MIT neuroscientists have discovered than an enzyme called HDAC1 could play a critical role in repairing age-induced DNA damage to cognitive and memory-related genes. HDAC1 is reduced in people with Alzheimer's or regular aging people.
Unlike these fish, we humans can't press pause on aging, so we have to rely on science advances to see how we can work around the issue.
By restoring this enzyme in aging people, or those suffering from cognitive diseases, the researchers propose that the effects could be reversed.
Their findings were published in Nature Communications on Monday.
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The MIT team studied mice and discovered that when the HDAC1 enzyme is lost, the mice experienced a specific type of DNA damage that built up over time. That said, the team also found out that they could reverse the damage and, in fact, improve cognitive function with a drug that activates the enzyme.
"It seems that HDAC1 is really an anti-aging molecule," said Li-Huei Tsai, the director of MIT's Picower Institute for Learning and Memory and the senior author of the study. "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."
The team studied engineered mice in which they could remove HDAC1 specifically in neurons. In the initial few months of observation, the researchers saw little to no difference between the mice that had been engineered and normal mice. However, as the mice got older, the differences started to become more clear.
The HDAC1-deficient mice started showing DNA damage and they started lose their ability to modulate synaptic plasticity. Moreover, these mice also showed signs of impairments in memory tests and spatial navigation.
Studies on Alzheimer's patients have also shown these types of DNA damage, which is usually caused by an accumulation of harmful metabolic byproducts. Typically as a person ages, they aren't able to remove these byproducts very easily.
In order to re-activate the enzyme that helps this process, the researchers realized HDAC1 had to be used. When HDAC1 is missing, the enzyme isn't able to function properly thus can't repair the DNA damage.
"This study really positions HDAC1 as a potential new drug target for age-related phenotypes, as well as neurodegeneration-associated pathology and phenotypes," Tsai said.