Deep learning-driven neuromorphogenesis screenings identify repurposable drugs for mitochondrial disease
Carmen MenachoiD, Satoshi OkawaiD, Iris Álvarez‐MerziD, Annika WittichiD, Mikel Muñoz‐OrejaiD, Paweł LisowskiiD, Tancredi Massimo PentimalliiD, Agnieszka Rybak‐WolfiD, Gizem Inak, Shiri ZakiniD, Mathuravani A. ThevandavakkamiD, Laura PetersilieiD, Andrea ZalianiiD, Barbara MlodyiD, Annette Seibt, Justin DonnellyiD, Kasey Woleben, José Carlos Fernández-ChecaiD, Diran Agaid HerebianiD, Ertan MayatepekiD, Nikolaus RajewskyiD, Antonella SpinazzolaiD, Markus SchuelkeiD, Ethan O. PerlsteiniD, Andrea Rossi, , Alessandro PrigioneiD
Abstract
Mitochondrial disease encompasses untreatable conditions affecting tissues with high energy demands. A severe manifestation of mitochondrial disease is Leigh syndrome (Leigh), which causes defects in basal ganglia and midbrain regions, psychomotor regression, lactic acidosis, and early death. We previously generated isogenic pairs of Leigh cerebral organoids and uncovered defects in neuromorphogenesis. Here, we leveraged on this disease feature to devise drug discovery pipelines. We developed a deep learning algorithm tailored for cell type-specific drug repurposing to identify drugs capable of promoting neuronal commitment. In parallel, we performed a survival drug screen in yeast and validated the repurposable hits on branching capacity in Leigh neurons. The two approaches independently highlighted azole compounds, Talarozole and Sertaconazole, both of which lowered lactate release and improved neurogenesis and neurite organization in Leigh midbrain organoids. Hence, targeting neuromorphogenesis has led to identify potential new drugs for mitochondrial disease and could prove an effective strategy for further drug discovery.
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