PITTSBURGH, April 28 -- Study results published by University of Pittsburgh researchers in today's Proceedings of the National Academy of Sciences offer a strong biological explanation for why cognitive processes become disordered in patients with schizophrenia.
"These results are important because even though psychosis -- the delusions and hallucinations associated with this disease is its most striking feature, disturbance in cognitive processing is often the most disabling, persistent and difficult to treat feature of schizophrenia," commented David A. Lewis M.D., professor of psychiatry and neuroscience and co-author of the study.
Schizophrenia is a serious and common mental illness that afflicts more than 2 million people in the United States. The onset of the disease usually occurs during late adolescence or early adulthood and frequently leads to a life of disability, and, in 10 to 15 percent of cases, ends in suicide. Families of patients with the illness often bear tremendous emotional and financial burdens related to it.
Dr. Lewis and his colleagues found that a specific component of the neural circuitry, or connections among brain cells, of the prefrontal cortex is substantially altered in a majority of people with the disorder. The affected component is called a chandelier neuron axon cartridge and plays a major role in controlling other neurons that process information within the prefrontal cortex and then send it to other brain regions. The prefrontal cortex is responsible for complex thinking processes, such as making judgments, formulating plans, organizing speech and other forms of communication. Disturbances in these processes severely affect the ability of an individual with schizophrenia to complete their education, gain employment and function in society.
The Pitt scientists examined post-mortem brain specimens from a total of 55 subjects whose families consented to the study. Dr. Lewis and his colleagues discovered that the number of chandelier neuron axon cartridges was reduced on average by 40 percent in subjects with schizophrenia compared to both normal controls and subjects with psychiatric disorders other than schizophrenia. Their study indicates that the alterations in chandelier neuron axon cartridges represent a disturbance in brain biology that may be specific to the disease process of schizophrenia. In addition, the findings do not appear to be a consequence of the treatment with antipsychotic medications.
"We can't determine from this study whether the alterations in chandelier neuron axon cartridges are the primary brain disturbance in schizophrenia, or if they represent the brain's response to some other abnormality," continued Dr. Lewis. "But the results do open options for the development of new treatments targeted at improving the cognitive symptoms of this disorder."
Co-authors of this study are Tsung-Ung Woo, M.D., Ph.D., formerly of Pitt, now a resident in psychiatry at UCLA and Richard E. Whitehead, B.S., research specialist and Darlene S. Melchitzky, M.S., research principal, from the department of psychiatry, University of Pittsburgh School of Medicine.
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Journal
Proceedings of the National Academy of Sciences