Long-term memory has been shown to be impossible without inflammation in the brain
When information is fixed in memory for a long time, DNA is damaged and a group of neurons in the brain become inflamed. This was found out by scientists from the USA, Denmark and Germany.
The memory center in the brain is the hippocampus. It is thanks to its work that it becomes possible to memorize a large amount of information for a long time. Information is processed even in sleep: it is transferred from short-term memory to long-term memory.
Researchers from Northwestern University (USA), Albert Einstein College of Medicine (USA), Aarhus University (Denmark) and Göttingen University (Germany) found out what happens in the brain when long-term memories are created. It turned out that this process is impossible without DNA damage and inflammation in the hippocampus. The corresponding scientific article was published by the journal Nature.
Inflammation of brain neurons is considered a bad thing, as it can lead to Parkinson's and Alzheimer's diseases. However, the inflammatory process in certain hippocampal neurons is necessary for information to move from short-term memory to long-term memory. According to the discovery of the authors of the publication, the stimulus triggers a cycle of DNA damage and repair in these neurons, resulting in the formation of memory nodes - clusters of brain cells in which "recorded" past experience.
This mechanism was revealed during an experiment involving eight-week-old mice. Scientists subjected the animals to short mild shocks of current, sufficient to form a memory of the shock event. Analysis of neurons in the hippocampal region showed that the mice activated genes that are involved in the Toll-like receptor 9 (TLR9) inflammatory pathway:
"This inflammatory pathway is best known for triggering immune responses by detecting small fragments of pathogen DNA. At first, we assumed that the TLR9 pathway was activated because the mice had an infection. But after taking a closer look, we found to our surprise that TLR9 was only triggered in clusters of hippocampal cells that exhibited DNA damage," explained the study authors.
The neuronal disruptions associated with long-term memory formation appeared to be more substantial and persistent compared to those that occur with other brain activity. DNA fragments were repaired in an unusual place - in centrosomes. These are the organoids that coordinate cell division. However, the researchers noted, in neurons that do not divide, centrosomes were involved in DNA repair and appear to help form memory nodes.
The authors of the research paper also found that in the week it took to complete the inflammatory process, the neurons encoding memory changed in the mice. These brain cells became more resistant to new information, "This is remarkable because we are constantly inundated with information, and the neurons encoding memories need to retain the information they have already acquired without being distracted by new input."
When the researchers blocked the TLR9 inflammatory pathway in hippocampal neurons, the mice not only failed to develop long-term memory, but also developed a profound genomic instability: the incidence of DNA damage in these cells became high. This phenomenon is considered a sign of accelerated aging, as well as cancer, mental and neurodegenerative disorders, such as Alzheimer's disease.