Scientists estimate that nearly half of the 322 million individuals affected by depression do not seem to benefit from treatment, which includes the multitude of prescription antidepressant medications available on the market today. Fortunately, the results of new brain research show promise of helping millions of individuals in need.
In the new study, recently reported by Inverse, researchers have theorized that antidepressant treatment isn’t helping because a majority of the available medications are based upon the concept that people experiencing depression symptoms are lacking “serotonin and norepinephrine, two important chemicals in the brain.”
The study, which is scheduled for publishing in the July edition of Neuroscience, suggests that some depressed individuals could be suffering from “a new type of depression” that is potentially driven by a protein referred to as RGS8.
Hiroshima University neuroscientist Yumiko Saito and co-author Yuki Kobayashi state that thirty percent of depressed individuals on antidepressant medications are not experiencing any relief from their symptoms. “Obviously we need a new drug. We need another explanation for what could cause depression.”
Saito and her team of researchers had previously learned that the protein RGS8 controls a hormone receptor known as MCHR1. The protein influences movement and regulation of mood. The prior study implied that decreased amounts of the protein could indicate an increased possibility for depression.
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The research group compared two groups of mice. One group remained a control group. The team genetically engineered the second group of mice to have more of the protein RGS8 in their nervous systems.
“A common behavioral analysis method” to assess “depressive behaviors in animals” is to force them to swim. The scientists documented the number of times that the mice were either immobile or active.
The team found that the group of mice that were genetically engineered was more active than those whose systems were not altered. This information suggests that the animals that had more of the protein were less depressed than the control group. “However, that resistance to depression didn’t happen when the mice were given a drug that stops the hormone receptor MCHR1 from working.”
In an effort to better understand the relationship between RGS8 and MCHR1, the researchers took a closer look at the brains of the mice. They learned that the mice had longer cilia, antennae-like organelles for cellular communication, in the hippocampus.
Dysfunctional cilia have been linked in many past studies to kidney disease, retinal disease, and obesity. More research is needed to determine whether or not dysfunctional cilia can be linked to mood disorders as well. The discovery of the longer organelles in the mice brains has prompted the team to believe that RGS8 may be “a promising candidate toward the development of new antidepressant drugs.”