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Aim Studies have reported that cognitive decline occurs after the onset of schizophrenia despite heterogeneity in cognitive function among patients. The aim of this study was to investigate the degree of estimated cognitive decline in patients with schizophrenia by comparing estimated premorbid intellectual functioning and current intellectual functioning. Methods A total of 446 patients with schizophrenia (228 male, 218 female), consisting of three sample sets obtained from 11 psychiatric facilities, and 686 healthy controls participated in this study. The Wechsler Adult Intelligence Scale-III (WAIS-III) was used to measure the participants’ current full-scale IQ (FSIQ). The premorbid IQ was estimated using the Japanese Adult Reading Test-25. Estimated cognitive decline (difference score) was defined as the difference between the estimated premorbid IQ and the current FSIQ. Results Patients with schizophrenia showed greater estimated cognitive decline, a lower FSIQ, and a lower premorbid IQ compared with the healthy controls. The mean difference score, FSIQ, and estimated premorbid IQ were −16.3, 84.2, and 100.5, respectively, in patients with schizophrenia. Furthermore, 39.7% of the patients had a difference score of 20 points or greater decline. A discriminant analysis showed that the difference score accurately predicted 81.6% of the patients and healthy controls. Conclusion These results show the distribution of difference score in patients with schizophrenia. These findings may contribute to assessing the severity of estimated cognitive decline and identifying patients with schizophrenia who suffer from cognitive decline.

Objectives Photosensitivity to ultraviolet A (UVA) radiation from sunlight is an important side effect of treatment with antipsychotic agents. However, the pathophysiology of drug-induced photosensitivity remains unclear. Recent studies demonstrated the accumulation of advanced glycation end products (AGEs), annotated as carbonyl stress, to be associated with the pathophysiology of schizophrenia. In this study, we investigated the relationship among skin AGE levels, minimal response dose (MRD) with UVA for photosensitivity, and the daily dose of antipsychotic agents in patients with schizophrenia and healthy controls. Methods We enrolled 14 patients with schizophrenia and 14 healthy controls. Measurement of skin AGE levels was conducted with AGE scanner, a fluorometric method for assaying skin AGE levels. Measurement of MRD was conducted with UV irradiation device. Results Skin AGE levels and MRD at 24, 48, and 72 hr in patients with schizophrenia showed a higher tendency for photosensitivity than in the controls, but the difference was statistically insignificant. Multiple linear regression analysis using skin AGE levels failed to show any influence of independent variables. MRD did not affect skin AGE levels. Conclusions Photosensitivity to UVA in patients with schizophrenia receiving treatment with antipsychotic agents might not be affected by skin AGE levels.

Introduction Treatment-resistant schizophrenia (TRS) refers to the approximately 20–30% of schizophrenia patients whose symptoms are resistant to any antipsychotic treatment. For the improvement of residual symptoms in TRS, augmentation therapy using anticonvulsants such as lamotrigine (LTG) has recently attracted attention. Randomized clinical trials (RCTs) have demonstrated robust evidence; however, the results have shown both positive and negative outcomes for the use of LTG. Although RCTs have merit, they also obscure informative clinical features present in each patient, such as the types of TRS that show the most significant effects from LTG. Thus, detailed case reports examining the efficacy of LTG may help to shed light on various treatments for complex, heterogeneous diseases such as schizophrenia. Methods We present detailed reports on the clinical course and features of TRS in five patients suffering from severe positive symptoms who were treated with LTG augmentation therapy. Results After the administration of LTG augmentation therapy, two patients did not show any improvement in their residual symptoms, while the remaining three patients did experience improvement. Remarkably, patients with more severe residual positive symptoms, especially those with auditory hallucinations, seemed to respond better to low-dose LTG (50 mg daily). Additional clinical variables, such as type and dose of ongoing antipsychotics, age of onset, duration of illness, duration of untreated psychosis, number of administration cycles, and genetic heritability, were not found to be related to the effectiveness of LTG augmentation. Discussion Low-dose LTG augmentation therapy seems to improve residual symptoms in some cases of TRS. The glutamatergic properties of LTG may be the decisive factor in these symptoms, as other glutamatergic agents have also been shown to be effective based on previous glutamate hypotheses in schizophrenia.

Aims: Schizophrenia is a major psychiatric disorder with complex genetic, environmental, and psychological causes, and oxidative stress may be involved in the pathogenesis of the disease. Glutathione (GSH), one of the main cellular non-protein antioxidants and redox regulators, and altered GSH levels have been reported in various regions in patients with schizophrenia. Three enzymes are responsible for GSH synthesis: glutamate cysteine ligase modifier (GCLM), glutamate cysteine ligase catalytic subunit (GCLC), and glutathione synthetase (GSS). Previously, positive associations between GCLM and schizophrenia were reported in Europeans, but not in the Japanese population. Thus, in this study, we investigated the association between the GSH synthesis genes (GCLM, GCLC, and GSS) and schizophrenia in Japanese individuals. Methods: Seventeen single-nucleotide polymorphisms (SNP) in GCLM, GCLC, and GSS were genotyped in 358 patients with schizophrenia and in 359 controls. Results: No SNP showed a significant association between their allelic or genotypic frequencies and schizophrenia. Case–control haplotype association analysis using windows of two or three SNP showed no significant associations with schizophrenia. The case–control haplotype analyses based on the ascertained linkage disequilibrium blocks also showed no significant associations in any genes with schizophrenia. Conclusions: The three primary GSH synthesis genes do not have an apparent degree of association with schizophrenia in the Japanese population.