Anxiety Disorders: Macromolecular Pathways and Interactions

Abstract

Fear and anxiety can be a normal adaptive reaction to help cope with stress in the short term, but when the emotional, cognitive, and physical manifestations are long lasting, extreme, and disproportionate to threat, whether real or preceived, anxiety is maladaptive and has become a disabling disorder. Anxiety disorders may be deconstructed to elementary behaviors/symptoms that can be conceptualized as quantitative characters determined by the combined effects of several risk genes and nongenetic factors (e.g., early‐life adversity). Progress in neurogenetics, molecular and cellular neuroscience, and neuroimaging is beginning to yield significant insights of how genetic and nongenetic factors contribute to specific manifestations of anxiety disorders. The aim of this overview is to summarize and integrate the current knowledge on anxiety‐related macromolecular pathways and mechanisms initiated by genetic risk and envionmental factors. These pathways interact with each other, often during specific periods of development, and could lead to alterations in the formation and function of neuronal circuits that encode emotional behavior.