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.

Background: Yoga therapy (YT) improves cognitive function in healthy individuals, but its impact on cognitive function among persons with schizophrenia (SZ) has not been investigated.

Objective: To evaluate the adjunctive YT for cognitive domains impaired in SZ.

Methods: Patients with SZ received YT or treatment as usual (TAU; n = 65, n = 23, respectively). Accuracy and speed for seven cognitive domains were assessed using a computerised neurocognitive battery (CNB), thus minimising observer bias. Separately, YT was evaluated among patients with bipolar I disorder (n = 40), major depressive disorder (n = 37) and cardiology outpatients (n = 68). All patients also received routine pharmacotherapy. Patients were not randomised to YT or TAU.

Results: In comparison with the SZ/TAU group, the SZ/YT group showed significantly greater improvement with regard to measures of attention following corrections for multiple comparisons; the changes were more prominent among the men. In the other diagnostic groups, differing patterns of improvements were noted with small-to-medium effect sizes.

Conclusions: Our initial analyses suggest nominally significant improvement in cognitive function in SZ with adjunctive therapies such as YT. The magnitude of the change varies by cognitive domain and may also vary by diagnostic group.

Objective: We showed previously that glycogen synthase kinase-3β (GSK-3β) levels are significantly elevated in the hippocampi of patients with major depressive disorder (MDD). However, the exact cause of this elevation and its function are unknown. Recent animal studies have suggested a mechanism involving the N-methyl-d-aspartate (NMDA) NR2B–GSK-3β loop.

Methods: To investigate the existence of an NR2B–GSK-3β loop in the hippocampi of patients with MDD, we examined the expression of NR2B. We also attempted to identify markers that correlate with NR2B levels in the hippocampus, using the Stanley Neuropathology Consortium Integrative Database (SNCID). The SNCID is a web-based tool used to integrate Stanley Medical Research Institute (SMRI) data sets.

Results: We found that hippocampal levels of NR2B and DLGAP1 mRNA were higher in the MDD group (n = 8) than in unaffected controls (n = 12) (p < 0.05). NR2B expression levels were correlated with the expression levels of NR2A, NR1, DLGAP1, GSK-3β and nitric oxide synthase 1, as well as with the number of calretinin-immunoreactive neurons in the hippocampus in all subjects in the SNC (n = 42, p < 0.001).

Conclusion: The results of our study show the possible involvement of excessive activation of the NR2B–GSK-3β loop in the overexpression of GSK-3β in the hippocampi of patients with MDD.

Objective: Vitamin A is a redox-active molecule and its inadvertent utilisation as a preventive therapy against ageing or neurodegeneration has become a harmful habit among humans at different ages. Mitochondrial dysfunction and redox impairment may be induced by vitamin A supplementation experimentally. Nonetheless, it is still not clear by which mechanisms vitamin A elicits such effects. Then, we performed this investigation to analyse whether mitochondria isolated from frontal cortex and hippocampus of vitamin A-treated rats are more sensitive to a challenge with amyloid-β (Aβ) peptides 1–40 or 1–42.

Methods: Adult Wistar rats received vitamin A at 1000–9000 IU/kg/day orally for 28 days. Then, mitochondria were isolated and the challenge with Aβ peptides 1–40 or 1–42 (at 0.2 or 0.1 μM, respectively) for 10 min was carried out before mitochondrial electron transfer chain enzyme activity, superoxide anion radical (O2−•) production and 3-nitrotyrosine content quantification.

Results: Mitochondria obtained from vitamin A-treated rats are more sensitive to Aβ peptides 1–40 or 1–42 than mitochondria isolated from the control group, as decreased mitochondrial complex enzyme activity and increased O2−• production and 3-nitrotyrosine content were observed in incubated mitochondria isolated from vitamin A-treated rats.

Conclusion: These data suggest that oral intake of vitamin A at clinical doses increases the susceptibility of mitochondria to a neurotoxic agent even at low concentrations.

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: The trait of experiencing positive affect could make a unique contribution to the pathogenesis of affective disorders. Animal models of positive emotionality are scarce but 50-kHz ultrasonic vocalizations (USVs) in rats have been associated with rewarding experience. We have previously reported that persistent inter-individual differences in expression of 50-kHz USVs (chirps) exist, and that male rats producing fewer 50-kHz USVs are more sensitive to chronic variable stress (CVS). In this study we examined the effect of CVS on extracellular serotonin (5-HT) levels in hippocampus, comparing high-chirping (HC) and low-chirping (LC) rats.

