Researchers have identified a potential drug therapy for a premature ageing disease that affects children causing them to age up to eight times as fast as the usual rate.
The study is the first to outline how to limit and repair DNA damage defects in cells and could provide a model for understanding processes that cause us to age.
The findings could have significant benefits, such as reducing degeneration of some tissues in older age, and could assist health management in countries, including the UK, where average life expectancy is extending, according to the researchers.
The first results of the 18-month study, led by Durham University, are published in the journal Human Molecular Genetics.
Researchers looked at a group of inherited degenerative disorders called Laminopathies that are caused by mutations in the gene LMNA. The most severe disorders linked to mutation in this gene include Hutchinson Gilford Progeria Syndrome (HGPS), a fatal disease that causes premature ageing in children.
The Durham University and University of Bologna team used in-vitro models and molecular imaging techniques to measure levels of oxidative stress and DNA damage in cells. Oxidative stress relates to the dynamics of cells and the body's ability to detoxify and repair itself. When cells are stressed, levels of highly reactive molecules known as reactive oxygen species (ROS) can increase dramatically. This can result in significant damage to cell structures and to DNA which is one underlying cause of premature ageing and standard ageing.
The team monitored changes in thousands of 'crinkly', damaged cells after administering NAC, a widely-used and well-tolerated drug. They found that while this drug did not affect some aspects of cell stress that are effectively controlled by currently used drugs, it very effectively controlled ROS generation and DNA damage. The results suggest that administration of NAC in combination
|Contact: Carl Stiansen|