Genetic modulation of senescent phenotypes in Homo sapiens

Single-gene mutations can produce human progeroid syndromes-phenotypes that mimic usual or "normative" aging. These can be divided into two classes-those that have their impacts upon multiple organs and tissues (segmental progeroid syndromes) and those that have their major impacts upon a single organ or tissue (unimodal progeroid syndromes). The prototypic example of the former is the Werner syndrome, a condition caused by mutations of the RecQ family of DNA helicases. Research on the Werner syndrome and a surprising number of other progeroid syndromes support the importance of the maintenance of genomic stability as a partial antidote to aging. The prototypic examples of the latter are Alzheimer type dementias. The three gene products that cause rare autosomal-dominant early-onset varieties of these disorders all participate in the modulation of the P amyloid precursor protein. They thus support the importance of the maintenance of proper protein processing and folding as a partial antidote to aging.