Linking Telomeres and Progerin
Progerin is the mutant form of lamin-A implicated in the accelerated aging condition progeria. It also shows up in normal aging, to a much lesser degree, and here researchers make progress towards understanding why: "Telomeres wear away during cell division. When they degrade sufficiently, the cell stops dividing and dies. The researchers have found that short or dysfunctional telomeres activate production of progerin, which is associated with age-related cell damage. As the telomeres shorten, the cell produces more progerin. ... This study highlights that valuable biological insights are gained by studying rare genetic disorders such as progeria. Our sense from the start was that progeria had a lot to teach us about the normal aging process and clues about more general biochemical and molecular mechanisms. ... the mutation that causes progeria strongly activates the splicing of lamin A [or LMNA] to produce the toxic progerin protein, leading to all of the features of premature aging suffered by children with this disease. But modifications in the splicing of LMNA are also at play in the presence of the normal gene. The research suggests that the shortening of telomeres during normal cell division in individuals with normal LMNA genes somehow alters the way a normal cell processes genetic information when turning it into a protein, a process called RNA splicing. To build proteins, RNA is transcribed from genetic instructions embedded in DNA. RNA does not carry all of the linear information embedded in the ribbon of DNA; rather, the cell splices together segments of genetic information called exons that contain the code for building proteins, and removes the intervening letters of unused genetic information called introns. This mechanism appears to be altered by telomere shortening, and affects protein production for multiple proteins that are important for cytoskeleton integrity. Most importantly, this alteration in RNA splicing affects the processing of the LMNA messenger RNA, leading to an accumulation of the toxic progerin protein."
Link: http://www.sciencedaily.com/releases/2011/06/110613121956.htm
This appears to be a newly-discovered fundamental cause of aging. However, the ultimate problem is the shortening of telemeres, which then causes the RNA disfunction. So therapies that lengthen telemeres should also minimize this destructive process.
It would be inhuman to not fight against the aging process!
All progress in life is basically just organisms trying to live as long as they can, which is why any organism eats, gets stronger, learns things, etc!
It's all just to live longer!
Reaching for escapes from death is the most "human" thing we can possibly do! We must do it with 100% urgency until we reach that goal! Any death is a just a big failure!