Keynote speaker

Dillin has made an intriguing discovery that mitochondrial stress in one tissue can be communicated to distal tissues. He has found that mitochondrial stress in the nervous system triggers the production of entities known as "mitokines". These mitokines are discharged from the nervous system, orchestrating a response in peripheral tissues that extends the lifespan of C. elegans and remodels metabolism in mice. The revelation came as a surprise, given the prevalent belief that cell autonomous mechanisms would underlie the relationship between mitochondrial function and aging. It was also surprising given the prevailing dogma that mitochondrial function must be increased, not decreased, to improve health and longevity.  His work also underscores the fact that mitochondria, which originated as a microbial entity and later evolved into an intracellular symbiont, have retained their capacity for intercommunication, now facilitated by signals from the nervous system. He has shown that this communication has evolved as a mechanism to reduce infection from pathogens.

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