What can progeroid syndromes tell us about human aging?
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.
Kipling
David
D
Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Davis
Terence
T
Ostler
Elizabeth L
EL
Faragher
Richard G A
RG
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
D005090:Exodeoxyribonucleases; D004265:DNA Helicases; D053484:RecQ Helicases; C098785:WRN protein, human; D000071657:Werner Syndrome Helicase