[Markers of apoptotic dysfunction in schizophrenia].

According to modern concepts, alterations of the apoptosis processes and its genetic regulation are involved in etiopathogenesis of schizophrenia. This is observed on the levels of both the brain and peripheral blood. However, studies in this aspect are on initial stage of development, and molecular and cellular mechanisms of abnormalities of apoptosis in schizophrenia are not clear. In the present study we determined the levels of apoptotic markers, annexin-A5 and ficolin-H proteins, in the serum of patients with chronic and first-episode schizophrenia and healthy controls. The potential association of functional single nucleotide polymorphism rs11575945 (-1C/T) of "Kozak" consensus sequence in the regulatory region of the annexin-A5 gene with schizophrenia was examined. In this study the enzyme linked immunosorbent assay and polymerase chain reaction with allele-specific primers were used. The results suggest that the pathogenesis of schizophrenia is characterized by increase rate of apoptosis, which is more pronounced in case of first-episode neuroleptic-free patients than in case of chronic patients treated with typical neuroleptic haloperidol. It was also shown that rs11575945 polymorphism of the annexin-A5 gene is associated with schizophrenia, and its minor allele is responsible for higher levels of the annexin-A5 protein in the blood and represent one of the risk factors for this disease.