394 – Implication of Genetic Polymorphisms and Changes in Expression Levels of Proteins Regulating Neuronal Plasticity and Apoptosis in Schizophrenia Disorder

Abstract

Introduction:

Pathologic changes in neuronal plasticity and apoptosis are important factors influencing alterations in synaptic transmission and impaired cognitive function, characteristic features of schizophrenia. Brain derived neurotrophic factor (BDNF), complexin-2, and annexin A-5 are known as members of regulatory pathways responsible for maintenance of neuronal plasticity and apoptosis.

Objectives:

The study was focused on assessment of possible association of functional single nucleotide polymorphisms (SNPs) and expression levels of BDNF, complexin-2, and annexin A-5 with schizophrenia.

Aims:

For this purpose we investigated functional polymorphisms and plasma levels of these proteins in schizophreniaaffected neuroleptic-treated and neuroleptic-free patients and healthy controls.

Methods:

DNA samples were genotyped by polymerase chain reaction with sequence-specific primers. Plasma levels of BDNF, complexin-2, and annexin A-5 were measured with an enzyme-linked immunosorbent assay. The significance of differences between allele and phenotype frequencies in study groups was determined using Pearson's χ2 test. For evaluation of intergroup differences in the levels of BDNF, complexin-2, and annexin A-5, both parametric and non-parametric statistics were used. The assessment of correlation between the measured parameters within each group was also performed. P-values less than 0.05 were considered significant.

Results:

In patients with schizophrenia, as compared to controls, the carriers of mutant alleles of the functional polymorphisms of BDNF, complexin-2, and annexin A-5 genes were overrepresented, and the blood levels of these proteins were altered.

Conclusions:

Functional polymorphisms of genes encoding BDNF, complexin-2, and annexin A-5 proteins are associated with schizophrenia resulting in altered expression levels of these proteins upon this disorder.