Telomeres are non coding regions of DNA involved in mantaining genome structure. Their length decreases with each cellular division and that fact is related with cellular and biological aging. Some of the most important endogenous mechanisms involved in regulation of telomere length is telomerase. This enzyme has 2 subunits, TERC and TERT, and it is able to increase telomere length. There are some mutations and polymorphisms of TERC and TERT taht provoke to telomerase dysfunction and are related to human diseases. One of these diseases is Werner Syndrome, a premature aging disease. In patients with this disease, some specific mutations of telomerase have been reported (Armanios M, Blackburn EH. The telomere syndromes. Nat Rev Genet 2012;13:693704). These patients have very short telomeres (Lee JW, Harrigan J, Opresko PL, Bohr VA. Pathways and functions of the Werner syndrome protein. Mech Ageing Dev 2005;126:79-86; Calado RT, Young NS. Telomere diseases. N Engl J Med 2009;361:2353-65), so some of the clinical manifestations of ageing appear in young people. One example is atherosclerotic phenomenons such as peripheral artery disease, coronary artery disease... (Massip L, Garand C, Turaga RV, Deschenes F, Thorin E, Lebel M. Increased insulin, triglycerides, reactive oxygen species, and cardiac fibrosis in mice with a mutation in the helicase domain of the Werner syndrome gene homologue. Exp Gerontol 2006;41:157-68).

In conclusion, you could try to connect Werner Syndrome with telomerase dysfunction and, after that, try to show that some of the clinical manifestations of this disease are due to cellular and biological aging because of this enzymatic lack of function.

The mutation in the WRN gene that causes Werner syndrome is autosomal and recessive, meaning that sufferers must inherit a copy of the gene from each parent. Patients display rapid premature aging beginning in young adulthood, usually in their early twenties. It is thought that the WRN helicase activity is important not only for DNA repair and recombination, but also for maintaining telomere length and stability. Thus, WRN helicase is important for preventing catastrophic telomere loss during DNA replication. In a normal cell, the telomeres (the ends of chromosomes) undergo repeated shortening during the cell cycle, which can prevent the cell from dividing and multiplying. This event can be counteracted by telomerase, an enzyme that extends the ends of the chromosomes by copying the telomeres and synthesizing an identical, but new end that can be added to the existing chromosome. However, patients with Werner syndrome often exhibit accelerated telomere shortening, indicating that there may be a connection between the loss of the WRN helicase activity and telomere and cell instability.