The aim of this review is to summarize the present state of findings on altered neurotrophic factor levels in schizophrenic psychoses, on variations in genes coding for neurotrophic factors, and on the effect of antipsychotic drugs on the expression level of neurotrophic factors. This is a conceptual paper that aims to establish the link between the neuromaldevelopment theory of schizophrenia and neurotrophic factors. An extensive literature review has been done using the Pub Med database, a service of the National Library of Medicine, which includes over 14 million citations for biomedical articles back to the 1950s. The majority of studies discussed in this review support the notion of alterations of neurotrophic factors at the protein and gene level, respectively, and support the hypothesis that these alterations could, at least partially, explain some of the morphological, cytoarchitectural and neurobiochemical abnormalities found in the brain of schizophrenic patients. However, the results are not always conclusive and the clinical significance of these alterations is not fully understood. It is, thus, important to further neurotrophic factor research in order to better understand the etiopathogenesis of schizophrenic psychoses and, thus, potentially develop new treatment strategies urgently needed for patients suffering from these devastating disorders.

Recent studies have suggested that DNA variations in the CCK-AR gene might predispose individuals to schizophrenia and particularly to auditory hallucinations (AH). The aim of this study is to assess the association between AH, using a specific scale for AH in schizophrenia (PSYRATS), and the CCK-AR polymorphism at 779 in a Spanish sample. A total of 105 DSM-IV schizophrenic patients with AH and 93 unrelated controls were studied. Twenty-two patients were considered as persistent auditory hallucinators, which showed similar clinical and demographic characteristic than patients with episodic AH, but with the exception of the PSYRATS values. The persistent AH group showed an excess of the A1 allele when was compared with episodic or control groups. Our data support the possible role of the CCK-AR gene in the development of persistent AH in schizophrenic patients.

The present study was designed to detect three single nucleotide polymorphisms (SNPs) located on 22q11 that was thought as being of particularly importance for genetic research into schizophrenia. We recruited a total of 176 Chinese family trios of Han descent, consisting of mothers, fathers and affected offspring with schizophrenia for the genetic analysis. The transmission disequilibrium test (TDT) showed that of three SNPs, rs10314 in the 3′-untranslated region of the CLDN5 locus was associated with schizophrenia (χ2 = 4.75, P = 0.029). The other two SNPs, rs1548359 present in the CDC45L locus centromeric of rs10314 and rs739371 in the 5′-flanking region of the CLDN5 locus, did not show such an association. The global chi-square (χ2) test showed that the 3-SNP haplotype system was not associated with schizophrenia although the 1-df test for individual haplotypes showed that the rs1548359(C)-rs10314(G)-rs739371(C) haplotype was excessively non-transmitted (χ2 = 5.32, P = 0.02). Because the claudin proteins are a major component for barrier-forming tight junctions that could play a crucial role in response to changing natural, physiological and pathological conditions, the CLDN5 association with schizophrenia may be an important clue leading to look into a meeting point of genetic and environmental factors.

The aim of the study was to explore the relationships between the performance in figure-ground segregation and the clinical dimensions in schizophrenia. Sixty-two schizophrenic subjects filled out the embedded figures test (EFT) and the schizophrenic symptomatology was rated using the brief psychiatric rating scale (BPRS). The BPRS items were grouped into four categories: positive, negative, general and disorganization. The results showed in male schizophrenics negative and significant correlations between EFT scores and negative or disorganization subscales. Taken into account that in schizotypic subjects EFT scores was negatively correlated with negative dimension of schizotypy we suggested that those relationship could constitute a trait of the disease.

We genotyped six SNPs in the genes of p450 family among paranoid schizophrenics and normal controls. All subjects are unrelated Han Chinese. Three showed polymorphic, and no significant differences in allele or genotype frequencies were detected between patients and controls. Thus we obtained no evidence for the involvement of the polymorphisms in paranoid schizophrenia in the population investigated.

We performed an association study between three SNPs in the genes of 14-3-3 family and paranoid schizophrenia. SNP rs983583 G/A in the YWHAZ gene showed significant association with paranoid schizophrenia. Our study indicated that the YWHAZ gene was a potential susceptibility gene for paranoid schizophrenia in the population studied.

As a practical strategy for reducing agitation in schizophrenia, low-potency neuroleptics have been commonly used as an adjunct in combination with high-potency neuroleptics that seem superior in reducing positive symptoms. There is no evidence, however, that giving more than one antipsychotics at a time enhances therapeutic effects. Antipsychotic polypharmacy has been rather considered an unproven and potentially harmful practice [4].

The low-potency neuroleptic levomepromazine has been in common use for agitated patients with schizophrenia in Europe and Japan [2,3], because of its markedly sedative property. In order to clarify whether levomepromazine as an adjunct to high-potency neuroleptics are beneficial or harmful, therefore, we compared the efficacy of the combined therapy with levomepromazine and high-potency neuroleptic haloperidol with the monotherapy with haloperidol for patients with acute exacerbation of schizophrenia.

In a double blind controlled study, rTMS results in a similar antidepressant effect to sham in combination with paroxetine. Both groups had the same delay in scale’s scores improvement. rTMS seems not to be efficient as an add-on treatment to pharmacological medication in non-resistant major depression.