Katharina Buczek
Now that the NPAS4-NuA4 complex has been identified, the team believes this discovery can aid a vast amount of research possibilities.
Pollina, for instance, hopes to study how this mechanism varies among shorter and longer-lived species.
Greenberg, on the other hand, wants to dive deeper into the mechanism’s details– studying what each protein in the complex is responsible for, how the process of repair is carried out, and what other molecules are involved.
For this research, he claimed that the next step is to replicate the mice study’s results in human neurons.
“I think there is tantalizing evidence that this is relevant to humans, but we haven’t yet looked in human brains for sites and damage. It may turn out that this mechanism is even more prevalent in the human brain, where you have so much more time for these breaks to occur and for DNA to be repaired,” Greenberg said.
If Greenberg’s theory is correct, then this may provide priceless insight regarding why neurons break down as adults age and develop neurodegenerative diseases like Alzheimer’s disease.
Likewise, the findings may help scientists develop tactics to protect neuronal genome regions that are more prone to damage.
To read the study’s complete findings, which have since been published in Nature, visit the link here.
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