A new study conducted by the Research Institute of the McGill University Health Centre has discovered a molecule that opens the door to the possibility of changing the amount of information the brain can store. The study highlights potential implication of FXR1P (Fragile X Related Protein 1) for neurodevelopmental and neurodegenerative diseases, such as Alzheimer’s and autism.
Function of FXR1P
The study used mice to study how brain cell connections produce new memories. FXR1P was shown to hold back the production of molecules required for building new memories. Researchers selectively removed FXR1P from parts of the brain and when they did, connections between brain cells were strengthened and this correlated with increased memory and recall in the mice.
Dr. Keith Murai, the study’s senior author said, “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.” He continued, “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.”
Dr. Murai further stated that, “the role of FXR1P was a surprising result.” Before the study, no research had been able to identify a function for this specific regulator.
The researchers believe that their discovery is providing “fundamental knowledge” to the field of neuroscience. They have shed just that much more light on the way the brain processes information and Dr. Murai hopes that FXR1P will be relevant to understanding and, in the future, creating treatments for brain diseases.
The implications of the discovery of FXR1P remain to be seen, however Dr. Murai seems to be optimistic that they have truly found something that could be used to treat widespread conditions, like autism spectral disorders and Alzheimer’s.
The study’s authors cited future research looking into identifying the compounds that control whether or not FXR1P is activated, thus altering the amount of brain activity. They would potentially be enhancing the activity for Alzheimer’s and decreasing certain activity in autism, for instance. Dr. Murai said, “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.”