An enzyme called HDAC1 is responsible for preventing DNA damage to genes involved in memory and other cognitive functions. As per research, enzymes diminish in conditions of Alzheimer’s and aging. Previous studies focus on the involvement of HDAC1 in repairing DNA but this new study focuses on what happens to DNA in the absence of HDAC1.
A study was conducted on mice to understand the role of Enzyme HDAC1. Neurologists engineered mice without HDAC1 enzyme and compare results with healthy mice. The study confirms that in the absence of HDAC1, specific DNA damages build up in mice as the mice age.
What Can It Mean?
Researchers found that HDAC1 loss led to a specific type of DNA damage called 8-oxo-guanine lesions. An enzyme called OGG1 repairs the damage to DNA. HDAC1 is responsible to activate the OGG1 enzyme in the body. Based on the results, researchers showed that they can reverse this damage and improve cognitive function with a drug that activates HDAC1.
This study really positions HDAC1 as a potential new drug target for age-related phenotypes, as well as neurodegeneration-associated pathology and phenotypes.Li-Huei Tsai, Director, Picower Institute for Learning and Memory, MIT
This study will be a major breakthrough in the treatment of Alzheimer’s and people suffering from cognitive problems in old age. Researchers tested an old dementia drug called exifone, which activates HDAC1 on mice. The result was beneficial as it reduced DNA damage in the brain, improving cognitive functions like memory. But exifone is harmful to the patient’s liver.