Fig 1.
Simplified Heuristic of the corticolimbic circuit and its potential link to disease pathogenesis.
It is posited that the translation of stress and emotion to disease outcomes involves bidirectional communication among several cortical and subcortical brain regions known to influence autonomic, endocrine, and immune system function via neural and hormonal mechanisms. Higher-order cortical regions involved in emotion regulation and stress perception, including the medial PFC, orbital PFC, and ACC, help modulate the function of subcortical regions, such as the hippocampus and amygdala, that are involved in emotion and stress processing (e.g., rapidly processing the emotional salience of an event). These subcortical regions, in turn, modulate lower-order brain structures such as the hypothalamus and brainstem, which are directly responsible for the release of catecholamines and glucocorticoids by peripheral systems (e.g., autonomic nervous system, the HPA axis). Repeated and/or prolonged activation of these peripheral systems may ultimately impair the structure and function of these corticolimbic regions. A dysregulated corticolimibic circuit may ultimately lead to disease states via repeated and/or chronic psychophysiological stress responses. Please refer to Fig 2 for visualization of relevant brain structures.
Fig 2.
Cortical (A-C) and Subcortical (D-E) Regions of Interest. Regions are delineated by the cross, and the colors are consistent throughout the figure. Regions are depicted on both a sagittal (left) and coronal (right) plane.
Table 1.
Demographic characteristics in the overall sample and across race and SES.
Table 2.
Multiple regression analyses: Interaction of SES and race on subcortical gray matter volumes.
Fig 3.
Graphical representation of significant SES by race interactions on various cortical brain regions.
For all the structures depicted, high SES Whites had greater brain volumes relative to all other groups. Error bars depict the standard errors.
Table 3.
Multiple regression analyses: Interaction of SES and race on cortical gray matter volumes.