Aging is the primary risk factor for multiple diseases and is influenced by inter-tissue communication mechanisms that remain poorly understood. My research focuses on how the nervous system coordinates systemic responses to cellular stress, with particular emphasis on mitochondria as signaling platforms.
Specifically, I study how mitochondrial dysfunction in defined neuronal populations is detected and transmitted to peripheral tissues, and how glial cells actively contribute to this process. I propose that neurons and glia form a functional unit that integrates and modulates stress signals, although the architecture and directionality of this communication are still unresolved.
Using Caenorhabditis elegans as an experimental model, I induce mitochondrial dysfunction in a cell type-specific manner to investigate how these signals propagate at the organismal level. This approach allows me to address key questions about when cellular stress becomes systemic, which mechanisms mediate neuron–glia communication, and how these interactions impact processes such as proteostasis and aging.
My goal is to define the mechanistic principles underlying inter-tissue communication in response to stress, and to understand how their dysregulation contributes to vulnerability to age-associated diseases.
