Panic disorder (PD) is one of the most common anxiety disorders, with a prevalence of 3.4–4.7%. Although PD seems to have no known cause, and its underlying aetiology is not well understood, studies have consistently shown that genetic factors explain about half of the variance. It is likely that most cases of PD have a complex genetic basis. Existing data suggest, however, that the genetic architecture underlying PD is heterogeneous and differs between cases. For example, the degree of genetic complexity, and the pattern of genes involved might differ in familial versus non-familial cases, in early- versus late-onset cases, or when different comorbid conditions, gender and potential intermediate or sub-phenotypes are considered. At the molecular genetic level, linkage and association studies—the latter including traditional candidate gene and recent genome-wide studies—have been used to study PD. Although no robust molecular genetic findings have emerged so far, it is conceivable that the first PD susceptibility genes will be identified in the coming years via the application of modern molecular genetic methods and through multicentre collaborations to bring together combined, large datasets. Such findings could have a major impact on our understanding of the pathophysiology of this disorder, and would provide important opportunities to investigate genotype–phenotype correlations, as well as the interaction between genetic and environmental factors involved in the pathogenesis of PD. Here, the authors summarise the latest genetics findings about PD, and give an overview of anticipated future developments.
- anxiety disorders
- trait marker
- molecular genetics
- molecular genetics
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Funding This study was supported by the National Genomic Network of the ‘Bundesministerium für Bildung und Forschung’ (BMBF), by an NIH/DFG Research Career Transition Award to JS, by the Alfried Krupp von Bohlen und Halbach-Stiftung to MMN, and by the Intramural Research Program of the National Institute of Mental Health, National Institutes of Health (IRP-NIMH-NIH) to FJM and JRW.
Competing interests None.
Patient consent Obtained.
Provenance and peer review Not commissioned; externally peer reviewed.
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