DNA lesions responsible for creating memories later destroys them, MIT

The mechanism which allows our brain to learn and develop new memories is also responsible for the destroying those memories with the age, claims MIT researchers through the study published in the journal Cell. According to scientists, the finding will give new insight in developing new approaches to prevent cognitive decline as we age. Researchers say that the study will help people suffering from disease like Alzheimer in which a person’s memory weakens.

Lead researcher Li-Huei Tsai, the Picower Professor of Neuroscience and director of the Picower Institute for Learning and Memory at MIT says that with every learning process brain cells physiologically breaks their DNA so that certain genes can be expressed which ultimately pave the way for the transcriptional program that supports learning and memory, and many other behaviors. In the process, DNA damage occurs which neurons must repair immediately. However, as we get older the ability to repair the damage weakens significantly, eventually leading to degeneration.

Previously, a research on mice showed that neurons in the hippocampal region of the brain contain a large number of DNA lesions, also called double strand breaks. To determine how these lesions occur, researchers injected toxic agent known as induce double strand breaks to the neurons. Scientists then collected RNA samples and found that 700 genes reflected changes after the damage. Most of them had reduced expression levels. While 12 genes including sensory experience displayed increased expression levels after double strand breaks. Tsai said that double strand break is naturally occurring phenomenon and essentially is physiological function of the brain cell.

With the study, MIT researchers have found that an enzyme named topoisomerase IIβ is responsible for the DNA lesions in response to stimulation. Researchers used computer models In order to determine the mechanism behind such drastic changes for genes to express itself. They found that DNA sequences were enriched with a motif for binding to a protein called CTCF. This protein is responsible for creating bends in DNA.

According to Tsai, these bends acts as a barrier in early responses and it prevents different elements of DNA from interacting with each other. Tsai further added that more research is needed to determine what affects these DNA repair system as we age.

Several scientists believe that this study has given new insight in better understanding DNA strand break formation by the enzyme topoisomerase IIβ and will help in several cognitive applications including treatment of diseases like Alzheimer.

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