Total recall: The science behind it

Total recall: The science behind it

Is it possible to change the amount of information the brain can store? Maybe, according to a new international study led by the Research Institute of the McGill University Health Centre (RI-MUHC). Their research has identified a molecule that puts a brake on brain processing and when removed, brain function and memory recall is improved. Published in the latest issue of Cell Reports, the study has implications for neurodevelopmental and neurodegenerative diseases, such as autism spectral disorders and Alzheimer's disease.

"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 does not take place," says RI-MUHC neuroscientist, Dr. Keith Murai, the study's senior author and Associate Professor in the Department of Neurology and Neurosurgery at McGill University. "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."

FXR1P: a controller of certain forms of memory

Dr. Murai and his colleagues used a mouse model to study how changes in brain cell connections produce new memories. They demonstrated that a protein, FXR1P (Fragile X Related Protein 1), was responsible for suppressing the production of molecules required for building . When FXR1P was selectively removed from certain parts of the brain, these new were produced that strengthened connections between and this correlated with improved memory and recall in the mice.

Disease link

Total recall: The science behind it
Credit: Cell Reports
"The role of FXR1P was a surprising result," says Dr. Murai who is part of the McGill Centre for Research in Neuroscience. "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 ."

"Future research in this area could be very interesting," he adds. "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 diseases."


Explore further

Carving memories at their joints

More information: FXR1P Limits Long-Term Memory, Long-Lasting Synaptic Potentiation, and De Novo GluA2 Translation, Cell Reports, www.cell.com/cell-reports/abst … 2211-1247(14)00882-1
Journal information: Cell Reports

Citation: Total recall: The science behind it (2014, November 13) retrieved 27 May 2019 from https://medicalxpress.com/news/2014-11-total-recall-science.html
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Nov 13, 2014
The "new" molecules" are the molecules used in the repair of damaged DNA.
The expression of those repairs were seen as that which " strengthened connections between brain cells ..."

"...changes in brain cell connections" do not "produce new memories". Existing memory is connected differently through the "changes in brain cell connections" brought about by the production of new molecules used in the repair of damage arising from continued external stimuli directed to those cells handling this specific external stimulus.

FXR1P (Fragile X Related Protein 1), is responsible for suppressing the production of molecules required for the repair [in building up] from damage FORMED with all new memory.
The subtleties here are extreme along with changes in the meaning of how memory is stored and formed.
http://medicalxpr...ain.html

Still, the article presented the research fairly accurately.
Spot on research.

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