Methods: Male rats were classified as HC- and LC-rats on the basis of stable levels of USV response using sessions of tickling-like stimulation. CVS procedure lasted 4 weeks. The administration of citalopram (1 μM) and measurements of levels of 5-HT were done by microdialysis. Corticosterone levels were also measured from trunk blood.

Results: Male LC-rats were more sensitive to CVS: the effect of stress on body weight gain was larger and corticosterone levels from full blood were higher in the stressed LC animals as compared to both the unstressed groups and the stressed HC animals. While no baseline differences in extracellular 5-HT levels in hippocampus were found between groups, the increase in extracellular 5-HT levels induced by citalopram was much higher in LC-rats.

Conclusion: Chronic stress appears to modify hippocampal 5-HT overflow in rats with low positive affectivity. This finding supports the notion of greater vulnerability to CVS in male rats with low positive affectivity.

Objective: Functional imaging studies of post-traumatic stress disorder (PTSD) have shown an increased activation of posterior cingulate gyrus (PCG) of the brain. The aim of this study was to explore white matter integrity of PCG in PTSD subjects.

Methods: White matter integrity, as determined from fractional anisotropy (FA) value using diffusion tensor imaging, was assessed for PCG in subjects with and without PTSD from a severe mine accident. All subjects were also measured by the PTSD Checklist Civilian Version (PCL-C), the State-Trait Anxiety Inventory (STAI), the logical memory subtest and the visual reproduction subtest of the Wechsler Memory Scale-Revised in China. Sixteen PTSD subjects (8 subjects in each group) in the longitudinal study and 13 PTSD subjects as well as 14 non-PTSD controls in the cross-sectional case–control study were respectively recruited.

Results: In the longitudinal study, subjects with PTSD showed increased FA values in left PCG during the follow-up scan. In the cross-sectional study, FA values in bilateral PCG in PTSD subjects were higher than controls. Within the PTSD group (n = 13), FA values in the left PCG correlated positively with logical memory and negatively with PCL-C intrusion and STAI-trait (STAI-t) subscores. FA values in right PCG correlated negatively with STAI-t and STAI-state subscores.

Conclusion: These findings suggest that alterations of white matter integrity in PCG link to mnemonic and affective processing in PTSD over the long-term follow-up period.

Objective: A case–control study was performed in Belgrade in order to investigate the association between Parkinson's disease (PD) and smoking, coffee and alcohol consumption.

Methods: During the period 2001–2005, 110 new PD cases and 220 hospital controls were interviewed. Cases and controls were matched by sex, age and place of residence (urban/rural). For the analysis of data conditional univariate and multivariate logistic regression methods were used.

Results: With PD were associated, independently from each other, current smoking [odds ratio (OR) = 0.44; 95% confidence interval (CI) = 0.23–0.82], alcohol consumption (OR = 4.78; 95% CI = 2.67–8.55) and coffee consumption (OR = 2.54; 95% CI = 1.36–4.75). In ever smokers the risk for PD significantly decreased with the increasing number of cigarettes smoked and with increasing duration of smoking. The risk for PD significantly increased with the increasing quantity of alcohol consumption. PD risk was significantly higher in subjects whose average daily consumption of coffee was 1 and 2–3 cups, and it was lower (but not significantly) in those whose daily coffee consumption was 4+ cups. Cases and controls did not differ in duration of alcohol and coffee consumption. The results of multivariate analyses did not substantially change after adjustment on family history positive on PD.

Conclusion: The findings of this study support the hypotheses of inverse association of smoking with PD, but an inverse association with coffee was not confirmed. PD was found to be positively associated with coffee and alcohol consumption.

Objective: Depression is suggested to involve disturbances in cholinergic as well as glutamatergic pathways, particularly the N-methyl-d-aspartate receptor-mediated release of nitric oxide (NO) and cyclic guanosine monophosphate (cGMP). The aim of this study was to determine whether the Flinders Sensitive Line (FSL) rat, a genetic model of depression, presents with corticolimbic changes in basal acetylcholine (ACh) levels and NO/cGMP signalling.

Methods: Basal levels of nitrogen oxides (NOx) and both basal and l-arginine-stimulated nitric oxide synthase (NOS) formation of l-citrulline were analysed in hippocampus and frontal cortex in FSL and control Flinders resistant line (FRL) rats by fluorometric and electrochemical high-performance liquid chromatography, respectively. In addition, ACh and cGMP levels were analysed by liquid chromatography tandem mass spectrometry and radioimmunoassay, respectively.

Results: Significantly elevated frontal cortical but reduced hippocampal ACh levels were observed in FSL versus FRL rats. Basal cGMP levels were significantly reduced in the frontal cortex, but not hippocampus, of FSL rats without changes in NOx and l-citrulline, suggesting that the reduction of cGMP follows through an NOS-independent mechanism.

