The tiny worm Caenorhabditis elegans has a toggle that flips on a long-life program. The trigger is a signal about oxygen starvation. Researchers already knew that flipping this toggle artificially makes the worm live longer. But how the signal gets from the nervous system to the organs remained a mystery.
The authors of the new study traced the entire wiring. They switched genes on and off in individual nerve cells of the worm and watched how that affected lifespan. The first link, it turned out, is the ADF neurons, which release serotonin. Activate these neurons, and the worm lives 26% longer. From there the signal travels to the RIS neuron through a dedicated receptor, SER-7. Remove the RIS neuron, and the effect vanishes. Other signaling molecules also join the chain: tyramine and the neuropeptide NLP-17. All of them converge on the fmo-2 gene in the gut, which is what actually sets longevity in motion.
So the toggle in the worm's neural circuit turned out to be not a simple on-off switch but a whole signal-transmission system. Now scientists know exactly which cells and molecules are responsible for longevity. That could help create drugs that slow aging without causing side effects.
The worm C. elegans has only 302 neurons, and scientists know each one by name. This work features neurons named ADF, NSM, RIS, RIM, BAG, URX, AQR, and PQR: a real zoo, but each plays its own role in the longevity circuit.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.