Integration and consolidation

Abstract

AbstractIn this book, leading experts have provided comprehensive and current reviews of the current state of knowledge regarding how genomics and brain imaging are defining the etiology and expression of bipolar disorder. Taken together, this state of knowledge begins to define a model of illness that is discussed in this chapter. As a starting point, the symptoms of bipolar disorder suggest that the disruption in brain systems that manage emotional homeostasis and reward processing (i.e., behavioral activation) must be represented in any proposed models of illness. Moreover, the typical onset in youth and progressive course of illness suggest a developmental component that persists until a recurrent mood disorder is established. Supporting these assumptions, neuroimaging research has steadily defined disruption in key ventral prefrontal-striatal-thalamic networks that may define the functional neuroanatomy of this condition. Differences from typical neurodevelopment in the formation of these networks, perhaps due to underlying multigenetic causes, likely establishes this disruption. The specific genetic basis has remained elusive, although studies of genes, gene combinations, and epigenetic events, including mitochondrial control, appear to be contributing components. These models offer an opportunity for focused, hypothesis-driven testing to drive future investigations, hopefully identifying the causes of bipolar disorder and ultimately providing specific targets for improved treatments.