In contrast to genetic loci related to extreme longevity, mutations in single genes underlie several human premature aging syndromes. Among these, Werner (OMIM: 277700), Bloom (OMIM: 210900) and Hutchinson-Gilford Progeria (HGP; OMIM: 176670) syndromes are segmental accelerated aging syndromes. These severe conditions are caused by mutations in DNA helicases in Werner and Bloom syndromes and in Lamin A in HGP patients [19], [20]. The consequences of these mutations are impaired DNA repair/maintenance or nuclear instability, which affect cell survival and tissue homeostasis [21]. This evidence together argues for specific ‘aging genes’ that may represent key components of pathways which when modulated results in pro- or anti-aging effects. Variation within such genes may be a factor in the inter-individual heterogeneity of human lifespan.
