Memory formation triggers inflammation and DNA damage in brain cells
A recent study, published in Nature, has unveiled that the formation of long-term memories can trigger inflammation and cause DNA damage in brain cells. A certain level of destruction is necessary for a new memory pattern to emerge. The research, conducted on mice, found that this process occurs in the hippocampus, a crucial part of the brain for memory storage.
Inflammation in brain neurons
Neuroscientist Jelena Radulovic from Albert Einstein College of Medicine states, "Inflammation of brain neurons is usually considered to be a bad thing, since it can lead to neurological problems such as Alzheimer's and Parkinson's disease." "But our findings suggest that inflammation in certain neurons in the brain's hippocampal region is essential for making long-lasting memories," she adds. This discovery challenges conventional understanding and opens new avenues for memory-related research.
Memory formation linked to inflammatory signaling
The team induced episodic memory in mice through brief, mild electric shocks. Examination of hippocampal neurons revealed gene activation in the Toll-Like Receptor 9 (TLR9) pathway, a significant player in inflammatory signaling. Intriguingly, this pathway was activated only in neuron clusters that also displayed DNA damage. Radulovic explains that these alterations appeared more substantial than common DNA breaks in the brain, which are typically repaired swiftly.
Inflammation-induced editing mechanisms in memory formation
The inflammation-induced editing mechanisms persisted for a week, after which the neurons storing memories became more resilient to external factors. This implies that memories are permanently secured and shielded from outside disruptions. A similar process likely occurs in the human brain as well. Radulovic notes, "This is noteworthy because we're constantly flooded by information, and the neurons that encode memories need to preserve the information they've already acquired and not be distracted by new inputs."
TLR9 pathway: A key player in memory recall
When scientists inhibited the TLR9 inflammatory pathway in mice, they were unable to recall the electric shocks. The absence of TLR9 also resulted in more severe DNA damage, similar to that seen in neurodegenerative disorders. This study prompts a reconsideration of the strategy to block the TLR9 pathway, as a treatment or preventative measure for long-term COVID-19. Radulovic emphasizes that these findings highlight the critical role of inflammation and DNA repair mechanisms in memory formation and recall.
