Kipling, David Glyn, Davis, Terence ![]() |
Official URL: http://dx.doi.org/10.1126/science.1102587
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.
Item Type: | Article |
---|---|
Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Subjects: | R Medicine > R Medicine (General) |
Publisher: | American Association for the Advancement of Science |
ISSN: | 0036-8075 |
Last Modified: | 14 Dec 2022 02:15 |
URI: | https://orca.cardiff.ac.uk/id/eprint/46694 |
Citation Data
Cited 162 times in Scopus. View in Scopus. Powered By Scopus® Data
Actions (repository staff only)
![]() |
Edit Item |