Think of a really vivid memory. Maybe it was a special birthday, a terrifying accident or a life-changing adventure. These memories stay in your brain—the sights, the sounds, maybe even the smells—much longer than the everyday details of your life. But how does your brain decide what to keep and what to let fade?
Albert Einstein College of Medicine scientists believe the answer lies in something surprising and slightly disturbing: controlled DNA damage and inflammation inside your brain cells. It sounds scary, but it could be the secret to how we form lasting memories, writes earth.com, which takes a study from Nature.
Inflammation is not always the enemy
“Inflammation of brain neurons is usually considered a bad thing because it can lead to neurological problems like Alzheimer’s and Parkinson’s”explains Dr. Jelena Radulovic, the neuroscientist who led the study. “But our findings suggest that inflammation in certain neurons in the hippocampal region of the brain is essential for creating long-lasting memories.”
The hippocampus is a part of the brain mainly involved in memory. The name “hippocampus” comes from the Greek words “hippos”, which means “horse”, and “kamppos”, which means “sea monster”, because the structure resembles a seahorse.
Now, Dr. Radulovic’s team has revealed a fascinating mechanism that operates within this structure.
Concussions, DNA damage and the construction of a memory
The researchers did experiments on mice, giving them short, mild shocks. This created a memory of the unpleasant event, known as episodic memory.
Analyzing the brains of the mice, the scientists discovered something striking – genes involved in an important inflammatory pathway had been activated in the hippocampus.
This pathway, called Toll-Like Receptor 9 (TLR9), is normally part of our immune response. This is designed to detect bits of foreign DNA from viruses or bacteria, triggering our defenses. But here, it seems to play a different role.
The mild shock caused small breaks in the DNA in certain neurons in the hippocampus. This type of routine DNA damage and repair happens all the time. However, in these memory-forming neurons, the damage appeared to be more significant and long-lasting.
The cell’s nucleus released the broken pieces of DNA and other resulting molecules, activating the TLR9 pathway.
“Memories in the Brain” Recreation Station
This inflammatory response then triggered a cascade of events: DNA repair phenomena shifted to an unusual place – the centrosomes.
Centrosomes are tiny structures in the cell, usually responsible for helping cells divide. But neurons don’t divide, so what are they doing here?
Dr. Radulovic’s team believes that this is where the magic of memory happens. Centrosomes, activated by inflammation, become centers of extensive DNA repair.
The process of restoring memory
This repair process appears to link these neurons together, creating a “memory pool” dedicated to storing that experience.
“Cell division and the immune response have been highly conserved in animal life over millions of years,” says Dr. Radulovic.
“It seems likely that over the course of evolution, hippocampal neurons have adopted this immune-based memory mechanism, combining the DNA-sensing TLR9 pathway within the immune response with a DNA centrosome repair function to form memories without progress toward cell division,” continued the expert.
When the brain recovers long-term memories, it rejects new information
Here’s another intriguing part: When these memory-encoding neurons are busy with this inflammatory repair process, they temporarily resist new information.
This makes sense – imagine trying to focus on building something complicated while someone is constantly interrupting you.
“This is noteworthy,” said Dr. Radulovic“because we are constantly inundated with information, and the neurons that encode memories must retain the information they have already acquired and not be ‘distracted’ by new input.”
The dark side of inflammation
It’s important to remember: messing with the brain’s inflammatory pathways is risky. These scientists found that if they completely blocked the TLR9 pathway, they stopped long-term memory formation and also led to genomic instability—that is, when DNA damage gets out of control.
“Genomic instability is considered a hallmark of accelerated aging as well as cancer and psychiatric and neurodegenerative disorders such as Alzheimer’s”warns Dr. Radulovic.
Implications of the study
This discovery, although still in its early stages, sheds light on a previously unexplored avenue for understanding and possibly treating memory disorders.
It gives hope in the fight against diseases known to steal our memory by opening the way to new therapies.
The understanding of the immune system has evolved. This research suggests that inflammation, carefully controlled and channeled, could hold unexpected power as a collaborator in the complex dance of memory formation and storage.
The implications are far reaching. Imagine a future where memory lapses are not an inevitable diagnosis.
How the TLR9 pathway is linked to the brain and memories
Our body has an immune system that helps us fight germs like bacteria and viruses. An important part of this system is the Toll-like receptor 9 (TLR9) pathway, which helps our body recognize and respond to certain types of DNA found in these germs.
What is TLR9 and where is it found?
TLR9 is like a special detector that our body uses to find bad germs. It is mainly found in two types of immune cells: plasmacytoid dendritic cells (pDC) and B cells. These cells keep TLR9 inside them until they need to use it to detect germs.
TLR9 looks for specific patterns in the DNA of bacteria and viruses. These patterns are like fingerprints that help TLR9 identify bad germs. When TLR9 finds these patterns, it latches onto the DNA and prepares to sound the alarm.
Once TLR9 latches onto germs’ DNA, it recruits a helper called MyD88. MyD88 then calls in more helpers, forming a team that works together to send signals to other parts of the immune system. These signals are like messages that tell our body to start fighting germs.
Fighting germs and maintaining balance
When the immune system receives the messages from TLR9 and its helpers, it starts producing special proteins called cytokines and interferons. These proteins are like soldiers that help our body fight germs.
They do this by activating other immune cells, such as macrophages, natural killer (NK) cells, and T cells, which work together to get rid of germs.
Our body has to be careful not to overreact to germs or it could start attacking itself. Therefore, the TLR9 pathway must be well controlled.
Sometimes, when this control doesn’t work properly, it can lead to problems like autoimmune diseases, where the body starts attacking its own cells.
The TLR9 pathway is like a special alarm system in our body that helps us detect and fight off bad germs.
By understanding how this system works, scientists can develop new ways to help our bodies fight infections and stay healthy.
Next steps in brain and memory research
Of course, turning all this knowledge into tangible help for those with memory problems requires years of careful research and clinical trials. This discovery is not the finish line, but a promising start.
It laid a vital foundation for exploring the intricate connection between the immune system and the brain—a connection that may hold the key to protecting our most precious memories.
This work, and what scientists will build on it, could open the doors to entirely new treatments. It’s a future where we could not only slow the diseases that steal our memory, but potentially restore some of what was lost.
The full study is published in the journal Nature.
Tags: Lasting memories cost DNA damage brain cell inflammation brain restores memories rejects information
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