Brooke the Immortal

Brooke the Immortal

Brooke Greenberg is almost 18, but she has remained mentally and physically at the level of a toddler. She has no hormonal problems, and her chromosomes seem normal. But her development is proceeding "extremely slowly," says Walker. [...] Her body stopped growing when she was two years old. She hasn't grown a centimeter or gained a pound. [...]

The girl's uniqueness lies precisely in the fact that her genetic material seems normal, whereas she is obviously not normal, says the professor. Despite the surprisingly unremarkable genetic analysis, complete chaos prevails inside the girl's body.

Her brain is hardly more developed than an infant's, but her bones have a biological age of about 10 years. Her teeth, including her baby teeth, are like those of an eight-year-old. The length of the telomeres, on the other hand, corresponds to her actual age. In addition, the development of various organ systems, like the digestive tract, is what the professor calls "disassociated." "Different parts of her body are developing at different rates, as if they were not a unit but parts of separate organisms," Walker explains. He believes that there is only one explanation -- a failure of central control genes. [...]

Walker believes that aging is merely the continuation of the body's development. He uses the image of a house to illustrate his point. First the house is built. When it's finished -- or, in the case of the body, when sexual maturity is reached -- the construction crew would normally leave the site. But in normal people the construction workers stay and keep building, according to a plan that's been fulfilled and a construction supervisor who says nothing but nonsense. Soon the crew builds things like contorted bay windows and shaky dormers. Supporting beams are suddenly sawed off, and then walls start falling. Finally the building collapses completely -- and death catches up with the body.

"Aging happens when developmental genes merely run out of meaningful information and subsequently cause chaos," Walker says. His idea is to simply shut off the master genes of development. This, he hopes, will put a stop to the aging process. A body manipulated in this fashion would no longer change, but would only perform repair work. Eternal life would be within reach.

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18 Responses:

  1. Sounds a lot like untreated congenital hypothyroidism.

  2. prog says:

    This reminds me of this recent interview at Wired Science with Aubrey de Grey. A fun read and a good update about what he and his research group have been up to lately.

    (What particularly reminded me was how quickly the author of this news story glommed onto the "omg immortality!!" angle, the sort of thing AdG sighs about in that interview...)

    • duskwuff says:

      What particularly reminded me was how quickly the author of this news story glommed onto the "omg immortality!!" angle...

      Because, of course, this girl has a body in perfect balance that we should all aim to emulate. :)

  3. skywaterblue says:

    I saw this girl on TV and there are no words for how creepy she is. Not herself persay, but the montage of all the family photos was extremely disturbing.

  4. lovingboth says:

    Who has the patent rights, I wonder.

  5. gryazi says:

    Looks like http://www.slideshare.net/tcha163/evans-ageing-2010-5573082 would be interesting to sit through if I weren't at work right now. Or at least, the references below the flashblock icon are.

  6. gryazi says:

    Interview with Dr. Walker over here: http://www.dovepress.com/interview-dr-walker-clinical-interventions-in-aging-d215-j4

    I'm thinking there's some confusion about specificity here - IIRC you can just use a microscope to look for gross defects in chromosomes, while sequencing the whole genome and finding the interesting portion in the diff (if there is one) is quite a bit more work.

    So everything looks good from 1,000 miles up, and "we have looked at her now for many years and have not been able to find a clear-cut defect in her genome." but "We're [still] searching now for the mutation that's causing her condition."

    If they find something, they'll have a good ol' genetic link. If they don't find anything, and/or get lucky and stumble onto something while looking at the regular genetics, it'll have to be epigenetic by definition.

    Although I guess mechanisms for looking for obvious epigenetic stuff ("Hey guys, look at all this methylation/... on the coding for the GH receptor!") are actually pretty well-developed by now, if you can spare the source material to try them and have an idea of where to look.

    (Having been tasked with finding evidence of poorly-defined stupid in 500GB of disk recently, I can sympathize and maybe feel relieved that I never had enough brain cells to get into bioinformatics.)

  7. sclatter says:

    This explanation of how aging works is completely full of crap. What this girl has is a developmental problem, not a failure to age. Despite what this guy is claiming the two aren't really related.

    Correct development to sexual maturity is under strong selective pressure by evolution. Aging is not directly under evolutionary pressure, but only indirectly. This is because normally, in the wild animals are die by misadventure long before they succumb to old age. So there are two models for how genes lead to aging. One is called mutation accumulation, which says that alleles with negative effects at old ages passively accumulate because they are not selected against. The other is called antagonistic pleiotropy which says that some gene alleles that are selected for positive effects in young animals also cause negative effects in older animals. There is evidence that both of these models come into play in the wild.

    There are a number of systems that contribute to aging, and none are what are really considered "developmental genes". Cellular senescence can be triggered by shortened telomeres, DNA damage, accumulated p16INK4a expression. In mammals SIRT1, an NAD-dependent deacetylase, is considered a big player in aging. The old idea that it's all accumulation of oxidative damage from reactive oxygen species has been largely debunked, though.

    (Sorry to nerd out. I'm teaching a class in molecular biology of aging this semester.)