an increased excretion of cortisol in depression have been described, the abnormalities of the HPA axis following stress may lead, or at least contribute, to the structural changes such as those evident in the hippocampus. These findings are supported by numerous studies, which have established an association between duration of the mood disorder/numbers of episodes (41, 42) and early traumatization (43), and the degree of hippocampal damage. In addition, the effect of stress on the hippocampus appears to be modulated by genetic factors (44). It should also be considered that structural abnormalities can represent a vulnerability factor for the development of mood disorders and hypercortisolism (45). Overall, imaging studies show that neurocircuitry dysfunction appears to occur in the same pathways in depression and cognition (9), similarly to the involvement of monoamines, glutamate, and gamma-aminobutyric acid (GABA) in both depression and cognition.
