- paranoia, delusions
- disorganized speech and thinking
- social withdrawal and a loss of motivation
The dystrobrevin-binding protein 1, or dysbindin, is a protein found in skeletal muscles cells, lysosomes, and neural brain tissue. The dysbindin protein in the brain is a constituent of axon bundles and is associated with nerve synapses, and it is this function of the protein that is correlated with schizophrenia.
Schizophrenia and Dysbindin Research
Previous research concerning the dysbindin protein has helped to establish correlations between dysbindin and schizophrenia. For example, the results of a 2002 research project found that the allele of the dysbindin gene expressed in mice seemed to be associated with the mental disorder. Thus, certain alleles of the dysbindin gene seemed more likely to result in the onset of schizophrenia. Another research project in 2009 found that dysbindin helps to control synaptic homeostasis. As a result, the protein is required presynaptically in the brain.
The newest research on dysbindin and schizophrenia was conducted by the Perelman School of Medicine at the University of Pennsylvania. The results of the study, entitled "Schizophrenia Genetics Linked to Disruption in How Brain Processes Sound," were published on October 16, 2011 in the Proceedings of the National Academy of Sciences and in Medical News Today. The goal of the study was to use high-speed imaging techniques to study schizophrenia on a cellular-level, and to better understand how the function of dysbindin affects the phenotypic symptoms of the disorder. The researchers hypothesized that a reduced amount of the dysbindin protein caused by a mutated gene could lead to schizophrenic symptoms. To test this hypothesis, in the study mice with a mutated dysbindin gene were exposed to sound and their neural responses were observed. The mice with the mutated gene expressed sound-processing deficits in the brain. Nerve cells that usually control fast brain activity became less effective in these mice. These nerves control brain activity by essentially turning cells "on and off" in order to process large amounts of information. Thus, in patients with schizophrenia, it is likely that many of their symptoms result from the ineffectiveness of nerve cells due to a reduced amount of the dysbindin protein and this research may lead to new treatment options for symptoms of schizophrenia that are currently untreatable.