A cure for<unk>  has not yet been discovered. It is often treated by managing the associated diseases and relieving symptoms to improve quality of life. The skin ulcers that accompany<unk>  can be treated in several ways, depending on the severity. Topical treatments can be used for minor ulcers, but are not effective in preventing new ulcers from occurring. In the most severe cases, surgery may be required to implant a skin graft or amputate a limb if necessary. Diseases commonly associated with<unk>  such as diabetes and cancer are treated in generally the same ways as they would be for a non-Werner syndrome individual. A change in diet and exercise can help prevent and control arteriosclerosis, and regular cancer screenings can allow for early detection of cancer. There is evidence that suggests that the cytokine-suppressive anti-inflammatory drug SB203580 may be a possible therapeutic option for patients with<unk> 's syndrome. This drug targets the p38 signaling pathway, which may become activated as a result of genomic instability and stalled replication forks that are characteristic mutations in<unk> . This activation of p38 may play a role in the onset of premature cell aging, skin aging, cataracts, and graying of the hair. The p38 pathway has also been implicated in the anti-inflammatory response that causes atherosclerosis, diabetes, and osteoporosis, all of which are associated with<unk> 's syndrome. This drug has shown to revert the aged characteristics of young<unk>  cells to those seen in normal, young cells and improve the lifespan of<unk>  cells in vitro. SB203580 is in the clinical trial stages, and the same results have not yet been seen in vivo. In 2010, vitamin C supplementation was found to reverse the premature aging and several tissue dysfunctions in a genetically modified mouse model of the disease. Vitamin C supplementation also appeared to normalize several age-related molecular markers such as the increased levels of the transcription factor NF-κB. In addition, it decreases activity of genes activated in human<unk>  and increases gene activity involved in tissue repair. Supplementation of vitamin C is suspected to be beneficial in the treatment of human<unk> , although there was no evidence of anti-aging activity in nonmutant mice. In general, treatments are available for only the symptoms or complications and not for the disease itself.
Werner syndrome
Mungan syndrome
Fechtner syndrome
Leschke syndrome
Klüver–Bucy syndrome
Ogden syndrome
Sugarman syndrome
Cowden syndrome