By Sunanda Creagh, The Conversation
Schizophrenia, bipolar disorder and depression share common genetic variations, a new study has found, with researchers saying they can now calculate how much of the risk for developing such disorders can be traced to genes.
The new findings improve our understanding of the complex interplay between genes and environmental factors in the development of mental illness and may one day help clinicians tailor better treatments.
The study, the result of collaboration between 372 researchers from across the globe, involved analysis of genetic data from 75,000 people, using a type of genetic variation called single nucleotide polymorphisms (SNPs).
The researchers were able to calculate that 23% of the risk of developing schizophrenia can be linked to the SNP genetic variation.
For bipolar disorder, 25% of the risk can be traced for genes, while for major depression the figure was 21%.
At least 17% of the risk of developing autism can be linked to genes, while for attention deficit hyperactivity disorder (ADHD), the figure was 28%.
Crucially, the researchers used data on unrelated people, meaning the results were purely a reflection of genetic risk rather than, for example, a common upbringing among siblings.
“Although a genetic underpinning of psychiatric disorders is mostly well accepted based on family records, occasional non-scientific literature has expressed doubt about this, suggesting shared family environment is responsible,” said lead researcher of the new study, Associate Professor Naomi Wray, from the Queensland Brain Institute.
“Our method for determining the genetic contribution uses information from DNA and uses unrelated people. In this way, our estimates demonstrate that genetic factors are responsible for an important proportion of risk.”
The paper was published in the journal Nature Genetics.
The results showed genetic similarities common to people with an increased risk of developing schizophrenia, bipolar disease or major depression.
However, Professor Wray noted that “disease only occurs when we carry a burden of risk variants as well as experience environmental risk factors – the lottery of life.”
“Part of the importance of our work is to demonstrate that there is a detectable genetic signal. Understanding the causes of psychiatric disorders has been an area of no-progress for so long. The genomics era has led to good progress in other disorders, but progress has been slower in psychiatry,” she said.
“Our results demonstrate a crack in the door that can be used to lever it open further.”
Philip Mitchell, Scientia Professor and Head of the School of Psychiatry at University of New South Wales, said the new study represented a major step forward.
“I think it’s a very important paper. There’s two take home stories in this paper,” he said.
“The first is we can now say that we now know that many genes contribute to the genetic risk and that about a quarter of the known inheritance of these conditions is accounted for by variants that are common,” he said.
“The other side of it is we now know, when you look at these specific genetic variations, there’s enormous genetic overlap between the conditions. It doesn’t account for all causation but there’s this substantial overlap. The big overlaps are between schizophrenia and bipolar, bipolar and depression, and also schizophrenia and depression.”
Professor Mitchell said it would be some time before these findings could be used in practice.
“But in a short space of time, we have gone from knowing hardly any of the genetic variations involved in these conditions, to knowing that common genetic variants explain about a quarter of the risk. That’s a huge step that’s happened very quickly,” he said.
“It confirms these are multi gene disorders. The risk of getting these conditions is determined by many genes. Ultimately, once we understand the genes, that tells you the biochemical pathways for molecular abnormalities and that helps us develop better treatments.”
This article was originally published at The Conversation.
Read the original article.