Although neurocognitive dysfunction and physical performance are known to be impaired in patients with schizophrenia, evidence regarding the relationship between these two domains remains insufficient. Thus, we aimed to investigate the relationship between various physical performance domains and cognitive domains in individuals with schizophrenia, while considering other disorder-related clinical symptoms.

Sixty patients with schizophrenia participated in the study. Cardiorespiratory fitness and functional mobility were evaluated using the step test and supine-to-standing (STS) test, respectively. Executive function and working memory were assessed using the Stroop task and Sternberg working memory (SWM) task, respectively. Clinical symptoms were evaluated using the Brief Psychiatric Rating Scale, Beck Depression Inventory, and State-Trait Anxiety Inventory. Multivariate analyses were performed to adjust for relevant covariates and identify predictive factors associated with neurocognition.

Multiple regression analysis revealed that the step test index was most strongly associated with reaction time in the Stroop task (β = 0.434, p = 0.001) and SWM task (β = 0.331, p = 0.026), while STS test time was most strongly associated with accuracy on the Stoop task (β=−0.418, p = 0.001) and SWM task (β=−0.383, p = 0.007). Total cholesterol levels were positively associated with Stroop task accuracy (β=−0.307, p = 0.018) after controlling for other clinical correlates. However, clinical symptoms were not associated with any variables in Stroop or SWM task.

The present findings demonstrate the relationship between physical performance and neurocognition in patients with schizophrenia. Considering that these factors are modifiable, exercise intervention may help to improve cognitive symptoms in patients with schizophrenia, thereby leading to improvements in function and prognosis.

The National Institute of Neurological Disease and Stroke-Canadian Stroke Network (NINDS-CSN) 5-minute neuropsychology protocol consists of only verbal tasks, and is proposed as a brief screening method for vascular cognitive impairment. We evaluated its feasibility within two weeks after stroke and ability to predict the development of post-stroke dementia (PSD) at 3 months after stroke.

We prospectively enrolled subjects with ischemic stroke within seven days of symptom onset who were consecutively admitted to 12 university hospitals. Neuropsychological assessments using the NINDS-CSN 5-minute and 60-minute neuropsychology protocols were administered within two weeks and at 3 months after stroke onset, respectively. PSD was diagnosed with reference to the American Heart Association/American Stroke Association statement, requiring deficits in at least two cognitive domains.

Of 620 patients, 512 (82.6%) were feasible for the NINDS-CSN 5-minute protocol within two weeks after stroke. The incidence of PSD was 16.2% in 308 subjects who had completed follow-up at 3 months after stroke onset. The total score of the NINDS-CSN 5-minute protocol differed significantly between those with and without PSD (4.0 ± 2.7, 7.4 ± 2.7, respectively; p < 0.01). A cut-off value of 6/7 showed reasonable discriminative power (sensitivity 0.82, specificity 0.67, AUC 0.74). The NINDS-CSN 5-minute protocol score was a significant predictor for PSD (adjusted odds ratio 6.32, 95% CI 2.65–15.05).

The NINDS-CSN 5-minute protocol is feasible to evaluate cognitive functions in patients with acute ischemic stroke. It might be a useful screening method for early identification of high-risk groups for PSD.

Major depressive disorder (MDD) is closely related to stress reactions and serotonin probably underpins the pathophysiology of MDD. Alterations of the hypothalamic-pituitary-adrenal axis at the gene level have reciprocal consequences on serotonin neurotransmission. Glucocorticoid receptor (GR) polymorphisms affect glucocorticoid sensitivity, which is associated with cortisol feedback effects. Therefore, we hypothesised that GR polymorphisms are associated with the susceptibility to MDD and predict the treatment response.

Ninety-six subjects with a minimum score of 17 on the 21-item Hamilton Depression Scale (HAMD) at baseline were enrolled into the present study. The genotypes of GR (N363S, ER22/23EK, Bcl1, and TthIII1 polymorphisms) were analysed. The HAMD score was again measured after 1, 2, 4 and 8 weeks of antidepressant treatment to detect whether the therapeutic effects differed with the GR genotype.

Our subjects carried no N363S or ER22/23EK genetic polymorphisms and three types of Bcl1 and TthIII1 genetic polymorphisms. The C/C genotype and C allele at Bcl1 polymorphism were more frequent in MDD patients than in normal controls (p < 0.01 and p = 0.01, respectively). The genotype distributions did not differ significantly between responders and non-responders.

These results suggest that GR polymorphism cannot predict the therapeutic response after antidepressant administration. However, GR polymorphism (Bcl1) might play a role in the pathophysiology of MDD. Future studies should check this finding in larger populations with different characteristics.