Are old axons capable of regeneration?
Age is not an obstacle to the regeneration of neurons, according to scientists from Yale
LifeSciencesToday based on Yale University materials: Age no obstacle to nerve cell regeneration, Yale researchers findThe ability of motor neurons to self-repair decreases with aging, but this phenomenon, at least in worms, does not depend on age, but on insulin.
A recent discovery by Yale University scientists suggests that deterioration of the nervous system may not be inevitable.
With age, all organisms show a decrease in the ability to regenerate the injured nervous system, but a recent study published in the journal Neuron (Byrne et al., Insulin/IGF1 Signaling Inhibits Age-Dependent Axon Regeneration) suggests that this decrease is not associated with the destructive effect of time.
"The nervous system regulates its response to age separately from what happens in the rest of the body," says study leader Marc Hammarlund, PhD, associate professor of genetics at Yale University School of Medicine. "By manipulating the insulin signaling pathway, we can create animals that live longer with a normally aging nervous system, or, conversely, animals that die at a normal age, but their nervous system remains young."
Alexandra Byrne, PhD, lead author of the study, identified two genetic pathways regulating insulin activity responsible for the age-related decline in the ability of C. elegans roundworms to regenerate axons of neurons. Scientists have also identified two other pathways that also regulate the ability of neurons to regenerate, but have nothing to do with the age of the worm.
The C. elegans nematode is a model widely used to study the genetics of aging and to manipulate a family of genes regulating insulin signaling, which has been proven to significantly increase the lifespan of this organism. A new study shows that insulin signaling directly affects the nervous system.
In aging C. elegans, the regeneration of axons of motor neurons is suppressed by the conservative DAF-2 receptor of the insulin/IGF-1 pathway. The function of DAF-2 in regeneration is mediated by the internal neuronal activity of the transcription factor of the Forkhead family DAF-16/FOXO. The DAF-16 factor regulates regeneration regardless of age, showing that neuronal aging is an internal, neuron-specific and genetically regulated process.
In addition, American scientists have found that, regardless of the age and signaling of FOXO through the TOR pathway, regeneration is inhibited by DAF-18/PTEN.
Finally, DLK-1, an evolutionarily conservative regeneration regulator, is suppressed by insulin/IGF-1 signaling associated in neurons with the DAF-16 receptor, and is necessary for regeneration mediated by both DAF-16 and DAF-18. Taken together, these data prove that insulin signaling specifically inhibits the regeneration of aging adult neurons and that this mechanism is independent of PTEN and TOR.
"We hope to understand how different signaling pathways co–ordinate neuronal aging and, in particular, how to induce an old neuron to regenerate after injury," says Dr. Byrne.
"We hope to increase not just life expectancy, but healthy life expectancy," adds Dr. Hammarlund.
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