One Disorder, Two Brains: Challenges in Modeling Epilepsy and Associated Movement Disorders in Mice
- 1Institute of Neuroscience, Lobachevsky State University of Nizhny Novgorod, 603022 Nizhny Novgorod, Russia
- 2Department of Genetics and Life Sciences, Sirius University of Science and Technology, 354340 Sochi, Russia
Abstract
Modeling epileptic syndromes co-occurring with movement disorders in mice often fails to fully recapitulate human phenotypes due to distinct gene-specific and anatomical mechanisms. This review categorizes these translational barriers into three primary groups. First, ortholog heterotopia and heterochrony drive spatiotemporal shifts in gene expression, causing orthologs to activate at disparate developmental stages or within different cell populations across species. Second, molecular redundancy and compensation obscure phenotypes through the upregulation of alternative proteins in response to target protein suppression, the activation of modifier genes, or neural network rewiring. Third, structural variations in striatal anatomy fundamentally alter corticostriatal loop functioning. Characterizing these divergent mechanisms is essential for improving the predictive validity of preclinical models and advancing targeted therapies.
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BibTeX
@article{travin2026disorder,
title = {{One Disorder, Two Brains: Challenges in Modeling Epilepsy and Associated Movement Disorders in Mice}},
author = {Daniil I. Travin and Polina E. Anisimova and Ksenia A. Bogovarova and Angelina O. Kustova and Victor S. Tarabykin},
journal = {International Journal of Molecular Sciences},
year = {2026},
month = nov,
doi = {10.3390/ijms27219916},
url = {https://www.mdpi.com/1422-0067/27/21/9916},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - One Disorder, Two Brains: Challenges in Modeling Epilepsy and Associated Movement Disorders in Mice
AU - Daniil I. Travin
AU - Polina E. Anisimova
AU - Ksenia A. Bogovarova
AU - Angelina O. Kustova
AU - Victor S. Tarabykin
PY - 2026
DA - 2026/11/05
JO - International Journal of Molecular Sciences
DO - 10.3390/ijms27219916
UR - https://www.mdpi.com/1422-0067/27/21/9916
AB - Modeling epileptic syndromes co-occurring with movement disorders in mice often fails to fully recapitulate human phenotypes due to distinct gene-specific and anatomical mechanisms. This review categorizes these translational barriers into three primary groups. First, ortholog heterotopia and heterochrony drive spatiotemporal shifts in gene expression, causing orthologs to activate at disparate developmental stages or within different cell populations across species. Second, molecular redundancy and compensation obscure phenotypes through the upregulation of alternative proteins in response to target protein suppression, the activation of modifier genes, or neural network rewiring. Third, structural variations in striatal anatomy fundamentally alter corticostriatal loop functioning. Characterizing these divergent mechanisms is essential for improving the predictive validity of preclinical models and advancing targeted therapies.
SN - 1422-0067
ER -