The defective protein is referred to as progerin, which causes the cell to "age".Consequently, HGPS patients develop classic diseases of old age such as atherosclerosis, osteoporosis, heart attacks and strokes. The disease is, therefore, regarded as a possible model system for the natural aging process in cells.

In order to find out which specific metabolic pathways are affected by the mutation and the defective protein, professor Karima Djabali and her team conducted a comparative study of diseased and healthy tissue cells in which they investigated the composition of proteins in the cell nuclei and looked for differences.

During the research, they found a substance in broccoli called sulforaphane that activates protein degradation in cells. The scientists treated the HGPS cells with the substance and found that significantly less progerin accumulated within the cells. Moreover, DNA damage and nuclear deformations, other effects of the disease, were also reduced in treated cells as compared with untreated cells.

"Of course our experiments are very basic, but every active substance and every new approach brings us a step closer to a treatment for HGPS patients. It could also help us develop anti-aging strategies in the future," Djabali said.

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