While it is important to search for unifying mechanisms of aging among a variety 
of model systems, evolutionary arguments suggest that the pathophysiological 
details of senescence may be, to some extent, species specific. Moreover, in 
species that are characterized by extensive genetic heterogeneity, such as our 
own, one is likely to find kindreds with both "private" and "public" markers of 
aging. Crude estimates of the number of loci with the potential to modulate 
aspects of the senescent phenotype of man suggest that thousands of genes could 
be involved. No single locus appears to modulate all features. Some affect 
predominantly a single aspect ("unimodal progeroid syndromes"); familial 
Alzheimer's disease is discussed as a prototype. Linkage studies indicate 
genetic heterogeneity for autosomal dominant forms of the disease. Some loci 
affect multiple aspects of the phenotype ("segmental progeroid disorders"); the 
prototype is Werner's syndrome, an autosomal recessive. Cells from homozygotes 
behave like mutator strains and undergo accelerated senescence in vitro. 
Elucidation of the biochemical genetic basis of such abiotrophic disorders may 
shed light on specific aging processes in man.