The problem we have to solve is cellular aging, especially with regards to Alzheimer's and other conditions. When DNA replicates from 5` to 3`, safety sequences of DNA known as telomeres get lost. This is a normal function of cell division, and causes aging, as when there are fewer telomeres available, the cell's "clock" keeps getting shorter.
The enzyme telomerase is responsible for keeping these in check. However, humans have very little telomerase.
The issue at hand is that if we present more telomerase, and thus extend the replication life of body cells, proofreading and repair mechanisms to repair illegal sequences caused by incorrect ligase bonding of Okazaki fragments may not be effective, as the statistical probability of errors increases. The other issue is that we don't know what can happen with an infinite telomerase supply. There could be ramifications on a molecular level that could be impossible to cure. Frameshifts, substitution errors -- there are an entire host of things to go wrong.
It's a long road to immortality. As no scientific data was published in the article, I'm not sure what exactly the girl has that causes her an inability to age. The only information given was obvious. Judging by her facial features, she seems like she has more of a growth disorder rather than a cellular stoppage of aging. If the latter were the case, she would still look very much like an infant, and would behave the same way as well.
That is a rather simplistic take on the problem of aging. I suggest you look up Aubrey de Grey and take a look at his work. I recall a telomerase + cancer gene activation therapy being successful in mice in the last year. Might even benefit myself later.
(rephrased from wikipedia) de Grey's list of seven problems is:
1. Mutations in chromosomes
2. Mutations in mitochondria
3. Junk inside cells
4. Junk outside of cells
5. Non-replaceable cells dying
6. Cell immortality (yes, this is a problem too)
7. Extracellular protein crosslinks
His contention is that we should approach the problem with engineering. Makes sense to me, sounds so Agile and Lean ;)
Are you aware of an accessible rebuttal to the list given in the parent comment? I'd like to know why biologists are skeptical of this direction of anti-aging research. Is it because AdG shows some fundamental misunderstanding of cellular biology? Could it be for political reasons?
My guess is that these cases are dysfunctions with aspects of the growth / maturation process, rather than outright stoppage of aging. If you look up images of Nicky Freeman, the 40-year-old referenced in the article who "looks like a 10-year-old", he in fact looks more like a 40-year-old with the size and stature of a 10-year-old:
I shudder to think a nydailynews.com article has made it to the top of HN. It's shock journalism with little information. You really don't need to read past two sentences to get the content of the whole article.
The site is pulling css and javascript over http instead of https - I've seen this too often to count, why aren't the webmasters fixing it? Are they using old browsers?
Aging is a complex process, which exists because evolutionary pressure decreases once an organism has lived past its reproductive lifespan. There is not one source of damage that leads to aging, or a small number of genes that lead to aging. Many things start going wrong in the body because there is no evolutionary, selective pressure for the problems to be fixed.
There is not a single gene that if mutated will lead to immortality. This girl will eventually die; her body will not last much beyond the average lifespan of a normal human. This is because all the other genes in her body have never been selected for to work past the range of a normal human lifespan.
The Hayflick limit only applies to healthy individuals (and their tissues) with no change in activity of the telomerase enzyme. If the girl exhibits her appearance because of a telomerase mutation, she is not subject to the normal apoptosis condition.
Isn't it conceptually just like a counter which effectively turns off the cell copying after enough copies are being made? Before the limit is reached, the length of telomerase doesn't influence the quality of the copying. I don't see how it has anything to do with 8 year old looking as one year old. That has to do with gene expression, not with the limit of cell copies. But the limit of the cell copies will limit the length of her life, if I understand? And that's only one of probably many built-in expiration dates we have.
If something is wrong with her telomerase activity she will be extremely prone to carcinogenesis.
Remember that a cell has to accumulate many mutations in order to become cancerous. One of the most important aspects of cancer is that its cells are immortal. The cells of a normal person have to overcome this barrier in order to become cancerous so that, if her cells are indeed changed as you postulated, turning into cancer cells will be much easier for them.
Really interesting article - I doubt she will hold "the key" to practical immortality, but researching her case may allow us to reverse engineer one or more of the many processes that contribute to aging.
I recently wrote a blog post on practical immortality that presents several arguments for age being a curable disease, and breaks down the things we'd need to do to cure the disease of age.
As we prevent more natal deaths due to better healthcare we also allow more mutated gene pool to survive. The by product of our medical advances hold the key to our evolution.
Right now I would be perfectly happy living to something like 75, but not having any ill effects on my health and mind as I age. Immortality seems like too long a time (although of course I could eventually end my own life).
I guess genetics is the new 'vehicle' to the fountain of youth. Plants, alchemy, ships, industrialization, computers, and now genetics. Seems like our quest moves further away from myth with each cycle. Albeit, when you have an infinite distance to travel even objectively large movements like these are insignificant.
The enzyme telomerase is responsible for keeping these in check. However, humans have very little telomerase.
The issue at hand is that if we present more telomerase, and thus extend the replication life of body cells, proofreading and repair mechanisms to repair illegal sequences caused by incorrect ligase bonding of Okazaki fragments may not be effective, as the statistical probability of errors increases. The other issue is that we don't know what can happen with an infinite telomerase supply. There could be ramifications on a molecular level that could be impossible to cure. Frameshifts, substitution errors -- there are an entire host of things to go wrong.
It's a long road to immortality. As no scientific data was published in the article, I'm not sure what exactly the girl has that causes her an inability to age. The only information given was obvious. Judging by her facial features, she seems like she has more of a growth disorder rather than a cellular stoppage of aging. If the latter were the case, she would still look very much like an infant, and would behave the same way as well.