The present study aimed to determine whether the number of hospitalizations in schizophrenia patients is associated with reduced cognitive performance, which may in turn imply that recurrences indirectly lead to a worsening in the disorder’s progression.

Cognitive performance in stable schizophrenia patients was assessed using the Brief Assessment of Cognition in Schizophrenia, Japanese-language version, on 30 patients who had not experienced any hospitalizations (G0), 57 patients who had experienced only one hospitalization (G1), 47 patients with two hospitalizations (G2), and 59 patients with three or more hospitalizations (G3).

Significant differences in motor function and attention and processing speed were found between patients with G0 and those with G1. Significant differences in working memory and verbal fluency were found between patients with G1 and those with G2. Patients with G3 performed even more poorly in comparison with those with G1, showing deficits in verbal memory, working memory, executive function, and composite score. The patients with G3 displayed a greater range of impairment and demonstrated deficits in executive function compared with patients with G2. Finally, G2 and G3 performed more poorly than G0, with deficits in the various cognitive areas.

The number of hospitalizations predicted cognitive performance, which suggests that relapse or recurrence may have a long-term neuropsychological impact. Prospective follow-up studies must be completed to explore this effect further because better treatment adherence may have a protective effect on neurocognitive function.

Higher daytime cortisol levels because of a hyperactive hypothalamic–pituitary–adrenal axis have been reported in patients with major depressive disorder (MDD). The elevated glucocorticoids inhibit the proliferation of the oligodendrocytes that are responsible for myelinating the axons of white matter fibre tracts.

To evaluate the relationship between white matter integrity and serum cortisol levels during a first depressive episode in drug-naive patients with MDD (MDD group) using a tract-based spatial statistics (TBSS) method.

The MDD group (n = 29) and a healthy control group (n = 47) underwent diffusion tensor imaging (DTI) scans and an analysis was conducted using TBSS. Morning blood samples were obtained from both groups for cortisol measurement.

Compared with the controls, the MDD group had significantly reduced fractional anisotropy values (P<0.05, family-wise error (FWE)-corrected) in the inferior fronto-occipital fasciculus, uncinate fasciculus and anterior thalamic radiation. The fractional anisotropy values of the inferior fronto-occipital fasciculus, uncinate fasciculus and anterior thalamic radiation had significantly negative correlations with the serum cortisol levels in the MDD group (P<0.05, FWE-corrected).

Our findings indicate that the elevated cortisol levels in the MDD group may injure the white matter integrity in the frontal–subcortical and frontal–limbic circuits.

We investigated an association between the polymorphism of brain-derived neurotrophic factor (BDNF) gene Val66Met and the response to mirtazapine in Japanese patients with major depressive disorder (MDD). We also examined mirtazapine's effects on the serum BDNF and plasma levels of catecholamine metabolites in these patients.

Eighty-four patients who met the DSM-IV-TR criteria for MDD were treated with only mirtazapine for 4 weeks. The BDNF Val66Met polymorphism was detected by direct sequencing in the region, and serum BDNF levels and plasma levels of catecholamine metabolites were measured by ELISA and HPLC-ECD, respectively.

Mirtazapine treatment for 4 weeks significantly increased serum BDNF levels in the responders, whereas nonresponders showed significant decreases. No association was found between either of the two genotypes (Val/Val vs. Met-carriers) and the response to mirtazapine at T4 or the serum BDNF levels at T0. Mirtazapine did not alter the plasma levels of homovanillic acid (HVA) or 3-methoxy-4-hydroxyphenylglycol (MHPG).

The dynamics of serum BDNF levels, but not plasma levels of HVA and MHPG, reflect the response to mirtazapine treatment; the BDNF Val66Met polymorphism in patients with depression is, however, associated with neither a particular response to mirtazapine treatment nor baseline serum BDNF levels.

Serum BDNF levels, but not plasma levels of HVA or MHPG, and BDNF Val66Met polymorphism are related to the mirtazapine response in MDD.