10 replies to this topic

[Danail Bulgaria]

I remember, that in one of the topics in this forum, I red about a girl, who doesn't age. I think, that I found a video of another such case. However, on the video they do not speak english, so I do not know from it, if she has had medical problems. The patient again is a girl, according to the video she is 20 years of age and does not develope. She also has some deformaties of the face, even though the defects of the girl, who I found are not so strong.

Here is the link from YouTube:

[Bonee]

i don't think she will be able evade other signs of ageing like atherosclerosis and the build up of non functional proteins by AGEs

[Danail Bulgaria]

There was another girl like that, very simmilar to this one, that was discussed some time ago. I managed to find a link to the video about her too. Maybe these girls will not evade atherosclerosis and the non functional proteins build up, but what we see here is definatelly a genetics, that holds the organism in one speciphic age. It is very likely that some mutation has happened in this girl's genome, and perhaps this mutation has happened whlie she was an embryo, and this is why this girl to have a stopped development after her birth. According to me it is very important for us to understand what exactly was this mutation before these girls die for one reason or another. Ofcourse, genetics may find nothing interesting, but imagine if genetics find a gene, that when damaged stops a large number of aging changes in the age at which it is damaged. Moreover, I found a video about a boy, whose "aging" was stopped when he was five years old. Why not suppose, that the same gene was damaged in his genome, when he was a five years old. Appeares the question what if the gene is found and what if it is possible to destroy it at the age of 30 - 40 -50? Will a 50 years old will never develope many aging changes whan he becomes 80 years old?



Here is the video about the boy, who do not age after his fifth year of age.

[Bonee]

i think the problem is there are no fundamental changes after some is like 20-25 years old, the bones mature, the brain mature etc, then comes the accumulation of trash what we call "becoming older"

[AgeVivo]

thinking/knowing/deducing/referring to something.

I think... it is interesting and could be linked to ageing. Sometimes specific cases are the key to uderstand the global picture. Who knows...

[AgeVivo]

the video in the top of the thread is in Portuguese, I understand it. The medical doctor says she likely has a thyroid hormon deficiency.

Perhaps in a couple of years, when full genome sequencing will become much cheaper, some researcher will sequence the genome of the parents and those babies, to see what could be the culprit(s) => to be thought about in a few years

Edited by AgeVivo, 17 August 2012 - 08:20 PM.

[Danail Bulgaria]

It is a pitty, that a genetics researchers do not have interest for these children at this moment. Some researchers have been researching different accelerated aging diseases and the genes, that provoke these diseases and their localisation are already known. Do You think, that they will find it interesting to find the genes, responsible for this "not growing" disease?

[niner]

i think the problem is there are no fundamental changes after some is like 20-25 years old, the bones mature, the brain mature etc, then comes the accumulation of trash what we call "becoming older"

That's just when it starts becoming noticeable. The damage begins to accrue in the womb. Small children show evidence of UV damage to skin, for example, and the beginnings of atherosclerosis can be seen in some teenagers. Most telomere loss occurs in the early years of life. Aging does accelerate late in life when certain forms of damage lead to higher rates of accumulation of other forms of damage, in an ever-increasing spiral.

Do You think, that they will find it interesting to find the genes, responsible for this "not growing" disease?

Yes, I think that it will eventually be understood when development is fully understood. Someone should get a DNA sample from these people and sequence it. It might provide some insight into normal development, and might even lead to a work-around that would allow them to continue developing.

[Veritas C. & E.]

There needs to be a clear distinction between development and aging. These kids don't develop, but they do age.

Think of aging as the damage from time (an alteration of nature) and think of development as metamorphosis (a change of nature).

We don't want to fight development, we want to fight aging.

[ihatesnow]

http://gma.yahoo.com...ews-health.html

[lemonhead]

Thanks for the link, ihatesnow.
I hadn't heard of the 'developmental inertia' theory before so I looked it up in PubMed and found this (unfortunately, not a free article):

PMID: 21767161 Rejuvenation Res. 2011 Aug;14(4):429-36. doi: 10.1089/rej.2011.1162. Epub 2011 Jul 18. Developmental theory of aging revisited: focus on causal and mechanistic links between development and senescence. Walker RF.
Abstract
Senescence violates the most basic tenet of natural selection by causing death rather than individual survival. Thus, current theories favor the concept of antagonistic pleiotropy (AP) to explain how aging emerged in metazoans. Presumably, pleiotropic genes reduce vigor and limit longevity in adults. However, they also promote fitness and reproduction in juveniles, causing them to be selected and retained in the gene pool. The general hypothesis presented herein is a special case of AP that identifies the common cause and mechanism of aging in iteroparous (i.e., capable of reproducing multiple times) animals. It ascribes senescence to unremitting, nonprogrammed change or remodeling forced upon the adult soma by postmaturation expression of developmental gene(s) affecting dynamic transformation of the single-celled conceptus into a complex, multicellular organism. Whereas persistent somatic change is necessary for development to proceed normally, it also has the potential to erode homeostasis in adults after maturation is complete. Thus, developmental inertia is the primary cause of senescence, whereas decay of internal order and integrated function among interdependent systems of the body is the general mechanism by which aging progresses over time. Accordingly, this global pathogenic process creates an environment in which the many recognized, age-associated physiologic and metabolic sequelae can arise as consequences of senescence rather than causes of it. Paradoxically, the genes that promote somatic remodeling essential for development and survival also guarantee aging and death by the same action whose outcomes differ only by the time it is expressed relevant to maturation.

Edited by lemonhead, 21 August 2013 - 02:00 AM.