Scientists have identified 17 genetic variants that appear to be linked to depression in individuals with European ancestry.
The study, carried out by pharmaceutical firm Pfizer and published in Nature Genetics, did not generate any new genetic data. Instead, the US research team analysed existing data from individuals who had purchased their own genetic profiles as part of the 23andMe online genetic sequencing service.
Prior to this study, efforts to identify genetic risks for depression had failed as there was insufficient genetic data to analyse. 'Everyone is recognising that this is a numbers problem', said Dr Ashley Winslow, director of neurogenetics at the Orphan Disease Center at the University of Pennsylvania and former neuroscientist at Pfizer, who led the study. 'It's hard, if not impossible, to get to the numbers that we saw in the 23andMe study.'
Although it is known that depression can run in families, the condition is the result of many different causes. This means that, if genetic data from individuals with different underlying causes of depression is grouped together, any statistical significance for a risk factor is diluted – which makes identifying genes associated with depression more difficult.
23andMe has sold over a million gene-test kits, and over half of its customers have agreed to allow their DNA to be used in further research. Using this data, researchers searched for common genetic differences in 75,607 individuals of European ancestry who self-classified as having been diagnosed or treated for depression, and compared this with genetic data 231,747 healthy controls.
The results were then combined with genetic data from a previous study using over 20,000 clinician-reported cases of depression and healthy controls of similar ancestry. Genetic sites that appeared statistically significant were followed up using an analysis in an independent 23andMe 'replication' sample.
In total, the research team identified 17 different genetic variants linked to depression, at 15 genome locations. Intriguingly, many of these genes are thought to play a role in regulating gene expression and neuron growth in the developing brain.
'We hope these findings help people understand that depression is a brain disease, with its own biology,' said Professor Roy Perlis, who also worked on the study.
'This study has proven that sample size is key,' said Elisabeth Binder of the Max-Planck Institute of Psychiatry, who was not involved in the study. 'It is also the first study to show that this can be achieved by repurposing large commercial databases for science, in this case from 23andMe. Without this collaboration such sample sizes could not have been achieved.'