If your car’s battery dies, you might call on roadside assistance—or a benevolent bystander—for a jump. When damaged neurons lose their “batteries,” energy-generating mitochondria, they call on a different class of brain cells, astrocytes, for a boost, a new study suggests. These cells respond by donating extra mitochondria to the floundering neurons. The finding, still preliminary, might lead to novel ways to help people recover from stroke or other brain injuries, scientists say.

“This is a very interesting and important study because it describes a new mechanism whereby astrocytes may protect neurons,” says Reuven Stein, a neurobiologist at The Rabin Institute of Neurobiology in Tel Aviv, Israel, who was not involved in the study.

To keep up with the energy-intensive work of transmitting information throughout the brain, neurons need a lot of mitochondria, the power plants that produce the molecular fuel—ATP—that keeps cells alive and working. Mitochondria must be replaced often in neurons, in a process of self-replication called fission—the organelles were originally microbes captured inside a cell as part of a symbiosis. But if mitochondria are damaged or if they can’t keep up with a cell’s needs, energy supplies can run out, killing the cell.

In 2014, researchers published the first evidence that cells can transfer mitochondria in the brain—but it seemed more a matter of throwing out the trash. When neurons expel damaged mitochondria, astrocytes swallow them and break them down. Eng Lo and Kazuhide Hayakawa, both neuroscientsists at Massachusetts General Hospital in Charlestown, wondered whether the transfer could go the other way as well—perhaps astrocytes donated working mitochondria to neurons in distress. Research by other groups supported that idea: A 2012 study, for example, found that stem cells from bone marrow can donate mitochondria to lung cells after severe injury.

To find out whether this kind of donation was taking place in the brain, Lo and Hayakawa teamed up with researchers in Bejing to test whether astrocytes could be coaxed into expelling healthy, working mitochondria. Previous studies hinted that astrocytes may pick up on neurons’ “help me” signals using an enzyme called CD38, Lo says. The enzyme, produced throughout the body in response to injury or damage, is also made by astrocytes. When Lo and colleagues genetically engineered mice to produce excess CD38, astrocytes from the rodents—extracted and deposited into fluid-filled dishes—expelled large numbers of still-functional mitochondrial particles. Researchers then dumped the mitochondria-rich fluid into another dish containing dying mouse neurons, and found that the cells did, in fact, absorb the mitochondria within 24 hours. The recharged neurons also grew new branches, lived longer, and had higher levels of ATP than cells not receiving the replacement batteries, suggesting that the astrocytes’ mitochondria were beneficial.

Next, the team needed to determine whether the same phenomenon happens in living animals. So they subjected live, anesthetized mice to a strokelike injury and then injected damaged brain regions with astrocyte-derived mitochondria. After 24 hours, scientists killed the mice, cut into their brains, and examined the tissue microscopically. They saw that the mice neurons had not only absorbed the mitochondria, but also had significantly higher levels of molecules known to promote survival in distressed cells than did mice that had not received the mitochondrial cocktail.

Finally, the team tested whether CD38 was necessary for the transfer. They injected mice with short segments of RNA designed to interfere with the enzyme’s function. Mice who received the treatment after their simulated “strokes” had far fewer astrocytic mitochondria in their neurons. The rodents also fared twice as badly on neurological tests compared with ones in which CD38 was unblocked , the team reports today in Nature . Lo emphasizes that the work is merely a “proof-of-concept study,” but adds that the outcomes of the neurological tests “tells you [the enzyme] is clinically relevant.”

Given that CD38 plays many important roles throughout the body, including the immune system, the data are “way too preliminary” to start pursuing drugs that would increase or alter its activity, cautions Frances Lund, a microbiologist at the University of Birmingham in Alabama. It’s not clear, for example, whether the transfer of mitochondria was caused by, or merely correlated with, CD38 levels, she says.

Still, Jun Chen, a neurobiologist at the University of Pittsburgh in Pennsylvania, is hopeful that the finding could lead to new treatments for diseases attributed to mitochondrial dysfunction. Parkinson’s disease, for example, is a neurodegenerative disorder strongly associated with mitochondrial dysfunction, in which dopamine-producing neurons in certain brain regions die en masse. If the new research pans out, he says, clinicians may one day be able to deliver healthy mitochondria into sick, but still viable, neurons.