In young animals and humans, injuries to nerve cells don’t have to lead to long-term damage because the youthful nervous system is relatively effective at repairing itself. But in adults this repair system falters, and nerve injury more often results in lasting effects.
To understand why aging reduces a neuron’s ability to regenerate, Alexandra B. Byrne, Ph.D., postdoctoral fellow, Marc Hammarlund, Ph.D., assistant professor of genetics, and colleagues turned to the tiny worm C. elegans. In young worms, the team found, 65 percent of axons—the long extensions of nerve cells—regenerated after injury. But in older animals, only 28 percent of injuries spurred regeneration.
Focusing on which signaling pathways are required for axon regeneration—and which are altered by aging—the team found that a pathway related to insulin was key to the change in older worms. But the pathway’s effects on neuron regeneration, they reported Feb. 5 in the journal Neuron, could be separated from aging: the regenerative abilities of older animals could be boosted by tweaking levels of the genes involved. The research has implications for treating not only brain injuries, but also aging-associated brain diseases such as Alzheimer’s disease.