Background: The suggestion that the neurohormone oxytocin may have clinical application in the treatment of schizophrenia was first published in 1972. Since then, a considerable body of research on a variety of fronts – including several recent double-blind treatment trials – has buttressed these early reports, providing support for the assertion that the oxytocin system is a promising and novel therapeutic target for this devastating malady. Herein, we review the diverse, convergent lines of evidence supporting the therapeutic potential of oxytocin in psychotic illness.

Methods: We performed a systematic review of preclinical and clinical literature pertaining to oxytocin's role in schizophrenia.

Results: Multiple lines of evidence converge to support the antipsychotic potential of oxytocin. These include several animal models of schizophrenia, pharmacological studies examining the impact of antipsychotics on the oxytocin system, human trials in patients examining the aspects of the oxytocin system and several double-blind, placebo-controlled clinical treatment trials.

Conclusions: There exists considerable, convergent evidence that oxytocin has potential as a novel antipsychotic with a unique mechanism of action. Auspiciously, based on the few chronic trials to date, its safety profile and tolerability appear very good. That said, several critical clinical questions await investigation before widespread use is clinically warranted.

Objective: Considering that mitochondria may be drug targets and some characteristics of drug–mitochondria interactions may still be misjudged because of the difficulty in foreseeing and understanding all possible implications of the complex pathophysiology of mitochondria, our study aimed to investigate the effect of escitalopram on the activity of enzymes of mitochondrial energy metabolism.

Methods: Animals received daily administration of escitalopram dissolved in saline [10 mg/kg, intraperitoneal (IP)] at 1.0 ml/kg volume for 14 days. Control rats received an equivalent volume of saline, 1.0 ml/kg (IP), for the same treatment period. Twelve hours after last injection, rats were killed by decapitation and brain areas were rapidly isolated. The samples were homogenised and the activities of mitochondrial respiratory chain complexes, some enzymes of Krebs cycle (citrate synthase, malate dehydrogenase and succinate dehydrogenase) and creatine kinase were measured.

Results: We verified that chronic administration of escitalopram decreased the activities of complexes I and II–III in cerebellum, hippocampus, striatum and posterior cortex whereas prefrontal cortex was not affected. Complex II activity was decreased only in striatum without affecting prefrontal cortex, hippocampus, cerebellum and posterior cortex. However, chronic administration of escitalopram did not affect complex IV and enzymes of Krebs cycle activities as well as creatine kinase.

Conclusion: In this study we showed a decrease in the activities of complexes I and II–III in most of the brain structures analysed and complex II activity was decreased only in striatum. However, it remains to be determined if mitochondrial dysfunction is rather a causal or a consequential event of abnormal signalling.

Objectives: Schizophrenia (SCZ) is a severe psychiatric disorder with a lifetime prevalence of approximately 1% in most of the populations studied. SCZ is multifactorial with the contribution of multiple susceptibility genes that could act in conjunction with epigenetic processes and environmental factors. There is some evidence supporting the association between genetic variants in dysbindin (DTNBP1) gene and SCZ in populations. In this study, we investigated the association between polymorphisms P1635 and P1655 in dysbindin gene with SCZ.

Methods: Totally, 115 unrelated patients with SCZ and 117 unrelated healthy volunteers were studied. Genomic DNA was extracted from blood. Genotyping was done with the PCR-RFLP method. The allele and genotype associations were analysed with X2 test. The Benjamini-Hochberg procedure was used to correct p values for multiple comparisons.

Results: The results showed no significant difference between patients and controls in allelic frequencies or genotypic distributions of SNP P1635 (p = 0.809), but a significant difference between the case and control groups for SNP P1655 (p = 0.009) was found. We could also find a significant positive association between A-C haplotype and SCZ (OR = 1.7, 95% CI 1.18–2.42; p = 0.004, pc = 0.02) and a protective effect for A-G haplotype (p = 0.003, OR = 0.57, 95% CI 1.18–2.42; p = 0.003, pc = 0.02).

Conclusion: This study may provide further support for the association between SNP polymorphisms in DTNBP1 and SCZ in the Iranian population. Studies with more markers and subjects for various populations will be necessary to understand the genetic contribution of the gene to the development of SCZ.

Objective: To understand the underlying mechanism of gastric symptoms in patients with depressive disorder.

Methods: This study tested in the rat depression model evoked with chronic mild stress whether the microstructure gastric mucosa is injured using scanning electronic microscopy and transmission electronic microscopy (TEM). In addition, the expression of heat shock protein 70 (HSP70) and fibroblast growth factor 2 (FGF2) proteins in the gastric mucosa were measured by Western blotting.

