Possible genetic link found between schizophrenia and how brain processes sound
By Ian Birch
Researchers in the USA have identified a number of sound processing deficits in mice with a mutated gene which they claim indicates a link between schizophrenia in humans and the way the brain processes sound. The study does not make any link between auditory hallucinations (hearing voices) and genetics however.
Recent studies have identified many genes that may put people with schizophrenia at risk for the disease. But, what links genetic differences to changes in altered brain activity in schizophrenia is not clear. Now researchers have come together using a range of approaches - along with a unique high-speed imaging technique - to understand how schizophrenia works at the cellular level, especially in identifying how changes in the interaction between different types of nerve cells leads to symptoms of the disease.
"Our work provides a model linking genetic risk factors for schizophrenia to a functional disruption in how the brain responds to sound, by identifying reduced activity in special nerve cells that are designed to make other cells in the brain work together at a very fast pace," explained lead author Gregory Carlson, assistant professor of Neuroscience in Psychiatry at Pennsylvania University. "We know that in schizophrenia this ability is reduced, and now, knowing more about why this happens may help explain how loss of a protein called dysbindin leads to some symptoms of schizophrenia."
The team discovered how a specific set of nerve cells that control fast brain activity lose their effectiveness when dysbindin protein levels are reduced. These specific nerve cells inhibit activity, but do so in an extremely fast pace, essentially turning large numbers of cells on and off very quickly in a way that is necessary to normally process the large amount of information travelling into and around the brain.
Other previous work at Penn in the lab of Michael Kahana, PhD has shown that in humans the fast brain activity that is disrupted in mice with the dysbindin mutation is also important for short-term memory. This type of brain activity is reduced in people with schizophrenia and resistant to current therapy. Taken as a whole, this work may suggest new avenues of treatment for currently untreatable symptoms of schizophrenia, says Carlson.
The research is published in the Proceedings of the National Academy of Sciences and was funded in part by the National Institutes of Mental Health.
External Links
Proceedings of the National Academy of Sciences abstract:
http://www.pnas.org/content/early/2011/09/29/1109625108.abstract
