We often remember our first day of school or a childhood bicycle ride decades after they happened, even though the cells and molecules in our brains are constantly replacing themselves. This biological paradox – how a memory can last a lifetime when its physical building blocks degrade in days – has finally been explained. An international team of neuroscientists has identified a protein called KIBRA that acts as a “molecular glue.” It anchors the key enzyme responsible for strengthening synapses, ensuring that memories remain stable even as the brain regenerates itself.
The biological problem: how memories outlive their molecules
For years, scientists knew that a brain enzyme called PKMzeta (protein kinase Mzeta) was essential for strengthening the connections between neurons, known as synapses. This strengthening is what allows us to store information. However, there was a major flaw in the theory: PKMzeta degrades and disappears after just a few days.
The “Ship of Theseus” in your brain
This created a puzzle that resembled the philosophical “Ship of Theseus” paradox: if every plank of a ship is replaced over time, is it still the same ship? Similarly, if the molecules storing a memory are replaced every week, how does the memory persist for fifty years?
Researchers from New York University and SUNY Downstate Health Sciences University have found the answer. Their study reveals that KIBRA serves as a persistent synaptic tag. It sits at the specific synapses involved in a memory and grabs onto new PKMzeta molecules as the old ones fade away. This continuous cycle allows the structure of the memory to outlast the lifespan of any single molecule.
How the KIBRA “glue” mechanism works
The team, led by Professors André Fenton and Todd Sacktor, used laboratory mice to observe these molecular interactions in real time. They discovered a distinct partnership between the two proteins.
Anchoring the memory
When the brain learns something new, specific synapses are activated. KIBRA selectively positions itself in these activated synapses. It then acts as a docking station for PKMzeta. The enzyme binds to KIBRA, and this connection keeps the synapse strong.
A cycle of renewal
Crucially, while the PKMzeta enzyme degrades, the KIBRA “glue” remains. It attracts newly synthesized PKMzeta to the same spot, ensuring the connection remains reinforced. The study published in Science Advances showed that disrupting this bond causes old memories to vanish. When researchers blocked the interaction between KIBRA and PKMzeta in mice, the animals lost long-term memories they had established weeks earlier, confirming that this handshake between proteins is the physical basis of memory maintenance.
Implications for treating Alzheimer’s and PTSD
This discovery moves neuroscience from theory to potential therapy. Understanding the mechanical basis of memory storage opens new doors for treating neurological and psychiatric conditions.
Restoring lost memories
In conditions like Alzheimer’s disease, synapses weaken and memories fade. This research suggests that the problem might not be a total loss of information, but a failure of the “glue” to hold the strengthening enzymes in place. Astrocytes act as essential partners to neurons for storing and recalling memories, and now we see that proteins like KIBRA are just as vital. Therapies that mimic or boost KIBRA could potentially stabilize weak synapses and recover fading memories.
Disrupting harmful memories
Conversely, this mechanism offers a target for treating Post-Traumatic Stress Disorder (PTSD). If scientists can selectively disrupt the KIBRA-PKMzeta bond at specific synapses associated with trauma, they might be able to weaken intrusive, harmful memories without damaging the rest of the patient’s memory.
What you can do about it
While we cannot yet buy a pill to boost KIBRA, this research validates lifestyle habits that support general brain plasticity.
- Prioritize sleep: Memory consolidation is a biochemical process that is heavily active during rest. Positive memory reactivation during sleep reduces negative memory recall, suggesting that quality sleep supports the molecular work of sorting and storing experiences.
- Keep learning: The “use it or lose it” principle applies to synapses. Engaging in complex tasks keeps synapses active, potentially recruiting more of these stabilizing proteins.
- Stay updated: This is a rapidly developing field. Watch for future news on “synaptic tags” or PKMzeta inhibitors, as these will likely be the basis for the next generation of memory drugs.
Sources & related information
Science Advances – KIBRA anchoring the action of PKMζ maintains the persistence of memory – 2024
Researchers Tsokas, Hsieh, Fenton, and Sacktor detail the experiments identifying KIBRA as the persistent synaptic tag that stabilizes PKMzeta to maintain long-term potentiation and memory despite molecular turnover.
NYU – How Do Our Memories Last a Lifetime? – 2024
A summary from New York University explaining the “Ship of Theseus” analogy and the collaboration between labs that led to identifying the molecular mechanism of long-term memory storage.
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