Etiology and neurobiology of social anxiety disorder.
Social anxiety disorder (SAD) is influenced by multiple genetic and environmental factors. Imaging genomics combines genotyping with neuroradiological techniques, such as functional MRI (fMRI) and positron emission tomography (PET), to investigate samples relevant to psychiatric pathophysiology. Neuroanatomical areas implicated in SAD include the amygdala, prefrontal cortex, hippocampus, and striatum. Recent investigations have suggested that allelic polymorphisms may play a role in the disorder; 2 candidate genes, the serotonin transporter (SLC6A4) and catechol-O-methyl transferase (COMT), are described. The biology of extinction learning is relevant to therapeutic approaches that aim to augment existing psychotherapies. In the future, novel uses of imaging genomics integrated with rational, biologically informed treatments will offer a more refined understanding of this complex and disabling disorder.
Mathew
Sanjay J
SJ
Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA. sanjay.mathew@mssm.edu
Ho
Stephanie
S
D001921:Brain / Q000000981:diagnostic imaging / Q000503:physiopathology*; D001931:Brain Mapping; D002394:Catechol O-Methyltransferase / Q000235:genetics; D002540:Cerebral Cortex / Q000000981:diagnostic imaging / Q000503:physiopathology; D023281:Genomics; D005838:Genotype; D006801:Humans; D008279:Magnetic Resonance Imaging; D010698:Phobic Disorders / Q000209:etiology* / Q000235:genetics / Q000503:physiopathology*; D011110:Polymorphism, Genetic; D049268:Positron-Emission Tomography; D050486:Serotonin Plasma Membrane Transport Proteins / Q000235:genetics; D015899:Tomography, Emission-Computed, Single-Photon
D050486:Serotonin Plasma Membrane Transport Proteins; D002394:Catechol O-Methyltransferase