Reducing brain activity could extend human lifespan, new research shows.

Although it is known that gene expression changes as people age, the mechanisms that extend human lifespan are not well understood. However, new research has revealed that differences in brain activity could be the reason some people live longer than others.

Extended longevity in humans has been found to correlate with the downregulation of genes related to neural excitation and synaptic function, and the upregulation of genes involved in immune function.

To investigate further, researchers studied the worm species C. elegans. The worm is a good model for human ageing studies as it shares many human genes and has a short lifespan of only 2-3 weeks. As C. elegans ages, its neural excitation increases. The researchers therefore wanted to see if inhibiting the age-related neural excitation could increase the lifespan of the worms.

C. elegans were treated with invermectin, a drug which blocks the chloride channels in nerve cell synapses. The drug was found to extend worm lifespan in a dose dependent manner. In a different experiment, histamine was used to dampen the neural excitation. The worms dosed on day one and day eight both displayed the same extended lifespan, suggesting that reduced neural activity at any stage of life still promotes longevity.

Neural activity can regulate neuropeptide signalling, which may be responsible for the lifespan extending effects. The worms were genetically engineered to give a mutation in the elg-3 gene, to disrupt the function of the EGL-3 proprotein convertase. The mutant worms displayed longer lifespans.

It is possible that these discoveries could enable the production of life-extending pharmaceuticals.

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