U.S. scientists find how brain cells regulate memories in mice study

WASHINGTON. KAZINFORM - The U.S. scientists have mapped a part of the molecular machinery that helps the brain maintain long-term memories, providing new targets against Alzheimer's disease characterized by memory loss, Xinhua reports.

The study published on Monday in the Proceedings of the National Academyof Sciences, outlined how a protein called CPEB3 primes neurons to storememories that stand the test of time in mouse cells.

The findings offered a never-before-seen view into one of the brain'smost universal and basic cellular functions.

«At its core, memory is a biological process, not unlike aheartbeat. With today's study, we've shed new light on the molecularunderpinnings behind our brain's ability to make, keep and recall memories overthe course of our lives,» said the study's co-senior author Eric Kandel,professor of brain science at Columbia University.

Kandel's team found in a previous study that CPEB3 plays a critical rolein strengthening synapses, the connection points where tiny branches of neuronsconnect to each other when all memories are made.

When they prevented mice from making CPEB3, those animals could form anew memory but could not keep it intact, according to the researchers.

Within the hippocampus, which is the brain's memory center, CPEB3 isproduced at regular intervals inside the centers of neurons. Kandel's teamfound that once CPEB3 is produced it is transferred to P bodies, chambers thatkeep CPEB3 dormant and ready for use.

P bodies do not have a physical barrier to contain CPEB3 and it is thedifference in densities holds P bodies together, according to the study.

Once laden with dormant CPEB3, P bodies leave a neuron's center andtravel down its branches toward the synapses. When an animal begins to form amemory, the P bodies dissolve, releasing CPEB3 into synapses to help create thememory, according to the study.

CPEB3, also present in the human brain, represents a potential to play arole in treating neurodegenerative diseases.

«By continuing to build this understanding, we could one daydevelop useful methods to boost CPEB3 in a way that prevents synapticdegradation, thus slowing memory loss,» said the paper's co-senior authorLuana Fioriti, who works in the Kandel lab.