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 beta amyloid precursor protein. They thus support the 
importance of the maintenance of proper protein processing and folding as a 
partial antidote to aging.