Perturbation of mitochondrial Fe homeostasis cause a decline in mitochondrial function that causes neuromuscular degenerative disease and other tissue dysfunction. C. Leeuwenburgh suggested that mitochondrial non-heme Fe represents a potential novel target for targeted interventions to slow ageing (C. Leeuwenburgh, University of Florida, USA) 8.

It was proposed that inadequate micronutrient intake leads to metabolic modification that has long term consequences such as cancer (DNA damage), severe infection (immune dysfunction) and cognitive dysfunction and accelerated ageing (mitochondrial decay). Much evidence supports the idea that micronutrient shortage accelerate ageing (B.N. Ames, University of California, Berkeley, CA, USA) 9.

The shortening of telomeres is supposed to be the molecular clock of ageing; indeed there is a strong correlation between age and telomere length and shorter telomeres directly correspond to shorter human life expectancy. For this purpose, several biotech organizations have accepted the challenge of finding ways to prevent telomere shortening by transiently inducing the activity of telomerase (L.A. Briggs, Reno, NV, USA). Another research has shown that therapy acting on the catalytic component of human telomerase, such as TAT2, a small molecule telomerase activator, could stabilize the telomere length and retard the loss of the immune control over viral infection (R. Effros, UCLA, Los Angeles, CA, USA) 10.

On the immunological side Dr Z. Cui has shown that cancer cells in vitro could be killed by the effector cells of the innate immune system such as macrophages and neutrophils. A similar activity was discovered in some healthy people concerning granulocytes and monocytes (Z. Cui, Winston-Salem, NC, USA) 11.

According to the fact that the immune system plays an important role in ageing, the group of Prof. C. Caruso, actively involved in immunosenescence studies 2345, has demonstrated that B naïve lymphocytes, are increased in the offspring of healthy old centenarians. It has been demonstrated that the children of centenarians, who are in their 70s and 80s, have a survival advantage when compared with control subject of the same age range whose parents died at an average life expectancy 3. The main lymphocyte differences observed between the two groups concern B cells. Indeed naïve B cells are more abundant as well as double negative B cells in centenarian children. These data are similar to that found in previously experiment on young subjects. So, B cell compartment of the offspring of centenarians seems to be more similar to that of young respect to the old one (S. Vasto, University of Palermo, Italy) 12.

It is well known that change in immune function are hallmarks of ageing and the group of Dr. A. Agrawal (University of California, Irvine, CA, USA) has shown that the reactivity of dendritic cells to self-antigens can be characteristic of ageing features. Furthermore, this over-reactivity induces lymphocyte T proliferation with subsequent higher risk of autoimmune diseases 13.

Interestingly, Effros's group suggests a possible involvement of hyper-activated T cells in bone loss associated with vascular disease in aged mice. The increased proportion of CD8 T cells lacking expression of the co-stimulatory receptor CD28 leads to decreased vaccine responsiveness and early mortality 14. ST Parish found that loss of CD28 expression is caused by increased Caspase-3 activity that can be induced by Tumor necrosis factor-alpha and suggested possible strategies for retarding the generation of senescent CD8 T cells during ageing (L.S. Graham, UCLA, Los Angeles, CA, USA).