Evidence map›Paper›PMID 41515912›Full record

ReviewInternational journal of molecular sciences2025

From Symptomatic Therapies to Disease-Modifying Approaches for Neuronal Sodium Channel Disorders.

Giorgia Dinoi, Ileana Canfora, Daniela D'Agnano, Brigida Boccanegra, Elena Conte, Annamaria De Luca, Antonella Liantonio, Vittorio Sciruicchio, Paola Imbrici

Abstract readReview
In one paragraph

Review in International journal of molecular sciences, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Targeting the non-coding RNA-PANoptosis axis: a novel frontier in disease diagnosis and therapy.Apoptosis : an international journal on programmed cell death · 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.

Giorgia DinoiDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0009-0007-9250-5610
Ileana CanforaDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-6357-316X
Daniela D'AgnanoChildren Epilepsy and EEG Center, San Paolo Hospital, ASL Bari, 70132 Bari, Italy.
Brigida BoccanegraDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-1078-8490
Elena ConteDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0001-8571-5125
Annamaria De LucaDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-5652-7341
Antonella LiantonioDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0002-4103-7577
Vittorio SciruicchioChildren Epilepsy and EEG Center, San Paolo Hospital, ASL Bari, 70132 Bari, Italy.ORCID 0000-0003-2388-573X
Paola ImbriciDepartment of Pharmacy-Drug Sciences, University of Bari "Aldo Moro", Via Orabona 4, 70125 Bari, Italy.ORCID 0000-0001-9140-5350

Funding

European Union - Next Generation EU - Ministero della Salute PNRR M6/C2 - Investment 2.1 Enhancement and strengthening of biomedical research in the NHS grant PNRR-MR1-2022-12376642 - Precision medicine in Dravet syndrome: from a national reg-istry to neuronal modelling based on individual genome dataNEXTGENERATIONEU (NGEU), Italian Ministry of University and Research (MUR), National Recovery and Resilience Plan (NRRP) project MNESYS (PE0000006) - A Multiscale integrated approach to the study of the nervous system in health and disease (DN.1553 11.10.2022)
6 · The paper itself

Abstract

Variants in neuronal sodium channel genes are responsible for a spectrum of neurological disorders, including developmental and epileptic encephalopathies (DEEs), with considerable genetic and phenotypic heterogeneity and drug resistance. Gene variants can produce loss-, gain-, or mixed-function effects, resulting in complex genotype-phenotype correlations. Current treatments rely mainly on symptomatic polytherapy with antiseizure medications, with sodium channel blockers contraindicated in loss-of-function cases but beneficial in gain-of-function forms. Existing therapies often provide limited benefit or even no seizure control at all and fail to address developmental impairments, highlighting the need for novel approaches. Emerging strategies include antisense oligonucleotides, gene therapy, and selective small-molecule modulators, which have shown antiseizure potential in preclinical models and in initial clinical studies by modulating

Indexed as

Epilepsies, MyoclonicSodium ChannelsAnimalsAnticonvulsantsGenetic TherapyHumansNAV1.1 Voltage-Gated Sodium ChannelNeuronsOligonucleotides, AntisenseSodium Channel BlockersAnticonvulsantsNAV1.1 Voltage-Gated Sodium ChannelOligonucleotides, AntisenseSodium Channel BlockersSodium ChannelsDravet syndromeelsunersenETX-101fenfluraminesodium channelszorevunersen

Identifiers

PMID41515912
PMCPMC12786012

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.