Employing zebrafish to understand genetic drivers of epilepsy-related comorbid behaviors.

Chinwendu Ononuju, Kharma Hall, Olivia Beatty, Scott C Baraban, Colleen Carpenter-Swanson

Abstract read

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Article in Frontiers in pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

5 authors.

Chinwendu OnonujuEpilepsy Research Laboratory and Weill Institute for Neuroscience, Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, United States.

Kharma HallDepartment of Biology, University of Richmond, Richmond, VA, United States.

Olivia BeattyDepartment of Biology, University of Richmond, Richmond, VA, United States.

Scott C BarabanEpilepsy Research Laboratory and Weill Institute for Neuroscience, Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, United States.

Colleen Carpenter-SwansonEpilepsy Research Laboratory and Weill Institute for Neuroscience, Department of Neurological Surgery, University of California San Francisco, San Francisco, CA, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Children with epilepsy frequently experience a range of significant comorbidities beyond seizures, such as motor dysfunction, cognitive impairment, and neurodevelopmental delays. In some cases, these comorbidities contribute more significantly to overall disease burden than the seizures themselves. To improve quality-of-life (QOL) for these children, treatment options should be selected that control seizures and ameliorate comorbidities. Unfortunately, such therapeutics remain largely elusive. Addressing this issue requires suitable preclinical models. Here we used CRISPR-generated zebrafish with single-gene mutations linked to pediatric epilepsy and applied clinically-relevant behavioral assays to study the effects of these mutations. Using high-throughput locomotion-based assays, we uncovered errors in sensorimotor integration in larval

Indexed as

behavioral phenotypesclemizolecomorbiditiesdisease modelingepilepsyzebrafish

Identifiers

PMID42158950

DOI10.3389/fphar.2026.1781517

PMCPMC13180867

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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.