Author

Georges Arielle Pêche

Centre National de la Recherche ScientifiqueORCID 0000-0002-5775-5696Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

Click to filter author papers

Molecular Biology· 1 Pharmacology & Toxicology· 1

Signature Assays, Organisms & Methods

Click to filter · or open tag

Approach:experimental assay· 2 Research Focus:cell type annotation· 1 Research Focus:differential expression· 1 Research Focus:drug response / drug discovery· 1 Organism:human· 1 Organism:mouse· 1 Research Focus:variant calling· 1

Frequent Co-Authors

Alexia Castiglione· 1 shared Antonia RattiiD· 1 shared Coralie SpiegelhalteriD· 1 shared Delphine BohliD· 1 shared Genries-Ferrand Sandrine· 1 shared Jennifer HuaiD· 1 shared Jocelyn LaporteiD· 1 shared Johann BöhmiD· 1 shared

Activity by Year

2020-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 24 mutual co-author links

Click any collaborator node to inspect or filter shared papers

Focal author (center)Selected co-authorORCID co-authorUnlinked name

Curved chords = mutual co-authorship

1 shared paperPharmacology & Toxicology

Alexia Castiglione

Mutual co-authors in cluster

Author profile →

2 papers

Recent·Most cited

Pre-clinical evaluation of a gene therapy candidate for SOD1-ALS shows improved survival and signs of inflammation in the CNS of treated mice.

Sonia Pezet, Jennifer Hua, Thibaut Marais, Marine Delamare, Sahar Elouej, Julia P. Lemos, Alexia Castiglione, Stéphanie Astord, Mathilde Cohen-Tannoudji, Georges Arielle Pêche, Mara Rigamonti, Nathalie Danièle, Genries-Ferrand Sandrine, Laurine Buscara, Antonia Ratti, , Maria Grazia Biferi

This study evaluates a gene therapy for SOD1-ALS, showing improved survival and CNS inflammation in treated mice with dose-dependent hSOD1 reduction.

bioRxiv · Oct 16, 2025 · PreprintPharmacology & Toxicology

Functional analyses of STIM1 mutations reveal a common pathomechanism for tubular aggregate myopathy and Stormorken syndrome

Georges Arielle Pêche, Coralie Spiegelhalter, Roberto Silva‐Rojas, Jocelyn Laporte, Johann Böhm

The paper shows that TAM and STRMK mutations in STIM1 cause similar functional defects leading to excessive Ca2+ entry and shared pathomechanisms.

Neuropathology · Oct 19, 2020Peer-reviewedMolecular Biology