Can a cure for Progeria syndrome lead to the "fountain of youth"?

Answer 1

Hyaluronic Acid
Can It Prevent Premature Aging?
http://www.ctds.info/hyaluronic_acid.html




Finding the Fountain of Youth

One of the lures of aging research is of course to find a fountain of youth—an elixir that prolongs life. Although several commercial entities are unleashing their resources at this tempting goal, given the inconclusive nature of most molecular aging pathways currently under consideration, these efforts seem unlikely to come to fruition in the near future. However, therapeutic intervention may be realistic for premature aging disorders as their molecular basis is becoming well defined. The feasibility of anti-aging intervention is made clear in the case of HGPS. Since the discovery of its genetic cause less than two years ago, at least two fascinating, yet realistic, strategies of molecular treatment have been opened. The first is based on correcting the primary defect at the level of pre-mRNA. This strategy involves correcting the aberrant splicing event caused by the HGPS mutation (Box 1). Proof of principle that this is possible has recently been provided by introduction of small oligonucleotides specifically targeted to the HGPS splice site, preventing its use and restoring normal splicing and cellular behavior [14]. If these results from cell culture experiments can be extended to organisms, they might provide a promising avenue of intervention. A second potential therapeutic approach for HGPS is founded in the complex post-translational processing of the lamin A protein by farnesylation (Box 1). Inhibitors of the farnesylation reaction, so called farnesyl transferase inhibitors, have recently been developed as potential cancer therapeutics and might also be effective in HGPS. The hope would be that these inhibitors will decrease the amount of harmful farnesylated pre-progerin in the cell and thus alleviate cellular HGPS symptoms. Fortunately, ongoing clinical trials on farnesyl transferase inhibitors show little toxicity, and early studies in cell culture have already shown a reversal of some of the cellular defects associated with HGPS [15–18].

The story of HGPS is an impressive example of the interplay of basic and clinical science. It is also a showcase for how modern biology deals with disease (Figure 2). Within less than two years, we have gone from only knowing the symptoms of the disease to identifying the disease-causing gene and learning much about how the mutant protein behaves in patient cells. The challenge ahead is to close the circle and to apply what we have learned about the cell biology of this disease to the development of therapeutic approaches. The insights from HGPS have also opened an entirely new and fascinating vista on the aging process. Who would have guessed two years ago that architectural elements of the cell nucleus might contribute to aging? These advances have put us in the rare and desirable situation of possibly being able to making significant steps towards understanding one of the most fascinating problems in biology—and at the same time do some good for patients and their families
http://www.imminst.org/forum/index.php?act=ST&f=44&t=11061&s=
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1283398
http://biology.plosjournals.org/perlserv?request=get-document&doi=10.1371/journal.pbio.0030395

http://www.sanzone.net/clients/primedia/antiaging/articlescode.asp?articleID=229

If You Could Live Forever
http://query.nytimes.com/gst/fullpage.html?res=9B05E4DC1F31F93BA35755C0A9659C8B63

Answer 2

Not in near future.