The levels of one gene in particular may play a key role in protecting from depression or accelerating its severity, according to a new study from researchers at the University of Maryland School of Medicine.
Depression, which affects over 300 million people, changing the way they interact with the world, is the most common cause of disability globally.
The study, published Thursday in the Journal of Neuroscience, pinpoints the importance of the levels of gene Slc6a15, which works in neurons of the brain involved with the brain’s reward system. The levels of this gene, which acts as a neutral amino acid transporter in brain neurons, could affect people’s mood, according to Dr. Mary Kay Lobo, the senior author of the study and an assistant professor in the department of anatomy and neurobiology at the University of Maryland School of Medicine.
The study focused on “vulnerable” neurons, or parts of the brain that react to stress. While previous studies had indicated Slc6a15 was “associated with depression susceptibility,” Lobo and her team wanted to examine how levels of this particular gene would correlate with “mediating susceptibility to stress.”
In their research, the team found that mice who had been genetically modified to have lower levels of the gene were found to exhibit depression-like outcomes after experiencing stress. In mice they had modified to enhance the level of the gene, they found a “resilient response to stress,” according to Lobo.
They also found that the level of gene Slc6a15 was reduced in the post-mortem analysis of individuals who had suffered from depression.
“If we can find ways to actually enhance levels of this molecule in this particular vulnerable neuron population that would be a way to combat depression,” Lobo said. “This is also a druggable target.”
Put more simply, the study of this previously understudied gene could be critical in advancing the understanding of depression and its underlying causes, according to Dr. A.J. Robison, a professor of physiology at Michigan State University who was not involved in the study.
“In order to improve, we really need to understand not only how the disease is happening and what went wrong to cause depression, but how the drugs work to combat it,” Robison said. “This study should lead to a continuing body of work that can really make genuine progress in understanding how depression works and maybe even in treating it.”
For Lobo, the next steps entail identifying more of these types of genes ― and their impact.
“We have to go in and find these vulnerable neuron subtypes, perhaps to alleviate depression-like symptoms,” she said.