The risk of depression is written in DNA and now a worldwide study, the first conducted globally on a large scale involving people of different ethnic groups, reveals over 200 genes associated with the 'sickness of living'. The work, published in 'Nature Genetics' and coordinated by University College London (UCL), will allow us to identify new treatment strategies that hit the identified 'targets'. Approaches that could also involve the repositioning of old drugs, i.e. the 'recycling' of medicines already known and used against other pathologies. Among those that could rise to new life there is also a pillar of the anti-diabetes armamentarium: metformin.
Various entities including international consortia, bodies and working groups in the UK, USA, China and Japan collaborated on the research, led by Karoline Kuchenbaecker of Ucl. The authors used data from various genetic investigation methods, genome and transcriptome studies (the part of the whole DNA that is 'translated' into RNA) and a meta-analysis, examining overall genetic information relating to 21 cohorts from different countries and including nearly one million participants of different origins (African, East Asian, South Asian, Hispanic/Latin American), including 88,316 patients with major depression. The authors thus discovered more than 50 new genetic loci (specific positions on chromosomes) and 205 new genes linked to depression.
For some of the genes identified, scientists have implications for the development of antidepressant drugs. In particular, the researchers focus on the Ndufaf3 gene which codes for a protein previously associated with mood instability and on which metformin, a first-line drug for the treatment of diabetes 2, acts. Tests on animals have suggested a possible link between taking metformin and the reduction of depression and anxiety: results which, in the light of the new study, deserve further investigation in the authors' opinion.
With this work, comments Kuchenbaecker, “we show beyond a doubt that our understanding of complex diseases such as depression will remain incomplete until we overcome the 'Eurocentric' bias in genetic research and look for the causes in people 'of different origins' around the world “.
The lead author of the study specifies: “Many genes previously thought to be linked to the risk of depression could influence its probability only in people of European origin. Therefore, for genetic research to contribute to new drugs capable of helping patients of all origins, it is It is vital to work on appropriately diverse genetic data sets.”
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