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Researchers have discovered a biological basis for the storage of long-term memories based on a molecule called KIBRA.

This study, published in the journal Scientific advancesshows how KIBRA acts as a “glue” to consolidate memory formation by interacting with other important molecules such as protein kinase Mzeta (PKMzeta).

Capture memories for a long time

“Previous attempts to understand how molecules store long-term memory have focused on the individual actions of single molecules,” said André Fenton, a professor of neuroscience at New York University and one of the study’s principal investigators. “Our study shows how they work together to ensure long-lasting memory storage.”

“A better understanding of how we retain our memories will help shed light on and treat memory disorders in the future,” added lead author Todd Sacktor, a professor at SUNY Downstate Health Sciences University.

Stability of memories over time

While neurons store information in the form of strong and weak synapses, the instability of the molecules in the synapses raises questions about the temporal stability of memories.

The study examined laboratory mice and focused on the role of KIBRA in memory. It identified KIBRA as a key component that ensures the persistence of memories. KIBRA acts as a “persistent synaptic marker” that binds to strong synapses and PKMzeta and avoids weak synapses. This allows PKMzeta to continuously strengthen certain synapses.

“During memory formation, the synapses involved in the formation are activated – and KIBRA is specifically positioned in these synapses,” explains Sacktor.

“PKMzeta then binds to the KIBRA synaptic tag and keeps these synapses strong. This allows the synapses to stick to newly formed KIBRA and attract more newly formed PKMzeta.”

Strengthening weak or faded memories

The experiments showed that disrupting KIBRA-PKMzeta binding can erase old memories, while increasing PKMzeta can enhance weak or faded memories. This persistent synaptic labeling explains the enhanced memory effect observed in previous studies.

“The persistent synaptic labeling mechanism explains for the first time these findings, which are clinically relevant for neurological and psychiatric memory disorders,” said Fenton.

Proteins are replaced to store long-term memories

Research supports a concept introduced by Francis Crick in 1984 that is similar to the philosophical idea of ​​Theseus’ ship, where new planks replace old ones to maintain the ship.

“The persistent synaptic marking mechanism we discovered is similar to the way old boards are replaced with new ones to maintain Theseus’ ship over generations. It ensures that memories are preserved for years, even when the proteins that maintain the memories are replaced,” Sacktor said.

“Francis Crick suspected this Theseus ship mechanism and even predicted the role of a protein kinase. But it took 40 years for him to discover that the components were KIBRA and PKMzeta and to decipher the mechanism of their interaction.”

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