Emotional intelligence and non-social cognition in schizophrenia and bipolar I disorder.

BACKGROUND: The different patterns of Emotional Intelligence (EI) deficits in schizophrenia and bipolar I disorder are are not yet well understood. This study compares EI levels among these groups and highlights the potential impact of non-social cognition on EI. METHOD: Fifty-eight schizophrenia and 60 bipolar outpatients were investigated using the Mayer-Salovey-Caruso Emotional Intelligence Test (MSCEIT) and the Brief Assessment of Cognition in Schizophrenia (BACS). Analyses of covariance were performed with adjustment for the BACS composite score. RESULTS: Compared to bipolar subjects, schizophrenia patients showed significantly lower levels in both EI and non-social cognition. After adjustment for the BACS composite score, the difference in EI was lost. The mediation analysis revealed that differences between schizophrenia and bipolar patients in strategic EI are almost fully attributable to the mediating effect of non-social cognition. CONCLUSIONS: Our findings suggest that in both schizophrenia and bipolar patients EI is strongly influenced by non-social cognitive functioning. This has to be taken into account when interpreting MSCEIT data in comparative studies in serious mental illness and emphasizes the importance of cognitive remediation.

Intravenous mirtazapine is safe and effective in the treatment of depressed inpatients.

Mirtazapine is a third-generation antidepressant with a dual mode of action. The oral administration has been shown to be effective and safe in the treatment of depressed patients. In this multicenter naturalistic study, we assessed the safety, tolerability, and therapeutic efficacy of intravenously administered mirtazapine in 80 moderately to severely depressed inpatients during a treatment period of 14 days. We found a significant decrease of the Hamilton Depression Rating Scale total score compared to baseline. Side effects were mild and transient. Our data indicate that intravenous mirtazapine is an effective, safe and well-tolerated treatment for depressed inpatients.

No nerve growth factor response to treatment with memantine in adult rats.

Nerve growth factor (NGF) is the most widely examined neurotrophin in the experimental models of Alzheimer's disease (AD) and has been shown to prevent the retrograde degeneration of cholinergic neurons. In this study we examined NGF and cholineacetyltransferase (ChAT) changes in several rat brain regions after excitotoxic lesion of the entorhinal cortex with quinolinic acid and tested the effect of memantine on spatial learning in the radial maze after lesion. We observed a significant increase (+26%, p=0.02) of NGF concentrations in the hippocampus of the lesioned rats when compared to sham-lesioned rats. Chronic treatment with memantine showed no significant effect on the NGF increase in the hippocampus (p=0.72). The ChAT activity was significantly increased in the lesioned rats when compared to controls (+16%, p<0.05) and did not depend on treatment with memantine. In spite of this, memantine improved performance of the radial maze. This indicates that memory improving effects of memantine observed in experimental animals and in clinical studies are probably not related to changes in brain NGF content, whereas the observed NGF increase in the denervated hippocampus is probably trauma-related reflecting impaired retrograde transport of hippocampal NGF.

Longitudinal study of antibody reactivity against HIV-1 envelope and a peptide representing a conserved site on Gp41 in HIV-1-infected patients.

This study was designed to distinguish between antibodies in HIV-1-infected patients directed against epitopes accessible on the native HIV-1 envelope (Env) complex and non-native Env epitopes. Peptide p#13 (Env. aa642-673) containing the neutralising 2F5 epitope and recombinant soluble glycoprotein 160 (rsgp160) were used in ELISA to determine the antibody (Ab) reactivity in sera of 116 HIV-1-infected individuals and 18 HIV negative controls. The reactivity of sera classified CDC stage C against p#13 was significantly decreased in comparison to stage A sera, while staying constant against rsgp160. Accordingly, in 6 out of 8 individual patients tested over time the response against p#13 was declining at later time points of infection. The reactivity of patients' sera against p#13 corresponded directly to the recognition of infected T cells and largely also to the CD4 cell count. The causal relationships of these phenomena are not clear. It is conceivable that antibodies against epitopes on HIV are lost or escape mutants arise and consequently control of HIV is lost and virus load increases as it is known for CDC stage C. Alternatively, increasing virus load may affect B cells recognising native Env epitopes and turn antibody production down by some mechanism. In this latter scenario helper T cells might have a critical role.