In the largest genetic study of anxiety disorders to date, new research from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s College London, in partnership with Texas A&M and the Institute of Psychiatric Phenomics and Genomics (IPPG) at LMU Munich, has identified 58 genetic variants associated with anxiety, most of which have not been identified before now.

The research, published in Nature Genetics, confirmed that, rather than being driven by a single “anxiety gene”, anxiety disorders are influenced by numerous genetic variants from across the genome, with each contributing a small effect.

The researchers compared the genetic data of 120,000 people diagnosed with an anxiety disorder to almost 730,000 people without.

Their analysis of the data notably highlighted the role of several genes involved in GABAergic signaling; a key system that regulates brain activity.

While the research provides a biological basis for anxiety, the researchers do not advocate for the use of genetic testing to diagnose anxiety.

Professor John Hettema, from the Department of Psychiatry at Texas A&M University Naresh K. Vashisht College of Medicine, another of the study’s senior authors said, “Anxiety disorders and their underlying sources of genetic risk have been understudied compared to other psychiatric conditions, so this study substantially advances this critical knowledge.”

Prof Jürgen Deckert, Julius Maximilians University, Würzburg, Germany wrote “The results of the study provide evidence for a role of several previously unknown molecular pathways in the etiology of anxiety, beyond the previously identified GABAergic system. They will provide the basis for future studies in cell culture, animal models and humans which will contribute to a better understanding of the neurobiology of anxiety and as a consequence to innovative and individualized therapies.”

 

Genome-wide association study of major anxiety disorders in 122,341 European ancestry cases identifies 58 loci and highlights GABAergic signaling (DOI 10.1038/s41588-025-02485-8) (Eley, Mattheisen, Hettema et al) was published in Nature Genetics.  

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