In an old male mouse, roughly every third hair follicle is left without a nerve. That nerve is what makes a hair stand up when it's cold or frightening. But the nerve itself hasn't died: its cell body sits in a ganglion near the spine and stays alive. Only the long extension, the axon that reaches toward the hair bulb, pulls back. Think of a cord that has come loose from an outlet, even though the outlet itself is still live.
Why does the cord pull away? Because the wall next to the outlet stopped holding it. In the skin, every hair has a tiny muscle that lifts it. With age, that muscle weakens and stops making the protein NGF, which tells the axon "stay here." Old female mice have more of this protein, so their nerves hold on better. When the researchers used a virus to put NGF back into the muscle of old males, the nerves once again reached the follicles, and hair grew back better.
So to bring nerves back into aging skin, you don't need to repair the nerve cells themselves. It's enough to shore up their surroundings, restoring the muscle's ability to support the axon. Then the cord finds its way back to the outlet.
In old male mice, about 35% of hair follicles are completely devoid of sympathetic nerves, yet the neurons themselves in the ganglia are intact, as if the cords were unplugged from the socket while the socket itself stays live.
The idea of reversible denervation and restoring the connection between nerve and tissue echoes a motif from William Gibson's novel Neuromancer, where damaged neural connections can be reprogrammed and restored by acting on the environment.
Not published on arXiv. Here are its page, the PDF and the formalization: you can check it yourself, not only read our account.