Author(s)

Peilin Wang

Corresponding Author

Peilin Wang

ABSTRACT

Anxiety disorders (AD), with early onset and probability of relapse, are the psychiatric disorder of the highest prevalence worldwide. Much is discovered about the synaptic mechanisms of AD, what has been utilized in medical treatment. However, there is a shortage of genetic cures, which may be possible along with the progress of genetic technologies. Based on family studies and twin studies, genetic epidemiological research has demonstrated a moderate level of familial aggregation. To date, Single nucleotide polymorphism (SNPs) and genome-wide association studies (GWAS) have found quite a few variants reaching genome-wide significant, such as on NTRK2, PDE48. Given that environmental factors substantially contribute to the onset of AD, Gene × Environmental (G×E) interaction can provide a new perspective into the pathology of AD, though it is now only limited to several candidate genes. Some variants are found related to anxiety sensitivity, which can predict AD and panic disorder (PD). Epigenetic modification of DNA, especially methylation, appears to exert great influences on the gene expression which modulates the effects of environmental factors on AD risk. A large-scale combination of GWAS, G×E interplay and epigenetics will enable us to fill the blank of genetic treatment and find more effective techniques, such as CRISPR or demethylation drugs, to prevent and cure AD. To convey new ideas of potential genetic treatment, this review provides an overview of the overall research in genetics of AD and discusses how genetics is expected to be utilized in the anxiety treatment.

KEYWORDS

Anxiety disorders, genetics, treatment, epigenetics, gene environmental interaction