[Brain isoforms of creatine kinase in health and mental diseases: Alzheimer's disease and schizophrenia]

Abstract

The paper analyzes the authors' own findings and the data available in the literature on the intensity, site, and possible causes of impairment of the creatine-creatine phosphate system of brain energy metabolism in mental diseases, such as Alzheimer's disease (AD) and schizophrenia. Examining the level of cytosolic BB creatine kinase in postmortem AD and schizophrenic's brain structures showed a significant decrease in BB creatine kinase as compared with the similar control brain structures. There was the maximum decline in AD cases. It was considerable as compared with both the control and schizophrenic groups (p < 0.01). The decrement was revealed by various techniques, including the determination of activity, immunological responsiveness and the analysis of two-dimensional protein maps. Immunocytochemical investigation indicated a decrease in responses to BB creatine kinase, mainly in astrocytes. The reduction in cytosolic BB creatine kinase levels is not a result of age, postmortem delay, or psychotic therapy. The causes of lower BB creatine kinase levels in the cell cytosol of the postmortem brain in mental pathology are discussed. The decrement in cytosolic BB creatine kinase in AD and schizophrenia occurs not only in the brain, but also in the peripheral tissues which contain BB creatine kinase. In all cases, it is greater in AD than in schizophrenia. Using immunosorbents with monoclonal antibodies to M-creatine kinase and to B-creatine kinase subunits makes it possible detect BB-creatine kinase in the extracts of human peripheral lymphocytes and platelets. A study of whether there is a relationship between the clinical data of mental patients and the level of BB creatine kinase in their blood elements is assumed to be useful in evaluating BB creatine kinase as a prognostic/diagnostic marker of mental diseases.