
Fabiola RojasInstitute of Biomedical Sciences (ICB), Faculty of Medicine & Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370035, Chile.
Polett GarcésInstitute of Biomedical Sciences (ICB), Faculty of Medicine & Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370035, Chile.
Xavier NavarroDepartment of Cell Biology, Physiology and Immunology, Institute of Neurosciences, Universitat Autònoma de Barcelona, Bellaterra 08193, Spain.
Petra Bloms-FunkeGrünenthal GmbH, Aachen 52099, Germany.
Brigitte van ZundertInstitute of Biomedical Sciences (ICB), Faculty of Medicine & Faculty of Life Sciences, Universidad Andres Bello, Santiago 8370035, Chile.
Mireia Herrando-GrabulosaDepartment of Cell Biology, Physiology and Immunology, Institute of Neurosciences, Universitat Autònoma de Barcelona, Bellaterra 08193, Spain.ORCID 0000-0002-6685-3220

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) form a continuous spectrum of aggressive neurodegenerative diseases affecting primarily motoneurons (MNs) and cortical frontotemporal neurons. Noncell autonomous mechanisms contribute to ALS/FTD, wherein astrocytes release toxic factor(s) detrimental to MNs. Because of the multifactorial nature of ALS, single-pathway-focused therapies have limited effectiveness in improving ALS. Therefore, novel combinatorial therapies are currently being pursued. Here, we evaluated whether the simultaneous activation of two complementary targets, the voltage-gated potassium channels 7.2/3 (Kv7.2/3) and the mitochondrial translocator protein (TSPO), by a novel synthesized compound (GRT-X) is an effective neuroprotective treatment in ALS in vitro models. We exposed primary rat ventral spinal cord neuronal cultures and rat spinal cord organotypic cultures to astrocyte-conditioned medium derived from primary mouse ALS astrocytes expressing mutant human SOD1 (SOD1

Indexed as

Amyotrophic Lateral SclerosisAstrocytesFrontotemporal DementiaKCNQ2 Potassium ChannelMotor NeuronsNeuroprotective AgentsReceptors, GABAAnimalsCells, CulturedCulture Media, ConditionedHumansMiceMice, TransgenicNerve DegenerationRatsRats, Sprague-DawleyBzrp protein, mouseCulture Media, ConditionedKCNQ2 Potassium ChannelNeuroprotective AgentsReceptors, GABASuperoxide Dismutase-1amyotrophic lateral sclerosisastrocyte conditioned mediumfrontotemporal dementiaGRT-Xmotoneuron deathoxidative and excitotoxity stress

Identifiers

PMID40671688
PMCPMC12333588

What Socratic holds

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LicenceCC BY
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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 Socratic graph.