I actually don not agree with xEva, that we live longer as old people than as young. The average life length of the people in the developed countries is about 80 years. If it is true, that we start to age at 40, then we averagely live as young the same time as we live old. If it is true, that the aging starts in the 50s or 60s then we live longer as young, rather as old.
I've heard some aspects of cardiovascular aging can be seen even in children. Noticeable external skin changes related to aging can start to be seen even in teens, though they tend to become more noticeable in mid-to-late 20s. Functional changes in certain organs related to aging can be slowed, halted and even reversed, though not all changes obviously.
Is this kind of aging dew to bad mitochondria or telomere shortening ?
Some types of progeria appear to be due to a defective nuclear lamin protein, called lamin A that has been affected by a mutation and the mutated form is called progerin, it appears it accumulates and it can affect nuclear structure and function.
No treatment is available, compatriot. Ashes to ashes and dust to dust!
By the way, no pharmaceutical company will make the effort to find the drug for so small number of patients.
One of the papers I linked elsewhere seemed to suggest that rapamycin was being considered or had shown some promise.
Here's a quick news article regarding it
n this latest study, Rapamycin was used on children with HGPS (Hutchinson-Gilford Progeria Syndrome), a devastating genetic condition in which the child ages quickly and reaches old-age by the time they are 12 years old. The accelerated aging is caused by an accumulation in every cell in the body of a protein called Progerin.
The scientists explained that Rapamycin got rid of the progerin in the cells, leaving them healthy.-link
The question is how strong does Rapamycin interact with mtor? Would prolonged protein restriction with intervals of adequate protein intake, be less strong, as strong, or stronger?
Mtor inhibition appears to be an extremely potent intervention. Some inactivation can reduce protein synthesis by more than 20%. It boosts autophagocytosis(recycling), reduces protein synthesis and appears to engage other mechanisms that increase resistance to stress. It appears to interact with mitochondrial function. Mtor inhibition has also been suggested to inhibit cells from becoming senescent and keeping those that already are senescent cells from expressing the senescent phenotype(if this is so, in my opinion it would be as if the cells were no longer there.). The recent scientific american magazine(I think it was january 2012 issue) has an overview article on mtor.
One of the nice things is that what is said to appear to kill many supercentenarians in most cases is some form of abnormal protein accumulation disease
"The superseniors deviate from the norm not just in how long they live but in how they die," says Coles, who arranges autopsies of the oldest old as part of his work with the recently established Supercentenarian Research Foundation. Only nine Supercentenarians have undergone postmortems -- Calment, for example, never agreed to one -- and Coles and colleagues have performed six of these procedures, including one earlier this year in Cali, Colombia, on a man who died at age 111.
Coles argues, based on these autopsies, that supers aren't perishing from the typical scourges of old age, such as cancer, heart disease, stroke, and Alzheimer's Disease. What kills most of them, he says, is a condition, extremely rare among younger people, called senile cardiac TTR Amyloidosis. TTR is a protein that cradles the thyroid hormone thyroxine and whisks it around the body. In TTR Amyloidosis, the protein amasses in and clogs blood vessels, forcing the heart to work harder and eventually fail. "The same thing that happens in the pipes of an old house happens in your blood vessels," says Coles.-link
If you drastically slow protein synthesis, increase the rate of recycling via autophagocytosis, and modify cellular function to resist damage. It seems like with such intervention
the wall limiting the supercentenarian lifespan barrier could hypothetically be broken.
Edited by steampoweredgod, 19 February 2012 - 02:03 AM.
