Comparing schizophrenia patients on the basis of familial and non-familial forms of the illness provides a promising approach to the identification of genes involved in schizophrenia. The aim of this study was to search for somatic factors that discriminate between patients with and without a family history of schizophrenia and between their relatives.

Ninety-five schizophrenia patients were structurally interviewed about mental and physical health and alcohol and substance use in themselves and their families. Besides this, complementary information was obtained from the patients’ case records. Patients with (41%) and without (59%) a family history were then compared.

The main differences were found in the patients’ relatives. Fewer patients with a family history, compared with patients without a family history, had relatives with cancer (p = 0.002). Conversely, there was a tendency towards that more patients with a family history, compared with patients without a family history, had relatives with cardiac infarction (p = 0.05).

The genetic risk associated with schizophrenia seems to cosegregate into a factor(s) that protects against cancer and possibly also increases the risk for cardiac infarction.

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.

The aims of this study were to research the following issues in a Spanish population of patients with schizophrenia. (a) The sensitivity and reliability of the Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) to detect cognitive impairment in schizophrenia. (b) The convergent validity of RBANS on a larger battery of neuropsychological tests sensitive to the cognition disorders typically observed in schizophrenia. (c) The correlates of poor performance in RBANS with clinical features and illness severity.

Thirty schizophrenia patients, 30 non-psychotic patients and 30 healthy participants were assessed using RBANS (form A). We administered a battery of neuropsychological tests and four scales to evaluate patient’s clinical status.

Schizophrenia patients and non-psychotic patients performed significantly worse than healthy controls on RBANS, and schizophrenia patients performed slightly worse than non-psychiatric controls, but this difference was not significant. Good inter-test reliability and concurrent validity were found. Only a moderate correlation between RBANS performance and illness severity was observed.

RBANS revealed coherence in identifying cognitive impairment in schizophrenia patients of a different cultural background, and it is shown to be a sensitive, valid and easy-to-perform tool for the neuropsychological assessment of Spanish patients with schizophrenia.

The purpose of this study was to investigate whether the effects of quetiapine on abnormalities of early auditory processing in patients with schizophrenia were reflected by mismatch negativity (MMN).

Subjects were 23 patients with schizophrenia and 23 controls. Psychopathology was rated in patients with the Positive and Negative Syndrome Scale (PANSS) at baseline and after 4-week and after 8-week treatments with quetiapine. Auditory stimuli for event-related potentials consisted of 100 ms/1000 Hz standards, intermixed with 100 ms/1500 Hz frequency deviants and 250 ms/ 1000 Hz duration deviants. A stimulus onset asynchrony of each was 300 ms. Electroencephalograph was recorded at Fz. BESA 5.1.8 was used to perform data analysis. MMN waveforms were obtained by subtracting waveforms elicited by standards from those elicited by frequency- or duration-deviant stimuli.

Quetiapine decreased all PANSS scores. Patients showed smaller mean amplitudes of frequency and duration MMN at baseline than did controls. A repeated measure analysis of variance with sessions (i.e. baseline and 4- and 8-week treatments) and MMN type (frequency versus duration) as within-subject factors revealed no significant MMN type or MMN type × session main effect for MMN amplitudes (for MMN type: F = 0.704, df = 1, p = 0.403; for MMN type × session: F = 0.299, df = 2, p = 0.796). Session main effect was significant (F = 3.576, df = 2, p = 0.031). Least square difference tests showed significant differences between MMN amplitudes at 8 weeks and those at both baseline (p = 0.025) and 4 weeks (p = 0.020). MMN amplitudes at 8 weeks were higher than those at baseline.

Quetiapine improved the amplitudes of MMN after the 8-week treatment. MMN offers objective evidence that treatment with the quetiapine may ameliorate preattentive deficits in schizophrenia.