Researchers believe that uncovering the role of a protein that is present in our bodies may revolutionize depression treatments.
In the most severe cases, it can lead to suicide.
It is normal to experience occasional sadness or grief after specific events, but depression is different.
It can lead to a variety of emotional and physical issues that reduce the ability to function at work and at home.
Depression is treatable, but it is important to talk to a professional to choose the best therapy based on the cause, symptoms, medical and family history, cultural factors, and environmental factors.
Most antidepressant drugs are made based on the belief that depression occurs because of two chemicals that people who have depression lack: serotonin and norepinephrine. The aim of medications is to adjust the levels of these two neurotransmitters.
According to the American Psychiatric Association, 80–90 percent of people respond well to therapies, but for some patients, the drugs available on the market today are not effective.
Researchers have been seeking new ways to treat depression. A study conducted at Hiroshima University in Japan, published in the journal Neuroscience, is based on the behavior of RGS8, a protein that in humans is encoded by the RGS8 gene.
This protein controls a hormone receptor called MCHR1, which helps to regulate sleep, feeding, and mood. In past years, scientists discovered “that RGS8 inactivates MCHR1 in cultured cells.”
Researchers at Hiroshima University conducted an experiment on mice to find out whether RGS8 can cause depressive behavior. First, the mice did a swim test, so the scientists could measure the time that each mouse was active, take that away from the total test time, and then uncover the immobility time period.
Results showed that “mice with more RGS8 in their nervous system recorded shorter immobility times than those with a normal amount of RGS8.”
When mice were given an antidepressant drug, the immobility times became shorter, but when the mice were given a drug that prevented MCHR1 from working, the immobility time was not affected.
These findings revealed a new possible cause of depression that highlighted the role of MCHR1.
The team also looked at the mice’s brains under the microscope to determine the relationship between MCHR1 and RGS8 by examining the size of cilia, which are hair-like projections from certain cells, in a region of the hippocampus called the CA1, where RGS8 levels were highest.
Results showed that mice that took the drug that stopped MCHR1 from working had longer cilia. In the past 10 years, studies about the role of cilia in diseases found that dysfunctional cilia are associated with health conditions such as obesity, kidney disease, and retina disease.
Scientists have to conduct additional experiments to uncover the role of cilia in depression, but the results of the studies conducted in Hiroshima showed that RGS8 plays a part in the development of depressive behavior.
These groundbreaking findings are paving the way for future experiments that aim to find new drugs to treat depression.