Ever wondered why your partner can recount every folly you’ve ever committed in absurd detail? We may finally have an answer to this rather pressing question, and it lies within our cells — more specifically, our DNA’s damage and repair mechanisms.
Here’s what researchers at the Albert Einstein College of Medicine in New York City have to say: the formation of a long-term memory entails certain brain cells experiencing a rush of electrical activity, and this pulse can be so strong that it can sever the neuron’s DNA. What follows is an inflammatory response, where the body’s immune system gets to work, trying to mend the damaged section and help etch the memory into the genes.
If you think about it, it’s pretty similar to the way tattoos work. When foreign tattoo ink enters our body, the immune system doesn't quite appreciate this intrusion and walls up the particles— essentially locking the ink there permanently.
But how did researchers link memory formation to inflammatory responses? We might have some mildly traumatised mice to thank.
Researchers subjected some adult mice to mild electric shocks in a specific environment, inducing a fear response in them when reintroduced to the same environment. Subsequently, the team analysed gene activity within the hippocampus, a region pivotal to memory processing. They observed an increase in the presence of inflammation-related genes in certain neurons four days after the shocks. However, three to four weeks later, there was a decline in these genes, indicating DNA repair and the establishment of long-term memories of the shocks.
Throughout the study, scientists pinpointed a specific protein, TLR9, responsible for initiating the immune response to DNA fragments. Despite the absence of infection, this process facilitates DNA repair, promoting healing without the need for immune cells to combat foreign bodies. When the researchers genetically modified mice to lack the TLR9 protein, they observed impaired memory recall and reduced fear responses to the shock-associated environment, suggesting an absence of long-term memory formation.
One intriguing discovery perplexed the researchers: the involvement of centrosomes, typically associated with cell division, in DNA repair. Although adult neurons do not undergo mitosis, the role of centrosomes in DNA repair within these cells remains enigmatic, but that’s a rabbit hole to go down another day.
While DNA damage might be associated with diseases like cancer, this example of the DNA damage-and-repair cycle offers a wholesome feature, no? What’s more, there’s also a chance that this cycle might be faulty in people with neurodegenerative diseases like Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says neuroscientist and study co-author Jelena Radulovic.
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