Publication Date:
2004-09-09
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kipling, David -- Davis, Terence -- Ostler, Elizabeth L -- Faragher, Richard G A -- New York, N.Y. -- Science. 2004 Sep 3;305(5689):1426-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15353794" target="_blank"〉PubMed〈/a〉
Keywords:
*Aging
;
Animals
;
Cell Aging
;
Cell Division
;
DNA Helicases/genetics/physiology
;
Exodeoxyribonucleases
;
Female
;
Gene Expression
;
Humans
;
Male
;
Mice
;
Models, Animal
;
Mutation
;
Phenotype
;
RecQ Helicases
;
Telomere/metabolism
;
*Werner Syndrome/genetics/pathology/physiopathology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
