Scientists learn how the brain decides what is important enough to remember

Memories shape our days in quiet ways. A smell can pull an old moment back. A sound can transport the mind to another time.

Some memories land softly and disappear. Others stick with surprising strength. Scientists have wondered why this difference exists.

A new study from The Rockefeller University offers a sharp look into that question and reveals a layered system inside the brain.

The research shows that a memory does not survive by chance. It earns its place through a slow and steady process. Each stage gives it more time to live.

How the brain shapes memories

The experts describe a chain of molecular timers that guide long-term memory. Each timer activates inside specific brain regions.

The researchers found that some timers help a memory settle into the brain, while others let it fade.

The team studied mice moving through custom virtual reality worlds. Repeated experiences created stronger memories. Less frequent moments faded faster.

Study co-author Priya Rajasethupathy is head of the Skoler Horbach Family Laboratory of Neural Dynamics and Cognition.

“This is a key revelation because it explains how we adjust the durability of memories,” said Rajasethupathy.

“What we choose to remember is a continuously evolving process rather than a one time flipping of a switch.”

Existing models of memory

Older theories placed short-term memory in the hippocampus and long-term memory in the cortex. It was an appealing idea, but far too tidy.

The concept was built on imagined switch-like molecules that flipped memories from one state to another.

“Existing models of memory in the brain involved transistor-like memory molecules that act as on/off switches,” said Rajasethupathy.

This view failed to explain why one memory stays for a month while another lasts a lifetime. A study in 2023 offered a clue. It pointed to the thalamus, a central region that acts like a sorting hub.

This region helps decide which memories deserve extra support and sends those selected memories toward the cortex.

The discovery raised deeper questions. What happens in the hours and days after a memory forms? What guides the brain’s choices during that period?

Strong vs. weak memories

A virtual reality model gave the team a clean way to test these ideas. Mice walked through controlled environments, forming memories tied to repeated events.

“Andrea Terceros, a postdoc in my lab, created an elegant behavioral model allowed us to break open this problem in a new way,” said Rajasethupathy. The design allowed clear comparisons between strong and weak memories.

Behavior alone could not answer everything. The team needed direct proof.

Celine Chen, who co-led the project, built a CRISPR screening system. The system allowed the team to adjust genes in the thalamus and cortex.

When specific molecules were removed, memory duration shifted. Some disappeared sooner and others held on longer. Each molecule shaped time in its own way.

Gene sequence that locks in memories

The results suggest that long-term memory grows through a sequence of gene programs. Early programs activate quickly and fade quickly. Later programs strengthen slowly and protect the memory.

The sequence acts like a path. A memory can travel far or fall off early.

The study highlights three regulators. Camta1 and Tcf4 act inside the thalamus. Ash1l works inside the anterior cingulate cortex. These molecules do not build the memory – they keep it alive.

When Camta1 or Tcf4 are disrupted, the thalamus and cortex lose effective communication, and the memory weakens.

Once a memory forms in the hippocampus, Camta1 offers the first layer of support. Later, Tcf4 strengthens the structure. Ash1l then changes chromatin to lock the memory into a more stable state.

“Unless you promote memories onto these timers, we believe you’re primed to forget it quickly,” explained Rajasethupathy.

Shared brain memory systems

Ash1l is part of a protein family that helps cells hold on to identity. These same molecules let the immune system recall past infections and keep developing cells committed to becoming neurons or muscle, Rajasethupathy noted.

The brain appears to use this shared biological language to protect cognitive memories.

This insight may help understand memory loss in disease. If scientists can support the second or third step of consolidation, the brain may work around damaged regions. Such strategies may help conditions like 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,” said Rajasethupathy.

The next challenge lies in understanding what activates each timer. The lab aims to uncover the signals that rank the importance of each memory.

“We’re interested in understanding the life of a memory beyond its initial formation in the hippocampus,” said Rajasethupathy. “We think the thalamus, and its parallel streams of communication with cortex, are central in this process.”

The study is published in the journal Nature.

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