Abstract

Progeroid syndromes have been the focus of intense research in part because they might provide a window into the pathology of normal ageing. Werner syndrome and Hutchinson–Gilford progeria syndrome are two of the best characterized human progeroid diseases. Mutated genes that are associated with these syndromes have been identified, mouse models of disease have been developed, and molecular studies have implicated decreased cell proliferation and altered DNA-damage responses as common causal mechanisms in the pathogenesis of both diseases.

Author affiliations

1. Department of Biochemistry, University of Washington, Seattle, Washington 98195, USA.
2. Department of Pathology, University of Washington, Seattle, Washington 98195, USA.
3. Department of Genome Sciences, University of Washington, Seattle, Washington 98195, USA.
4. Departments of Molecular and Cellular Biology Program, University of Washington, Seattle, Washington 98195, USA.

Correspondence to: Brian K. Kennedy¹ Email: bkenn@u.washington.edu

Correspondence to: Raymond J. Monnat, Jr^2,3 Email: monnat@u.washington.edu

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