The Molecule That Might Give Us All Super-Memories

At the very least, FXR1P should be able to help treat Alzheimer's and autism.

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Nov 15 2014, 8:25pm

Image: Dan Vogel/Flickr

Total recall would be a pretty sweet special skill, particularly if the recaller finds themselves witnessing crimes and/or playing poker on a regular basis. It's probably handy in other situations too … like quoting movies or the digits of pi. I'd be happy enough just having a reasonably functional memory again. Like a whole lot of people in my demographic, my short-term memory began a slow and steady wither starting right around the same time Google appeared. I don't remember, I connect.

What if total recall was something that could just be switched on, like night vision goggles only for the darkened past instead of the actual dark? Researchers at Montreal's McGill University have identified a molecule in the brain that appears to inhibit brain processing ability such that when the molecule is removed, memory recall and overall neuro-functioning appear to improve.

The molecule, described in an open-access paper in week's edition of Cell Reports, could prove to be key in treating neurodegenerative diseases like autism and Alzheimer's. Specifically, the researchers explored the functioning of the FXR1P protein, aka Fragile X Related Protein 1, kin to FXR2P and Fragile X Mental Retardation Protein (FMRP), both molecules implicated in the functioning of memory and synaptic plasticity, or the brains interconnectivity.

"For long-term synaptic plasticity and memory formation to occur properly, new proteins must be synthesized in a temporally and spatially precise manner in response to specific patterns of activity, a process that is tightly controlled at the level of mRNA translation," the McGill study explains. "We have identified the RNA-binding protein FXR1P as a key player in controlling specific aspects of synaptic protein expression, synaptic plasticity, and memory formation."

The researchers, led by neuroscientist Keith Murai, found that by knocking out FXR1P in the brains of mice, those brains responded by increasing production and transport of a key neuroreceptor, GluA1, boosting L-LTP, one of the cellular processes crucial for learning and memory, and increasing long-term memory capability overall.

"These findings define a molecular pathway that regulates distinct features of synaptic plasticity and cognitive function," Murai and his team write.

Murai notes in a separate statement that with the identification of compounds influencing the "braking potential" of FXR1P it should be possible to influence memory formation/capability and overall synaptic 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," Murait explains. "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."