New insights into non-coding DNA could help to unlock new treatments for neurological disorders, scientists believe.
Researchers from the University of Sheffield’s Neuroscience Institute and Healthy Lifespan Institute say their new findings provide important information about so-called junk DNA and how it impacts on neurological disorders such as Motor Neurone Disease (MND) and Alzheimer’s disease.
The study, which is published in the latest edition of *Nature*, found junk DNA is more vulnerable to breaks from oxidative genomic damage than previously thought, which has crucial implications on the development of neurological disorders.
The researchers also identified the pathway of how oxidative breaks are formed and repaired.
Professor Sherif El-Khamisy, chair in molecular medicine at the University of Sheffield and co-founder and deputy director of the Healthy Lifespan Institute, said: “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.
“Until now the repair of what people thought is junk DNA has been mostly overlooked, but our study has shown it may have vital implications on the onset and progression of neurological disease.
“The research also shows that it could have implications for making cancer treatments more effective.”
Professor Ilaria Bellantuono, co-director of the Healthy Lifespan Institute at the University of Sheffield, added: “This work is important as it paves the way towards being able to identify new drugs to prevent the development of multiple diseases simultaneously and boost resilience in older people.”
The research, which is funded by the Wellcome Trust and the Lister Institute, could have important implications for new cancer treatments because it is believed inhibiting NuMA, the activity of a key component of the pathway, could help to stop the survival of non-dividing dormant cancer cells, which are difficult to treat.
Further research is expected to centre on working with patients to investigate the pathogenic variants linked to this pathway and working with industry to develop therapeutic interventions to which may help those with common neurological disorders.
A mechanism for oxidative damage repair at gene regulatory elements *Nature* 28 September 2022 [abstract]
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