The African Turquoise Killifish can pause aging. Unfortunately, we cannot do the same without science advances. That is why researchers around the world spend their lives searching for ways to help us live longer. And a team of MIT neuroscientists is onto something.
Back in 2013, they linked an enzyme called HDAC1 to DNA repair in neurons. Now, they’ve discovered that the enzyme is critical for repairing age-related DNA damage to genes involved in cognitive functions, such as memory. This enzyme is often missing in aging adults, particularly those with Alzheimer’s, but it can be restored. The researchers suggest developing a drug that reactivates HDAC1 in aging adults to reverse cognitive decline.
The team experimented with mice by engineering a group of them to be HDAC1 deficient. Those mice ended up experiencing a specific type of DNA damage build up as they age. However, by administering a drug that activates the enzyme, the mice saw an improvement in cognitive function and reversal of neuron damage. These results show that restoring the protein could be a potential treatment for Alzheimer’s and age-related cognitive decline. Although, the drug they gave the mice is out of the question as it is known to cause liver damage in humans.
Li-Huei Tsai, the director of MIT’s Picower Institute for Learning and Memory and the senior author of the study, said:
It seems that HDAC1 is really an anti-aging molecule. I think this is a very broadly applicable basic biology finding because nearly all of the human neurodegenerative diseases only happen during aging. I would speculate that activating HDAC1 is beneficial in many conditions.
This study really positions HDAC1 as a potential new drug target for age-related phenotypes, as well as neurodegeneration-associated pathology and phenotypes.
Other studies on Alzheimer’s patients have also found the same sort of DNA damage. It’s caused by a buildup of harmful metabolic byproducts – which occurs because the aging body starts having a hard time removing them. There’s a separate enzyme called OGG1 that is responsible for repairing the DNA damage, but it needs HDAC1 to work.
Now that the researchers know they can restore HDAC1 and it fixes the problem, they’ve moved on to exploring whether DNA damage and the enzyme also play a role in the formation of Tau tangles – misfolded proteins in the brain. Tau tangles are a signature of Alzheimer’s and other neurodegenerative diseases. If a link is established, restoring HDAC1 will likely help treat the condition.
