Why do some neurons cope with lifelong stress, while others fail and degenerate? In this research line, we investigate neuronal resilience as an active, molecularly encoded property that shapes brain aging and disease. We focus on how chromatin readers, energy metabolism and ER redox biology work together in vivo to determine whether neurons adapt or cross the point of no return.
Using Drosophila as a discovery platform and neuronal models for validation, we have identified YEATS-domain chromatin readers as key integrators of transcription and metabolism. Our work on YEATS2 and ENL/AF9 shows that these factors do not simply "read" histone marks, but tune mitochondrial function, stress responses and, ultimately, lifespan and neurodegeneration trajectories. In parallel, we study how ER oxidoreductases such as ERO1 couple ER and mitochondrial redox stress to neuronal vulnerability and aging. Together, these projects aim to build a mechanistic map of the pathways that keep neurons resilient — or push them towards degeneration.
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