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We all know how environmental factors or phases of one’s life can influence a person’s mental state; little do we know about the genetics involved.

In a recent study at the University of Maryland School of Medicine, scientists have uncovered a gene that plays a central role in the mental state of a person- either protecting from stress or triggering a downward spiral, depending on its level of activity or simply put, a gene that could protect from depression or accelerate its severity.

Depression is a serious mood disorder, affecting over 300 million people globally every year, changing the way they interact with the world. Nearly 800,000 die from suicide every year—it is the second-leading cause of death among people between the ages of 15 to 29.

Not only contributing to the mortality, but it also affects tens of millions of patients and their families, destroying their lives.

The study which was published on Thursday in the Journal of Neuroscience, stresses 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 called the nucleus accumbens. This region plays a central role in the brain’s “reward circuit.” Meaning when you eat a delicious meal, indulge in pleasurable activity, drink alcohol, or have any other kind of enjoyable experience, neurons in the nucleus accumbens are activated, letting you know that the experience is pushing the proper buttons.

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 depression, any kind of enjoyment becomes difficult or impossible; this symptom is known as anhedonia, which in Latin means the inability to experience pleasure. Therefore, they focused on a subset of neurons in the nucleus accumbens called D2 neurons. These neurons respond to the neurotransmitter dopamine, which plays a central role in the reward circuit.

They proceeded to study these neurons using animal models- mice, when they were subjected to social stress—exposure to larger, more aggressive mice—they were seen to withdraw and exhibit behaviour that indicated depression, such as social withdrawal and lack of interest in food that they would normally enjoy. Dr. Lobo found that in such situations, the levels of the Slc6a15 gene in the D2 neurons of the nucleus accumbens were markedly reduced.

The researchers also studied mice in which the gene had been reduced in D2 neurons. When those mice were subjected to stress, they also exhibited signs of depression. Alternatively, when the researchers enhanced Slc6a15 levels in D2 neurons, the mice showed a resilient response to stress.

“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.”

“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,” said Dr. A.J. Robison, a professor of physiology at Michigan State University who was not involved in the study. “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.”

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