Scientists have discovered dozens of genes that increase the risk of depression, an important finding that highlights the complexity of the disease and shows why antidepressants work well for some people, but are completely ineffective for others.
A Global Consortium of More than 200 scientists identified 44 gene variants or small changes in genes, each contributing in a minor way to a person's risk of depression. Thirty of the gene variants had not been identified in any previous study.
The hope is that the discovery will pave the way for new, diverse therapies for depression, an often debilitating disease affecting nearly 1
Depression is one of the most serious but elusive public health issues. Steven Hyman, director of the Stanley Center for Psychiatric Research at MIT's Broad Institute and Harvard, who was not involved in this study
"Despite decades of effort, there have only been few insights into its biological mechanisms," Hyman told Live Science , "This groundbreaking study represents an important step in elucidating the biological foundations of depression."
The massive study published yesterday (26 April) in the journal Nature Genetics analyzed the genomes of more than 135,000 major depression patients, commonly referred to as major depression, and compared them to the genomes of nearly 350,000 People without depression.
Many of the genes associated with depression are also associated with other psychiatric disorders, such as schizophrenia and bipolar disorder, as well as health issues. Related to depression, including obesity and insomnia, the study found.
Some of the gene variants control neurotransmitters in the brain, such as dopamine and adrenaline, which can target the current class of antidepressants. However, other gene variants have nothing to do with neurotransmitters, which is why antidepressants do not work for some people when the genetic bases of their depression are elsewhere in the brain, the researchers say. [7 Ways Depression Differs in Men and Women]
Each of the newly identified gene variants is essentially a target that could be addressed with drug therapy, Dr. Patrick Sullivan, director of the Center for Psychiatric Genomics at the University of North Carolina School of Medicine. (Sullivan, along with several other researchers, has ties to pharmaceutical or genetic companies.)
In the new study, researchers found no single gene variant that would be a strong risk factor for depression, such as mutations in BCRA1 Genes often lead to breast cancer. Instead, each gene variant contributes incrementally to depression.
"If there was something important, we would have found it," Sullivan told Live Science.
All people carry some of these gene variants for depression, but some people are more than others and more at risk of depression, said senior study author Naomi Wray, a professor at the University of Queensland in Australia.
Previous studies on identical twins have revealed that genes are responsible for half of all cases of depression. At other times, the cause may be stress or trauma. Some people may remain resilient for reasons that are not understood, even though they experience something that would depress others.
"We know that many life experiences also contribute to the risk of depression, but the identification of genetic factors opens new doors for research biological drivers," said Wray in a statement .
Sullivan compared the study on depression and genetics with research conducted decades ago on cardiovascular disease, leading to drug therapies that significantly reduce the risk of heart attacks and stroke. Most of the antidepressants used today have been discovered by accident, but now the search for new drugs can be "rationally controlled" by biological discovery.
For example, gene variants are associated with RNA and the movement of molecules of the nucleus of nerve cells, Sullivan noted. This discovery could lead to "biologically driven therapeutics" targeting RNA.
The scientists involved in this study are working on an online tool that will allow subjects with depression to participate in further genetic studies. Members of the public who wish to be informed about the start of the study can send an e-mail to: firstname.lastname@example.org
Follow Christopher Wanjek @wanjek for daily tweets about health and science with a humorous touch. Wanjek is the author of Food at Work and Bad Medicine. His column, Bad Medicine appears regularly on Live Science.