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Brain Mosaicism Matters: Organoids in focus to unveil mechanisms in epileptogeni...

Brain Mosaicism Matters: Organoids in focus to unveil mechanisms in epileptogenic cortical malformations Epilepsy, a global neurological disorder affecting around 70 million people, poses a significant medical challenge, with one-third of patients facing drug-resistant epilepsy. Cortical malformations such as focal cortical dysplasia... ver más

31/03/2026

MINISTERE DE L'ENS...

196K€

Presupuesto del proyecto: 196K€

Líder del proyecto

MINISTERE DE L'ENSEIGNEMENT SUPERIEUR ET DE... No se ha especificado una descripción o un objeto social para esta compañía.

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Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2024-03-13

Línea de financiación objetivo El proyecto se financió a través de la siguiente ayuda:

HORIZON-MSCA-2023-PF-01-01: MSCA Postdoctoral Fellowships 2023

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Duración del proyecto: 24 meses Fecha Inicio: 2024-03-13
Fecha Fin: 2026-03-31

Presupuesto del proyecto 196K€

Descripción del proyecto Epilepsy, a global neurological disorder affecting around 70 million people, poses a significant medical challenge, with one-third of patients facing drug-resistant epilepsy. Cortical malformations such as focal cortical dysplasia type II (FCDII) are associated with pediatric drug-resistant epilepsy for which surgical intervention serves as the main therapeutic approach for seizure control. FCDII is marked by cortical dyslamination and the presence of abnormal cytomegalic cells. Recent findings show that FCDII results from brain mosaicism due to postzygotic mutations in genes of the mTOR pathway, which produces excessive activation of the pathway. Nevertheless, as the human surgical FCDII samples represent an advanced disease stage, we poorly understand its developmental origin and mechanisms. Moreover, the link between mTOR activation and epileptogenesis remains unclear. To address these critical knowledge gaps, a disease-relevant FCDII model is needed. For the preservation of human-specific features, I will use a mosaic cortical organoid model that expresses an inducible MTOR-S2215F mutant construct to reflect the somatic nature of FCDII. Induction of the mutation at different time points will shed light on the specific time frame during which mutations occur in FCDII patients and enable us to generate a preclinical model replicating an FCDII-like phenotype. Next, I will perform single-cell transcriptomic profiling at various developmental stages to uncover the cellular and molecular mechanisms behind FCDII development. Finally, the neuronal network activity of mosaic FCDII cortical organoids will be characterized, focusing on identifying the primary drivers of epileptiform activity among mutant cytomegalic or non-mutant nearby cells. In brief, this preclinical FCDII model has the potential to unveil novel developmental mechanisms, offer new non-invasive avenues for treating FCDII patients with drug-resistant epilepsy, and boost my career trajectory in the field.

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