LONGECITY

I am going to ask folks to review this Dateline clip. This reflects a heretofore unknown condition where a child has not aged physically past 6 months in her twelve years of life. I apologize that it is the NBC Dateline show and in some respects barely more credible than the National Enquirer IMHO but if confirmed I consider it too significant to ignore.

Baby Frozen in Time

Supposedly they have done a genetic analysis and found no anomalies. Considering this child has been studied at John's Hopkins and Sloane Kettering among other institutes I would think there may be some professional studies out there that merit review. It is said that no one understands what is happening to her so please feel free to speculate so long as it is a scientific based speculation.

This child's condition is debilitating as there are serious complications with this type of arrested development, including and not the least of which is that her mind has not progressed past the same six months of development her brain is locked into.

However like the studies of Werner's Syndrome and Progeria that are now yielding some genetic results of importance ( Lamin A gene, SGS1 WRN ) I suggest that this *abnormal* condition is one that deserves some attention by us.

I have put this topic here because I suspect the followup should focus on the scientific aspects and not be simply a general discussion although I do encourage some open speculation on the subject because this is apparently an uncharted area.

For example please take a moment to consider the importance of this poor child's infirmity to us if we are looking at a series of genes that have never been turned on to trigger normal development that might also hint at a genetic switch that could be theoretically turned *off* at a more advantageous period in life.

The same *switch* that could allow her to grow might have more important ramifications obviously. It is no panacea and doesn't address the other more important aspects of cellular senescence but the possibility that a genetic switch (or some other mechanism) could possibly arrest total physiological development is too important to ignore IMHO.

Also I think it has reached a point were it would be beneficial if we began a listing and links page for every related protein and gene that has been discovered and confirmed with respect to aging, perhaps even a few of those just suspected.

Perhaps even our own informal relational map of how where they sequence on the human genome.

There are no grounds to speak of aging (in any of the commonly used definitions) based on the data that has been reported in this case. What has been reported is, like you say, a developmental defect, and there is no reason whatsoever to believe that this might have anything to do with what happens to us in our later decades of life. In particular, there is no reason to believe that this girl will not suffer from aging just like we do if she lives to be old enough.

I agree -- there seems to be some confusion in semantics here. Aging in the sense of development is not the same as aging in the sense of senescence. Although I have read of research showing that adults who had suffered from some underproduction of HGH during childhood have shown slightly elongated telomeres, due to their cells not having undergone a full number of cell divisions.

I agree that we must be cautious about the common misuse and misunderstanding of the word and processes of aging but that wasn't actually the focus I was trying to encourage. I also clearly understand this is a developmental defect and I doubt seriously that cellular senescence is actually slowed but I would be curious about a number of aspects of that question and that is why I was interested about how much of the actual case history is out there in the web.

What concerns me more is what I suspect is the *genetic switch* involved and let me clarify why. Recently breast cancer for example was linked to just such a switch that may *turn off* later in life.

Gene 'switches off' breast cancer

I am curious if a similar process but extremely rare anomaly essentially turned off during prenatal development. We can presume from the description of the developmental problems that the problems for this child began in the womb but it may be that understanding how such developmental problems begin also can allow a whole host of new interventions later in life to essentially counter act the effects of cellular senescence in the manner that may soon be possible with Breast Cancer.

Moreover I suspect that in the ESC debate it may be possible to hijack the developmental process in vitro by simply manipulating just such switches (probably similar in approach to the current suggestion) and then by controlling a series of system and specific switches to actually culture DNA organ tissues directly and perhaps even assemble organs in vitro.

What I am suggesting can be better understood from this case and maybe learned is where the more generalized *system switches* are. I think we are looking at two types of genetic switch (there are most probably more) one that controls whole systems of development and others that control very specific functions.

In this particular case there have been a number of very serious developmental defects that have debilitated the child and were seriously detrimental but I still wonder if there is a way to use this advantageously at other periods of life?

When is development over?

At the end of puberty?

At the end of menstruation?

While I agree that we are talking about development stages here I am also suggesting that it is invalid to just ignore *development* when talking about aging. Some aspects of development are directly related to aspects of aging. Speaking of which do you have some support for this manofsan?

Although I have read of research showing that adults who had suffered from some underproduction of HGH during childhood have shown slightly elongated telomeres, due to their cells not having undergone a full number of cell divisions.

It sounds familiar to me but it is unclear how the process would work except as retarded growth. However I am curious. But my curiosity is what if we could selectively deter some systems in favor of others that would prolong the development of longer telomers or ones more resistant to shortening?

What if we could find the mechanism that allows the oocyte to mass produce mitos after fertilization and then create replacement mitos in vitro that can be reinserted to the body's cells through protofection?

BTW I am still interested in why we can't redesign the mitochondria since its genome is far simpler than taking the more radical approach that SENS depends on of moving the function into the nuclear DNA?

Alright this last question deserves its own thread and doesn't really belong here but I still think it is worth asking.

A more appropriate question for this thread is:

Are we sometimes confusing gene switching for mutation; especially in the case of certain common cancers like breast and prostate?

The Role of Methylated BRCA1 in Breast Cancer


'Start of life' gene discovered

Scientists complete map of human genetic variation
http://news.yahoo.co...ience_hapmap_dc

Nature Article and other resources on the HAPMAP
http://www.nature.co...nome/index.html

http://www.genome.gov/11511175

Yahoo News about DNA Map


HAPMAP Home

BTW I have a suggestion for a Methuselah Mouse experiment involving this hypothetical switch (if such a switch mechanism is discovered).

What if it is possible to switch off development at a more opportune developmental stage (for example during mid adolescence) and allow a mouse to sustain that level of physical plasticity for a far longer period?

Is there a commensurate cellular resistance in late puberty, one that includes not
merely healing from damage but immunity?

Is this idea of genetic switching also leading to better understanding why certain viral infections like mumps and herpes zoster have such different impacts physiologically depending upon whether they strike early or late in life?

Hi Laz, I don't immediately have any links on the longer telomeres thing, but I will look for some to post.

Hmm, but are you suggesting that we somehow manipulate the natural growth cycle to try and stave off aging?

I once read that Neanderthal children reached full body size much earlier in life than homo-sapiens do. Would this have been a survival strategy purely for coping with environmental threats like predators, or could there have been some senescence-related advantage to this?

You yourselves have pointed out to me that aging is partly the result of cessation of the rapid cell division which was allowing the body to outrun the effects of lipofuscin accumulation. Therefore, shouldn't optimal pacing of cell division across time be chiefly dictated by the need to maintain mitochondrial quality and to stave off lipofuscin accumulation and its oxidative effects?

Anyway, here is an interesting news link about stem cells continuing to repair heart walls years after implantation:

http://www.betterhum...03/Default.aspx

what if we could selectively deter some systems in favor of others that would prolong the development of longer telomers or ones more resistant to shortening?

That's the general idea. We have to wait for someone to do the lab work.

why we can't redesign the mitochondria since its genome is far simpler than taking the more radical approach that SENS depends on of moving the function into the nuclear DNA

Eminently more sensible. We can and we should. Once more it is a matter of lab work.