title: What can progeroid syndromes tell us about human aging?
abstract: Human genetic diseases that resemble accelerated aging provide useful models for gerontologists. They combine known single-gene mutations with deficits in selected tissues that are reminiscent of changes seen during normal aging. Here, we describe recent progress toward linking molecular and cellular changes with the phenotype seen in two of these disorders. One in particular, Werner syndrome, provides evidence to support the hypothesis that the senescence of somatic cells may be a causal agent of normal aging.
authors.affiliation: Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
authors.forename: David
authors.initials: D
authors.lastname: Kipling
authors.forename: Terence
authors.initials: T
authors.lastname: Davis
authors.forename: Elizabeth L
authors.initials: EL
authors.lastname: Ostler
authors.forename: Richard G A
authors.initials: RG
authors.lastname: Faragher
mesh_terms: D000375:Aging; D000818:Animals; D002455:Cell Division; D016922:Cellular Senescence; D004265:DNA Helicases / Q000235:genetics / Q000502:physiology; D005090:Exodeoxyribonucleases; D005260:Female; D015870:Gene Expression; D006801:Humans; D008297:Male; D051379:Mice; D023421:Models, Animal; D009154:Mutation; D010641:Phenotype; D053484:RecQ Helicases; D016615:Telomere / Q000378:metabolism; D014898:Werner Syndrome / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D000071657:Werner Syndrome Helicase
chemical_list: D005090:Exodeoxyribonucleases; D004265:DNA Helicases; D053484:RecQ Helicases; C098785:WRN protein, human; D000071657:Werner Syndrome Helicase