Sergio Casas‐Tintó

This study identifies extracellular proteoglycan remodeling as a shared mechanism driving brain repair and tumor progression through Hpsl and glypican interactions.

This study identifies Ca-alpha1T and Slowpoke channels as essential for pro-tumorigenic Ca2+ signaling in Drosophila gliomas, with Slowpoke showing therapeutic potential.

This paper shows that parental exposure to light stress reduces offspring brain fitness, accelerating glioblastoma progression in Drosophila.

The paper shows that glial cells in Drosophila can transdifferentiate into neurons after CNS injury, providing a new mechanism for neurogenesis.

This study shows that synaptic proteins in glioblastoma cells contribute to tumor progression and lethality in Drosophila models.

This paper investigates the haplolethal region of the Drosophila wupA gene, showing that haplolethality arises from the combined insufficiency of multiple TnI isoforms requiring chromosomal integrity for proper expression.

This paper shows that glioblastoma produces ImpL2, which disrupts neuronal insulin signaling, leading to neurodegeneration and premature death, and that restoring insulin signaling can rescue these effects.

This study shows that PI3K activation prevents Aβ42-induced synapse loss and promotes amyloid deposit formation in Drosophila and human cell cultures.