Cultured skin fibroblasts from four patients with Alzheimer's disease had life spans comparable to those of six age-sex matched controls, whether measured by passages to phase-out, cumulative population doublings to phase out, or percentage of nuclei incorporating [3H]thymidine (Cristofalo index). These results provide direct experimental evidence that Alzheimer's disease is not simply a form of accelerated aging. They suggest that the abnormalities, described by several groups, in Alzheimer fibroblasts reflect the disease rather than the physiological age of the donor, making the cultured cell a valid tool for studying the cellular pathophysiology of this disorder. Together with other data, these observations raise the possibility that some forms of Alzheimer's disease may represent inborn error(s) of metabolism of late clinical onset.