Scientists Identify New Protein Involved In Memory And Brain Function

Chuck Bednar for redOrbit.com – Your Universe Online
Experts from the Research Institute of the McGill University Health Centre (RI-MUHC) have identified a molecule in the brain that effectively serves as a limiter for the amount of information a person is capable of retaining, and found that removing it could improve our mental function and memory recall.
In the study, senior author Dr. Keith Murai, an associate professor in the Department of Neurology and Neurosurgery at McGill University in Montreal, and his colleagues used a mouse model to examine the role that the brain’s cellular connections play in producing new memories. They demonstrated that a protein, FXR1P (Fragile X Related Protein 1), was responsible for suppressing the production of the molecules required for building new memories.
“Previous research has shown that production of new molecules is necessary for storing memories in the brain; if you block the production of these molecules, new memory formation does not take place,” Dr. Murai explained in a statement Thursday. “Our findings show that the brain has a key protein that limits the production of molecules necessary for memory formation. When this brake-protein is suppressed, the brain is able to store more information.”
Writing in the latest edition of the journal Cell Reports, Dr. Murai and his fellow researchers reported that when they selectively removed FXR1P from certain regions of the brain, new molecules were produced that actually strengthened the connections between brain cells. The findings correlated with improved memory recall in the mice, and could ultimately be used to devise new treatments for neurodevelopmental and neurodegenerative diseases like autism and Alzheimer’s disease.
“The role of FXR1P was a surprising result,” explained Dr. Murai, whose laboratory focuses on understanding how proteins and their signaling complexes regulate synaptic morphology and function. “Previous to our work, no-one had identified a role for this regulator in the brain. Our findings have provided fundamental knowledge about how the brain processes information. We’ve identified a new pathway that directly regulates how information is handled and this could have relevance for understanding and treating brain diseases.”
“Future research in this area could be very interesting,” he added. “If we can identify compounds that control the braking potential of FXR1P, we may be able to alter the amount of brain activity or plasticity. For example, in autism, one may want to decrease certain brain activity and in Alzheimer’s disease, we may want to enhance the activity. By manipulating FXR1P, we may eventually be able to adjust memory formation and retrieval, thus improving the quality of life of people suffering from brain diseases.”
In addition to Dr. Murai and his colleagues from McGill University, scientists from the Baylor College of Medicine, the National Institute of Neuroscience at the University of Brescia in Italy, the Department of Cellular and the University of Ottawa were involved in the study. Their research was supported by funding from the Canadian Institutes of Health Research (CIHR), the Natural Sciences and Engineering Research Council of Canada, and National Institutes of Health (NIH).
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