Scientists have identified 19 genes that could cause depression when they alter the levels of their corresponding proteins in the brain, an important finding for the development of new treatments, according to a study published on Monday in Nature.
The research, led by the Veterans Affairs Medical Center and Emory University (Atlanta, Georgia), highlights that the detection of certain pairs of genes and their proteins opens the door to designing more effective drugs for this metal disease.
The experts in charge of this work, Aliza Wingo and Thomas Wingo, began their research based on the theory that certain genetic variants could cause depression by altering brain proteins.
They then turned to a novel approach that combines genome-wide association analysis (GWAS) with proteome-wide association analysis (PAWS).
GAWS, Thomas Wingo points out in a statement, is a very useful tool because of its ability to detect variants associated with certain diseases, such as depression, but it does not explain how they increase the risk of suffering from them.
Therefore, he explains, they designed the aforementioned study model to find out how variations in brain protein levels can explain some of the inherited risks of depression.
They were able to identify a total of 25 “proteins of interest,” 20 of which were missed in previous GAWS studies because they could not label them as being involved in cases of depression.
The authors also determined that the aforementioned 19 genes “contribute to the pathogenesis of depression by modulating the abundance of brain proteins,” says Thomas Wingo.
The brain protein fluctuations observed through this new study methodology are probably the first biological changes that alert to the existence of depression and, perhaps, predispose the individual to the disease, adds Aliza Wingo.
“These findings could also prove useful in identifying biomarkers of depressive symptoms. An effective biomarker, such as hemoglobin A1C in diabetes, could help in the diagnosis and treatment of depression,” concludes Thomas Wingo.