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Animals chronically exposed to increased levels of corticosterone display an anxiodepressive-like phenotype, providing a neuroendocrine animal model for stress-related disorders (Darcet et al, 2014; David et al, 2009).
However, extrapolation of findings of this animal model to humans may not always be appropriate, for example when studying human brain activation patterns during specific challenges or resting state.
The effects of hypercortisolism on brain functional connectivity have yet to be investigated.
One important network that should be investigated in light of hypercortisolism is the limbic network, consisting of the hypothalamus, hippocampus, amygdala, insula, and parts of the nucleus accumbens (Janes et al, 2012; Maclean, 1952).
These findings suggest that hypercortisolism may cause persisting changes in the brain.
Effects of hypercortisolism on brain structure include a reduction of hippocampal volume (Bourdeau et al, 2002; Simmons et al, 2000; Starkman et al, 1992) that is reversible after successful abrogation of the hypercortisolism (Bourdeau et al, 2002; Starkman et al, 1999).
Our data indicate that previous exposure to hypercortisolism is related to persisting changes in brain function.
In various stress-related psychiatric disorders such as major depressive disorder and posttraumatic stress disorder (PTSD), alterations in the activity of the hypothalamic–pituitary–adrenal axis (HPA axis) are present, with hyperresponsivity or chronic activation of the HPA axis often resulting in increased levels of cortisol (Carroll et al, 1976, 2007; Friedman et al, 2007; Inslicht et al, 2006; Schlechte et al, 1986; Steudte et al, 2011; Young and Breslau, 2004).
RSFC of these three networks of interest was compared between patients in remission of Cushing’s disease (n46.5 years), using probabilistic independent component analysis to extract the networks and a dual regression method to compare both groups.