The Quotes are Powered By Forexpros, the Forex, Futures, and Stock Markets Portal.

Competitiveness / Healthand Welbeing



Swedish Research: New findings may stop the early aging

Friday, 17 May 2013
Progeria otherwise know in as HGPS (Hutchinson-Gilford Progeria Syndrome) an extremely rare, fatal genetic condition which affects children and gives them an appearance of accelerated aging seems to be opening up to the route of cure led by researchers in Sweden.
Researchers from Sahlgrenska Academy at the University of Gothenburg believe in their findings that Pharmaceuticals that inhibit a specific enzyme may be useful in treating progeria, or accelerated aging in children. A new study performed at the Sahlgrenska Academy indicates that the development of progeria in mice was inhibited upon reducing the production of this enzyme.

Therefore the researchers have identified a mechanism that blocks an enzyme associated with accelerated aging according to their finding published today in the journal Science.

"This study is a breakthrough for our research group after years of work," said senior author Martin  Bergö in a news release. "When we reduce the production of the enzyme in mice, the development of all the clinical symptoms of progeria is reduced or blocked."

The disease is very rare and not hereditary. Only a few hundred children worldwide are affected. Researchers in Gothenburg are now cooperating with a university in Singapore that has developed two possible medications, according to Swedish media reports.

More about Progeria and the research

Progeria is a rare genetic childhood disorder characterized by the appearance of accelerated aging. The classical form of progeria, called Hutchinson-Gilford Progeria Syndrome (HGPS), is caused by a spontaneous mutation, which means that it is not inherited from the parents.

The progeria mutation occurs in the protein prelamin A and causes it to accumulate in an inappropriate form in the membrane surrounding the nucleus. The target enzyme, called ICMT, attaches a small chemical group to one end of prelamin A. Blocking ICMT, therefore, prevents the attachment of the chemical group to prelamin A and significantly reduced the ability of the mutant protein to induce progeria.

"We are collaborating with a group in Singapore that has developed candidate ICMT inhibitor drugs and we will now test them on mice with progeria. Because the drugs have not yet been tested in humans, it will be a few years before we know whether these drugs will be appropriate for the treatment of progeria," Martin Bergö explains.

Although there are only a few hundred children in the world with progeria, the disease, children, and research have attracted a great deal of attention.

"The reason is obvious: the resemblance between progeria patients and normally-aged individuals is striking and it is tempting to speculate that progeria is a window into our normal aging process. The children develop osteoporosis, myocardial infarction, stroke, and muscle weakness. They display poor growth and lose their hair, but interestingly, they do not develop dementia or cancer," says Martin Bergö, who is also studying the impact of inhibiting ICMT on the normal aging process in mice.


  • Mohamed X. Ibrahim, Volkan I. Sayin, Murali K. Akula, Meng Liu, Loren G. Fong, Stephen G. Young, and Martin O. Bergo.(2013) Targeting Isoprenylcysteine Methylation Ameliorates Disease in a Mouse Model of Progeria. Science, 16 May 2013.
  • Swedish Television
  • Sahlgrenska Academy

Print Friendly and PDF