Depression affects more than 150 million people worldwide, with symptoms that can impact every aspect of an individual’s life. People develop depression for a number of reasons, including both genetic predispositions and the impact of stressful life events.
No one's life is free of stress, of course, yet some people seem to be far less affected by stress than others.
New research offers insight into why some people seem relatively immune to the effects of stress, while others find it difficult to shake off and become depressed. It also suggests we may need to change how we think about treating depression.
Treatment of depression has historically been directed at regulating neurotransmitters such as serotonin.
The study identified a different molecule which scientists believe may control the degree to which our brain effectively deals with stress.
While most prior efforts in antidepressant drug discovery have focused on ways to undo the bad effects of stress, our findings provide a pathway to generate novel antidepressants that instead activate mechanisms of natural resilience.
Beta-catenin is found in the brain and plays a number of biological roles. When beta-catenin was activated in mice, the animals became protected against stress, the researchers noted. Conversely, those with inactive forms of the molecule eventually develop depressive behaviors.
Further evidence implicating beta-catenin in resistance against depression came from post-mortem samples. Beta-catenin was suppressed in the brains of people who were depressed at their time of death, regardless of whether they were receiving antidepressant therapy.
Researchers have begun to trace the brain pathway that requires beta-catenin for depression resistance. While they have identified certain genes involved, future studies are needed to fully understand the molecular basis of this process.
“While most prior efforts in antidepressant drug discovery have focused on ways to undo the bad effects of stress, our findings provide a pathway to generate novel antidepressants that instead activate mechanisms of natural resilience,” stated Eric J. Nestler, one of the study authors and Director of the Friedman Brain Institute, Icahn School of Medicine at Mount Sinai in New York.
The study is published in Nature.