Junk DNA sheds light into neurological disorders

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SHEFFIELD, England (Commonwealth Union) – The role of junk DNA has differed throughout the last few decades. Researchers have recently found that ‘Junk’ DNA, which are regions of DNA that are noncoding, can pave the way for new treatments for neurological disorders and have found how its breaks and repairs, impact our defense against neurological diseases.

The University of Sheffield’s Neuroscience Institute and Healthy Lifespan Institute paved the way for significant new details into the so-called junk DNA and the role it plays on neurological disorders such as Motor Neurone Disease (MND) and Alzheimer’s disease.

Until now, the repair of junk DNA, of the body which can make up 98% of DNA, has been largely left out by researchers, but the new findings saw that it is much more vulnerable to breaks from oxidative genomic damage than previously assumed. This has a significant impact on the progress of neurological disorders.

The scientists also noted the pathway of how oxidative breaks are produced and fixed. Repairing these breaks in junk DNA is vital to permit the body to synthesize proteins which defend us against disease.

Oxidative stress is generally caused by free radical damage when an unpaired electron that is unstable can cause genetic destruction. Oxidative stress which can occur due to cellular metabolism is impacted by diet, lifestyle and environment. Oxidative stress that causes damage on the long run to cells can play a role in neurological disorders like dementia.

Researchers hope further studies of the findings could assist in accelerating the identification for biomarkers of disease, which could lead to early intervention to stop the advancing of neurological conditions such as Alzheimer’s disease and the MND in individuals with the relevant gene.

“The significance of repairing DNA breaks in the invisible non-coding genome will open up a whole new field of research, including new targets for therapeutic interventions and biomarkers. By therapeutically targeting components of the pathway, it may help us delay or treat neurological diseases such as dementia,” said Professor Sherif El-Khamisy, Chair in Molecular Medicine at the University of Sheffield, Co-founder and Deputy Director of the Healthy Lifespan Institute.

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