The study concludes that Slc6a15 caused enhanced susceptibility to a subthreshold social defeat stress
In a path-breaking discovery, researchers have identified the gene that leads to depression, which according to the World Health Organization (WHO) has affected 350 million people worldwide.
According to the WHO figures, 6.9 percent of the total population in the world is facing depression and it is a major cause of disability.
The new gene found by US researchers either amplifies or reduces stress depending on the level of its activity. They presume that the discovery will open doors for devising a new treatment for mental health disorder.
According to the study, nearly 800,000 people commit suicide every year, which has now become the second biggest reason for deaths of people aged 15 to 29.
The new gene has been named Slc6a15 and is common in both humans and animals. The researchers, who conducted the study on a lab mouse, found that altering the particular gene, which is found in the brain, leads to depression or can make the mice resilient.
“The study highlights how levels of this gene in these neurons affects mood,” said Dr Mary Kay Lobo, assistant professor at the University of Maryland, US said to Science Daily.
“It suggests that people with altered levels of this gene in certain brain regions may have a much higher risk for depression and other emotional disorders related to stress,” Lobo added.
In an early stage of their research back in 2006, Lobo and her colleagues had found that the Slc6a15 gene was common among specific neurons in the brain and now they have found that these neurons are the important factors that trigger depression.
According to Lobo, she and her team delved into the part of the brain called Accumbens, which is also called brain’s “reward circuit”.
This specific part of the brain is activated at different times during a day such as while eating a delicious meal, having sex, drink alcohol or while having other similar experience.
One of the major symptoms of depression is the inability to enjoy the moments of happiness, a state which is medically termed anhedonia.
According to the abstract of the study, “The Slc6a15 reduction in nucleus accumbens (NAc) occurred selectively in striatal dopamine receptor 2 (D2), which are neurons. Next, we used Cre-inducible viruses combined with D2-Cre mice to reduce or overexpress Slc6a15 in NAc D2-neurons. Slc6a15 reduction in D2-neurons caused enhanced susceptibility to a subthreshold social defeat stress (SSDS) as observed by reduced social interaction, while a reduction in social interaction following CSDS was not observed when Slc6a15 expression in D2-neurons was restored.”
The study concludes that Slc6a15 reduction in dopamine receptor neurons caused enhanced susceptibility to a subthreshold social defeat stress (SSDS) and reduced social interaction. In the meanwhile, a reduction in social interaction was not observed when the Slc6a15 expression in D2-neurons was restored.
The study has been authored by Indian American researcher Ramesh Chandra of Department of Anatomy and Neurobiology, University of Maryland School of Medicine, along with T Chase Francis, Hyungwoo Nam, Lace M. Riggs, Michel Engeln, Sarah Rudzinskas, Prasad Konkalmatt, Scott J. Russo, Gustavo Turecki, Sergio D. Iniguez and Mary Kay Lobo.
Ramesh Chandra’s bio on the official website of the University says “I am further investigating these mitochondrial changes in a mouse model of depression through funds from a 2015 NARSAD Young Investigator Grant from the Brain & Behavior Research Foundation.”