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In a new study, researchers from research institutions such as the University of Sheffield in the United Kingdom found that the breaking and repair of junk DNA affects the body's protection against neurological diseases, so junk DNA may open up new therapies
Previously, the repair of junk DNA, which makes up 98 percent of genomic DNA, was largely overlooked by scientists, but the new study found that junk DNA is more susceptible to damage
The authors also identify pathways
Oxidative stress is an inevitable consequence of cellular metabolism and can be influenced by factors such as diet, lifestyle, and environment
The authors hope the new study could pave the way for further research that could help speed up detection of disease biomarkers and allow for early intervention to help prevent those who carry the gene from developing or developing neurological disorders, such as Alzheimer's disease and motor neuron disease
Professor Sherif El-Khamisy, corresponding author and director of molecular medicine at the University of Sheffield, said: "The significance of repairing DNA breaks in invisible non-coding genomes will open up a whole new field of research, including new targets and biomarkers for therapeutic interventions
Professor Ilaria Bellantuono, co-director of the Institute for Healthy Life Research at the University of Sheffield, said: "This new study is important as it paves the way for being able to identify new drugs to prevent multiple diseases from occurring simultaneously and improve the
The new study could also have important implications for new cancer treatments, as the authors argue that inhibiting the activity of a key component of the pathway (NuMA) may help prevent the survival
Future research is expected to revolve around working with patients to explore pathogenic variants associated with this pathway and working with industry to develop therapeutic interventions to help those with common neurological conditions such as dementia, Alzheimer's disease, motor neuron disease, and Huntington's disease
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