Wie das Gehirn entscheidet, woran es sich erinnert: Mit einem auf der virtuellen Realität basierenden Verhaltensmodell bei Mäusen entdeckten die Wissenschaftler, dass das Langzeitgedächtnis durch Schlüsselregulatoren gesteuert wird, die Erinnerungen entweder in immer dauerhaftere Formen bringen oder sie herabstufen, bis sie vergessen werden

>The results suggest that long-term memory is not maintained by a single molecular on-and-off switch, but by a cascade of gene-regulating programs that unfold over time and across brain regions like a series of molecular timers.
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>Initial timers turn on quickly and fade just as fast, allowing for rapid forgetting; later timers act more slowly but create more durable memories. This stepwise process allows the brain to promote important experiences for long-term storage, while others fade. In this study, the researchers used repetition as a proxy for importance, comparing memories of frequently repeated contexts to those encountered less often. The team identified three transcriptional regulators: Camta1 and Tcf4 in the thalamus, and Ash1l in the anterior cingulate cortex, which are not necessary for initially forming memories, but are crucial for maintaining them. Disrupting Camta1 and Tcf4 impaired functional connections between the thalamus and cortex, leading to memory loss.
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>The model suggests that, after the basic memory is formed in the hippocampus, Camta1 and its targets ensure the initial persistence of the memory. With time, Tcf4 and its targets are activated providing cell adhesion and structural support to further maintain the memory. Finally, Ash1l recruits chromatin remodeling programs that make the memory more persistent.
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>“Unless you promote memories onto these timers, we believe you’re primed to forget it quickly,” Rajasethupathy says.
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>Interestingly, Ash1l belongs to a family of proteins called histone methyltransferases that retain memory in other biological systems as well. “In the immune system, these molecules help the body remember past infections; during development, those same molecules help cells remember that they’ve become a neuron or muscle and maintain that identity long-term,” Rajasethupathy says. “The brain may be repurposing these ubiquitous forms of cellular memory to support cognitive memories.”
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>The findings may have implications for memory-related diseases. Rajasethupathy suspects that, by identifying the gene programs that preserve memory, researchers may eventually find ways to route memory through alternate circuits and around damaged parts of the brain in conditions such as Alzheimer’s. “If we know the second and third areas that are important for memory consolidation, and we have neurons dying in the first area, perhaps we can bypass the damaged region and let healthy parts of the brain take over,” she says.

[Thalamocortical transcriptional gates coordinate memory stabilization | Nature](https://www.nature.com/articles/s41586-025-09774-6)