[extropy-chat] [fwd] Werner's Syndrome Mice

[Joao Magalhaes]

Hi,

I've read the paper and these animals do not display such a marked 
accelerated aging phenotype as do human patients with WS. Therefore, the 
possibility exists that Werner Syndrome mice suffer from accelerated 
pathology rather than accelerated aging, a bit like it appears to happen in 
the Lamin A mutant mice. The reference for the LMNA mutants:

Nikolova V, et al (2004) Defects in nuclear structure and function promote 
dilated cardiomyopathy in lamin A/C-deficient mice. J Clin Invest 113:357-69.

Actually, WRN appears to interact with at least 17 other proteins 
(http://genomics.senescence.info/genes/entry.php?id=13). On the issue of 
protein interactions and aging, there was a fun paper by Daniel Promislow 
arguing that proteins more likely to be involved in aging are the ones with 
the higher connectivity--that is, with the higher number of protein-protein 
interactions. The reference is:

Promislow DE. Protein networks, pleiotropy and the evolution of senescence. 
Proc R Soc Lond B Biol Sci. 2004 Jun 22;271(1545):1225-34.

His ideas are a good complement to my own recent paper:

de Magalhães, JP and Toussaint, O (2004) "GenAge: a genomic and proteomic 
network map of human ageing." FEBS Letters 571(1-3):243-247.

Lastly, those of you interested in telomeres and telomerase as a way to 
delay aging may be interested in another recent paper of mine:

de Magalhães, JP and Toussaint, O (2004) "Telomeres and telomerase: a 
modern Fountain of Youth?" Rejuvenation Research 7:126-132.

All the best,

Joao


---

Joao Pedro de Magalhaes, PhD

Harvard Medical School, Dept. of Genetics
Avenue Louis Pasteur, 77, Room 238
Boston, MA 02115
Telephone: 1-617-432-6550

http://www.senescence.info