Results: We found that the gastric epithelial cells were ruptured and the gastric pits were widened in rats with depression. The amount of mucous granules was also reduced in the surface mucous cells. Moreover, parietal cells became active, and the secretory canaliculi were magnified. Expression of HSP70 and FGF2 was reduced in the gastric mucosa.

Conclusions: These findings suggested that gastric symptoms in rats with depressive-like behaviour were caused by the injury of the gastric mucosa, AQ1 and HSP70 and FGF2 may be key molecules in the pathogenesis.

Objective: Fas (CD95), commonly categorised as a death receptor due to its well-defined role in apoptosis, can paradoxically also promote neuroprotection. We have previously found that defects in Fas signalling render mice highly susceptible to neural degeneration in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine mouse model of Parkinson's disease (PD). Decreased activity of the ubiquitin proteasome system and accumulation of protein aggregates are implicated in PD pathogenesis. Here, we investigate the relationship between Fas and ubiquitin proteasomal activity in neuronal cells.

Methods: We performed proteasome assays in neuroblastoma cells and in midbrain cultures of wild-type and Fas-deficient mice.

Results: Neuroblastoma cells upregulated proteasomal activity in response to an activating Fas antibody in vitro. Furthermore, neural tissue from Fas-deficient mice showed decreased proteasomal activity compared with the tissue from wild-type mice when exposed to a PD-inducing toxin in vivo.

Conclusion: These findings suggest that mechanisms for Fas-mediated neuroprotection may include Fas-induced upregulation of proteasomal activity, and consequently less accumulation of toxic protein aggregates.

Objective: Previous studies indicated that the levels of serum interleukin (IL)-12 at baseline were elevated in obsessive-compulsive disorder (OCD) patients compared with control subjects, suggesting that IL-12 maybe involved in the etiopathogenesis of OCD. Therefore, we study the relationship between 1188A/C polymorphism of IL-12(rs3212227) and OCD in Chinese Han population.

Methods: We genotyped 194 OCD patients and 322 healthy individuals by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP), then analyzed the data using case-control association test.

Results: No significant differences were found in 1188A/C genotypic and allelic frequencies between OCD cases and controls (X2 = 2.12, df = 2, P = 0.35 by genotype; X2 = 0.005, df = 1, P = 0.94 by allele).

Conclusions: Our results suggested that there may be lack of an association between OCD and IL-12 1188A/C polymorphism in Chinese Han population.

Objectives: The heterogeneity of schizophrenia mainly results from variations in clinical expressions of the disease, such as age at onset, gender differences in onset of illness, symptoms and response to antipsychotic treatment. Enhanced sensitisation of dopamine pathways in males, having consistently an earlier onset, might be implicated as disease modifiers for schizophrenia in males.

Methods: In this study, we performed a case (n = 87)-control (n = 100) association study between the DBH5′-ins/del and DBH-444g/a polymorphisms of the DBH gene and also compared the level of psychotic symptoms between patients with different DBH genotypes/haplotypes with respect to antipsychotic therapeutic response and gender difference.

Results: No significant differences between allele and genotype and haplotype frequencies at either groups (p < 0.05). When the age is considered in patient group, a significant difference was observed between patients with ID genotype and with II genotype (p = 0.018). Patients with ID genotype have been diagnosed as schizophrenics in early ages when compared to II genotype carriers. We also found a significant difference between II and ID genotype (p = 0.007) when the gender had taken into account, showing that the ID genotype carriers had an early onset to schizophrenia.

Conclusions: This association was more significant in male schizophrenia patients than females. Thus, this finding may constitute a novel biological support for the prior finding that onset of schizophrenia varies with gender. The results also showed that critical genetic vulnerability may be associated with the presence or absence of the ID genotype of DBH5′-ins/del.

Objective: Delirium is a common problem, but often misdiagnosed and unidentified. Apart from the manifold clinical picture variable durations can also be an obstacle for its diagnosis.

Methods: We present a case of protracted delirium that has developed after severe somatic illness in association with previously undiagnosed Sheehan's syndrome.

Results: The variety of psychiatric symptoms with initial psychotic disorder and the long run of the disease delayed the diagnosis of delirium and meantime gave reason to assume personality change.

Conclusion: This case report calls attention to the possibility of protracted delirium in patients with neuropsychiatric deficit symptoms that persist subsequent to somatic illness.

Objective: MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) is a neurodegenerative disorder caused by mitochondrial dysfunction. Multiple systems of the body, including cognitive function and heart conduction, can be affected by this disorder. We report a case with global cognitive impairment.

Method: A single-case report.

Results: The patient got improved cognitive function, especially visuospatial function, under coenzyme Q10 treatment.

Conclusion: First, coenzyme Q10 may give some benefit to control MELAS. Second, cognitive functions and intellectual abilities decline with disease progression. Routine neuropsychological tests should be performed.