Conclusions: These data confirm a bidirectional change in ACh in the frontal cortex and hippocampus of the FSL rat, as well as provide evidence for a frontal cortical ACh-cGMP interaction in the depressive-like behaviour of the FSL rat.

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: The ability to reflect rationally on one's own anomalous experiences and to recognise that their conclusions are incorrect is called as cognitive insight. It influences the delusion proneness of patients with schizophrenia. Structured instruments to assess cognitive insight have not been validated in any Indian languages so far. Hence, we aimed to evaluate the validity and factor structure of Tamil version of Beck Cognitive Insight Scale (BCIS-T).

Methods: One hundred and fifty consecutive patients with schizophrenia completed BCIS-T. We assessed their clinical insight with the reference standard, Schedule for Assessment of Insight-Expanded version (SAI-E). An independent psychiatrist evaluated their psychopathology using Brief Psychiatric Rating Scale (BPRS).

Results: BCIS-T was internally consistent with Cronbach's α 0.67 and Guttman's split-half coefficient as 0.63. BCIS-T composite index documented convergent validity with SAI-E total score (ρ = 0.38; p < 0.001) and discriminant validity with BPRS (ρ = −0.02; p = 0.85). Factor analysis showed a four-factor structure, namely self-certainty, self-reflectiveness, openness to external feedback and infallibility of self-reflection. BCIS-T composite index had significant linear relationship with clinical insight and treatment compliance on multivariate analyses (p < 0.01).

Conclusion: Our findings support the validity of BCIS-T to assess cognitive insight of the patients with schizophrenia. We suggest addressing the intricacies of cognitive insight beyond the traditional two-dimensional models in cross-cultural settings.

Objectives: Based on the hypothesis that energy impairment may be involved in the pathophysiology of depression, we evaluated the activities of citrate synthase, malate dehydrogenase, succinate dehydrogenase (SDH), mitochondrial respiratory chain complexes I, II, II-III, IV and creatine kinase (CK) in the brain of rats submitted to chronic administration of bupropion.

Methods: Animals received daily administration of bupropion dissolved in saline (10 mg/kg, intraperitoneal) at 1.0 ml/kg body weight. The rats received injections once a day for 14 days; control rats received an equivalent volume of saline. Twelve hours after the last administration, the rats were killed by decapitation and brain was rapidly removed and kept on an ice plate. The activities of the enzymes were measured in different brain areas.

Results: We observed that the activities of citrate synthase and malate dehydrogenase, mithocondrial respiratory chain complexes I, II-III and IV and CK were not altered after chronic administration of bupropion. However, SDH activity was increased in the prefrontal cortex and cerebellum. In the hippocampus, cerebellum and striatum the activity of complex II was increased after chronic administration of bupropion.

Conclusions: Our results demonstrated that bupropion increased some enzymes of brain energy metabolism. These findings are in accordance with other studies which showed that some antidepressants may improve energy metabolism. The present results reinforce the hypothesis that antidepressants modulate brain energy metabolism.

Background: It has been claimed that schizophrenia can be linked to the magnocellular system by way of N-methyl-d-aspartate (NMDA) receptors. The present report examines this claim.

Methods: A review is made of relevant research literature.

Results: The NMDA studies that have been referenced to connect visual deficits in schizophrenia to the magnocellular system are based on the cat, a species whose visual system is fundamentally different from that of primates. The cat visual system cannot easily be divided into magno- and a parvocellular portions.

Conclusions: Owing to the substantial differences between the visual systems of cats and primates, it is difficult to link sensory abnormalities in schizophrenia specifically to the magnocellular system based on data from the cat.

Introduction: Depressive syndromes are common following cerebrovascular accident (CVA) and many patients do not respond to pharmacotherapy. Electroconvulsive therapy (ECT) is a safe and effective treatment for mood disorders arising with many comorbid medical conditions. In this paper, we describe the successful treatment of post-CVA depression with ECT.

Methods: Retrospective chart review of 24 patients hospitalised for depression on an in-patient Medical Psychiatry unit between 2000 and 2010. Medical, neurologic and psychiatric histories, physical examination findings, results of laboratory, imaging and neurophysiologic investigations and treatment response with medications and ECT were recorded.

Results: Twenty patients (83%) showed a positive response to treatment with ECT. None had worsening of depression after the ECT or experienced exacerbation of post-stroke neurological deficits. Three patients suffered from minor complications of ECT (prolonged confusion or short-term memory problems).

Conclusions: This review supports the use of ECT after a stroke with appropriate clinical observation. The treatment was well tolerated and the majority obtained clinical benefit.