Over 170 genes linked to depression, may lead to new blood test for mental health

NEW HAVEN, Conn. — Although the mind is the central focus in the battle to treat depression, a new study finds a person’s genes also play an important role in their mental health. Researchers at Yale University have discovered more than 170 genes with a link to depression. The breakthrough may even lead to a blood test that can more easily diagnose the condition.

Experts analyzed data from 2.5 million individuals worldwide in the biggest study of its kind to date. The findings reveal the “roots of major depression in all its genetic complexity,” according to the study authors. The results may also lead to better drugs for a disorder that affects one in five people in their lifetime.

“One of the real goals of the research is bringing forward new ways to treat people suffering from depression,” says co-senior author Professor Murray Stein from UC-San Diego, in a university release.

The team adds these genetic clues open the door to a screening program for the world’s biggest cause of disability. The findings also shed light on related psychiatric diseases, such as PTSD (post traumatic stress disorder). A blood or saliva sample would help doctors prescribe personalized medications best suited to treat mental illness.

Ancestry company helping to uncover depression gene mutations

Psychiatrists uncovered 178 mutations by pooling genetic and health information on 1.2 million people from Britain, Finland, and customers of genetics company 23andMe. Researchers then compared the data to an entirely separate batch of 1.3 million DNA samples from 23andMe. Study authors discovered “statistically significant” variations in the genes with a link to depression.

“What is most heartening is we could replicate our findings in independent data sets,” says co-lead author Dr. Daniel Levey of Yale University. “Replication is a hallmark of good science, and this paper points to just how reliable and stable results from GWAS studies are becoming.”

These Genome Wide Association Studies (GWAS) involve mapping the complete DNA of healthy and diseased volunteers to pinpoint key differences. Depression and other mental illnesses are genetically complex, featuring combinations of many mutations.

“That’s why we weren’t surprised by how many variants we found,” adds co-senior author Prof. Joel Gelernter. “And we don’t know how many more there are left to discover — hundreds? Maybe even thousands?”

Additionally, this study included more than 300,000 U.S. veterans. The results may provide medical professionals with “polygenic risk scores” to pinpoint those most at risk of developing major depression, anxiety, or PTSD. In the case of veterans, physicians could check on the health of military personnel before and after battle.

Could drugs for other diseases find a new role battling depression?

It also provides deep insights into the underlying biology of genetic disorders. For instance, one mutation, NEGR1, is a protein in the hypothalamus, an area of the brain with a connection to depression. Dr. Levey notes their findings confirm research by the late Yale neuroscientist Ronald Duman.

“It’s really striking when completely different kinds of research converge on similar biology, and that’s what’s happening here,” Levey explains.

Insights into the functions of the variants could lead to drugs that target them. Riluzole, for instance, treats symptoms of motor neuron disease by controlling glutamate. Several of the mutations with a link to depression affect the same brain chemical, suggesting a possible new application.

Researchers have long struggled to identify the causes of depression. The condition affects around 16 million Americans at any one time. Rates have risen during the last decade and doubled during the coronavirus pandemic. Symptoms include low mood, lethargy, loss of pleasure, no appetite, decreasing libido, and more.

The study, appearing in the journal Nature Neuroscience, adds to growing evidence depression is hiding in the genes.

SWNS writer Mark Waghorn contributed to this report.

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