The researchers bred mice to lack a key gene in a pathway in the brain that seems to determine how neurons grow and form connections with one another, according to Cheyette. The mice without this gene were found to develop normally, but showed “behavioral abnormalities” compared to their siblings who were not missing the gene. They took longer to eat when introduced to a new environment, gave up faster during an escape task, and were less social than their peers. When the more troubled mice were given lithium, their behavior returned to normal.

Cheyette’s group also examined the difference between the brains of the “wild-type” mice and the mice who were missing the gene. The brains of the experimental mice had fewer dendritic spines—tree-like parts of a neuron that branch out and form connections with other neurons. On its own that might suggest this gene shapes the development of these connections, and that the lack of those connections likely explains the mice’s abnormal behavior. Cheyette’s group also treated some of the experimental mice with lithium, and found that they developed more connections, leaving them with about as many as the normal mice. And while Cheyette wouldn’t say this is “the absolute 100 percent answer” to the question of why lithium works, it “adds a lot of weight” to the argument that it targets this pathway.

The study also looked at thousands of cases worth of human genetic data from Cheyette’s collaborators to see if defects in the same gene in humans were associated with bipolar disorder, schizophrenia, or ASD (autism spectrum disorder). It’s important to note here that very few people have these mutations to begin with, according to Cheyette. And while mutations in this gene were quite rare, among the small number who had them, there were nearly twice as many cases of people with those disorders (.9% of the total cases) than those without the disorders (.5% of the total cases).

This research does have its limits: As Cheyette said, “mice are not humans.” Some things are bound to be lost in translation when using animal models for human psychiatric symptoms. He also emphasized that “by itself, this gene is only going to account for a small increase in risk in small numbers of patients.” It by no means explains every occurrence of bipolar disorder, schizophrenia, and ASD. Instead, he believes it may be one of many overlapping, interacting genes that contribute to risk. “But it’s an still important clue in [figuring out] the kinds of defects in patients that may exist at the biological level,” Cheyette said. And, according to Cheyette, that deeper understanding may answer questions that have plagued the field for decades.

With little working understanding of the brain, psychiatrists have always done the best they could to categorize diseases based off what they could observe in their patients. And, working with what they had, they built diagnostic categories around these behaviors with the hope that, eventually, “those disorders would correspond to very different underlying biology when we finally understood it,” Cheyette said. For years, luck and careful observation were quite helpful—several other psychiatric drugs that formed the basis for current treatments were discovered by accident. But that approach has only come so far, and pharmacological treatments for psychiatric disorders have “hit a wall” in the past decade, Cheyette says.