Scientists have uncovered the mechanism of long-term memory in the brain

Long-term memories are formed through a sequence of molecular timers that gradually reinforce important impressions, allowing less significant ones to disappear. Experiments with virtual reality have shown how different molecules coordinate memory retention in different areas of the brain. This was reported on November 30 in the journal Science Daily.

Every day, the brain turns short-term impressions, emotional experiences, and creative discoveries into long-term memories, shaping personality and influencing decisions. The central question of neuroscience is how the brain determines what is worth remembering and how long those memories last.

A new study has shown that long-term memories are formed through a sequence of molecular mechanisms with different time scales that are activated in different parts of the brain. Using virtual reality, scientists have observed how individual regulatory molecules move memories to a more stable state or allow them to gradually disappear.

The work demonstrated the interaction of several brain regions — the hippocampus, thalamus, and cortex —and their joint role in processing memories with a system of "checkpoints" that assesses the significance and durability of each event. Pria Rajasethapathi, head of the Laboratory of Neurodynamics and Cognitive Research, noted that this important discovery demonstrates how the brain controls the longevity of memories, and the process of selecting what to remember is constantly evolving, rather than happening once.

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The classical memory model considered the hippocampus as the center of short-term memory and the cortex as a long-term storage, where memories are stored "on" or "off." New data have shown that long-term memory does not depend on a single "switch", but on a sequence of gene—regulating programs - molecular timers activated in stages.

Experiments with virtual reality in the laboratory revealed three key regulators: Camta1 and Tcf4 in the thalamus and Ash1l in the anterior cingulate cortex. They are not involved in the formation of the original memory, but they are critically important for its preservation. Disruption of these molecules weakened the connection between the thalamus and the cortex, leading to memory loss. According to the model, memory formation begins in the hippocampus. Camta1 supports early memories, Tcf4 strengthens cellular connections and structural support, and Ash1l is responsible for chromatin remodeling, consolidating longevity.

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In addition, Ash1l molecules belong to histone methylation enzymes involved in maintaining "cellular memory" in other body systems, including the immune system and cell differentiation. This discovery suggests that the brain uses universal cellular memory mechanisms to maintain cognitive functions.

As noted in the article, the results may be important for the treatment of memory diseases such as Alzheimer's disease, allowing redirecting the ways of preserving memories through healthy areas of the brain.

"If we know which secondary and tertiary regions are important for memory consolidation, and in the first region neurons die, perhaps we can bypass the damaged area and allow healthy parts of the brain to take over the function," concluded Rajasethapathi.

On November 9, Medical Xpress magazine reported on the ability of physical activity to reduce the risk of Alzheimer's disease. According to the publication, this effect was observed when passing 3 thousand steps, and the best indicator was at 5-7.5 thousand steps. It was also clarified that people who walked more had improved cardiovascular health.

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