Werner Syndrome

Publication Title: 
Biogerontology

The premature ageing ataxia telangiectasia (AT) and Werner syndromes (WS) are associated with accelerated cellular ageing. Young WS fibroblasts have an aged appearance and activated p38 MAP kinase, and treatment with the p38 inhibitor SB230580 extends their lifespan to within the normal range. SB203580 also extends the replicative lifespan of normal adult dermal fibroblasts, however, the effect is much reduced when compared to WS cells, suggesting that WS fibroblasts undergo a form of stress-induced premature senescence (SIPS).

Author(s): 
Davis, Terence
Kipling, David
Publication Title: 
Mechanisms of Ageing and Development

The phenomenon that caloric restriction increases life span in a variety of species from yeast to mice has been the focus of much interest. Recent observations suggest that a protein important for heterochromatin formation, Sir2, is central for caloric restriction-induced longevity in lower organisms.

Author(s): 
Hasty, P.
Publication Title: 
Aging Clinical and Experimental Research
Author(s): 
Butler, Robert N.
Warner, Huber R.
Williams, T. Franklin
Austad, Steven N.
Brody, Jacob A.
Campisi, Judith
Cerami, Anthony
Cohen, Gene
Cristofalo, Vincent J.
Drachman, David A.
Finch, Caleb E.
Fridovich, Irwin
Harley, Calvin B.
Havlik, Richard J.
Martin, George M.
Miller, Richard A.
Olshansky, S. Jay
Pereira-Smith, Olivia M.
Smith, James R.
Sprott, Richard L.
West, Michael D.
Wilmoth, John R.
Wright, Woodring E.
Publication Title: 
La Revue Du Praticien
Author(s): 
Belmin, JoÎl
Konrat, CÈcile
Publication Title: 
Journal of Alzheimer's disease: JAD

As the basis for the lifelong clock and as a primary cause of aging, a process of shortening of hypothetical perichromosomal DNA structures termed chronomeres is proposed in the CNS. The lifelong clock is regulated by the shortening of chronomere DNA in postmitotic neurons of the hypothalamus. Shortening of these DNA sequences occurs in humans on a monthly basis through a lunasensory system and is controlled by release of growth hormone discharged from the anterior pituitary directly into the hypothalamus via local blood vessels.

Author(s): 
Olovnikov, A. M.
Publication Title: 
The Journal of Cell Biology

Werner and Bloom syndromes are human diseases characterized by premature age-related defects including elevated cancer incidence. Using a novel Saccharomyces cerevisiae model system for aging and cancer, we show that cells lacking the RecQ helicase SGS1 (WRN and BLM homologue) undergo premature age-related changes, including reduced life span under stress and calorie restriction (CR), G1 arrest defects, dedifferentiation, elevated recombination errors, and age-dependent increase in DNA mutations.

Author(s): 
Madia, Federica
Gattazzo, Cristina
Wei, Min
Fabrizio, Paola
Burhans, William C.
Weinberger, Martin
Galbani, Abdoulaye
Smith, Jesse R.
Nguyen, Christopher
Huey, Selina
Comai, Lucio
Longo, Valter D.
Publication Title: 
FEBS letters

Caloric restriction (CR) is known to effectively elongate mammalian life-spans. The compound 2-deoxy-D-glucose (2DG), which is often used as an inhibitor of glucose utilization, is a mimetic agent of CR. In this study, we examined the changes of telomerase and Werner's syndrome RecQ (WRN) helicase after treatment with 2DG, because of the involvement of recQ helicase in the regulation of telomeres. Interestingly, 2DG treatment increased the expression of WRN protein in accordance with induction of its promoter activity and gene expression.

Author(s): 
Zhou, Bei
Ikejima, Takashi
Watanabe, Takeshi
Iwakoshi, Keiko
Idei, Yohei
Tanuma, Sei-ichi
Uchiumi, Fumiaki
Subscribe to RSS - Werner Syndrome