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Winning the Mprize


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#1 richardschueler

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Posted 14 October 2007 - 01:06 AM


From watching the sens3 conferences, I've come the the conclusion that it's GREAT to be a mouse. The number of diseases cured in mice, and the great brain surgery, and the great nanotech hemostat, and all kinds of really amazing technolgoy to make healthy long living powerful mice.

This leads me to 2 conclusions. 1. It should be pretty easy to win the mprize as it currently stands by finding 2 strategies which don't overly rely on the same factors, combine them, and you'll have the oldest mice yet. Perhaps calorie restrcition plus growth hormone gene knockout (yeah, i picked 2 that work simlar functions...the panel to choose from in my mind is quite small right now.)

If it's true that it would be pretty easy to wint he mprize as it currently stands, then I assume the reason more people aren't trying is because it's not a good profit for them? The cost of making such mice exceded the ammt of prize they'd receive?

How much did it cost the last mprize winner to win, and how much was his profit?

Until I understand the economics of the research and implementation vs the profit of the prize it's hard for me to bring on science teams and investors...

P.S. was there a better forum to post this in?

#2 niner

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Posted 14 October 2007 - 04:09 AM

There's a lot of stuff that works better in mice than people. Oh well. I wish that the MPrize was designed to be more applicable to humans. The knockouts may well give us some amount of improved understanding, I know, but it's not like we can easily apply them to ourselves. Sorry for the OT semi-rant...

#3 John Schloendorn

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Posted 14 October 2007 - 05:18 PM

The economics are currently far away from making any scientist do something they weren't going to do anyway. This is in part due to the formula that lets you win only a fraction of the pot for incremental achievements. On the other hand, this design has allowed repeated press releases when somebody won, which an all-or-nothing design would not have allowed. The current design is consistent with the Mprize being a message, more than a research incentive. It's real value is that people can show their face and say, yes I want aging cured, and I want it enough to give a few bucks. When this is done by not hundreds, but millions of people, there will also be enough cash to inspire scientists, as a side-effect...
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#4 Avatar of Horus

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Posted 29 May 2013 - 02:35 AM

... one of the Methuselah Mouse Prize winning was achieved by the manipulation of the growth hormone thing, with a "Growth Hormone Receptor Gene Knockout transgenic mouse"; the second one on the MPrize web page:
http://www.mprize.or...j_mprize_record

Life extension in the dwarf mouse
Bartke A, Brown-Borg H.
Curr Top Dev Biol. 2004;63:189-225.
Geriatrics Research, Department of Medicine, Southern Illinois University School of Medicine, Springfield,
Illinois, USA.
http://www.ncbi.nlm....pubmed/15536017
Abstract
Ames dwarf mice and Snell dwarf mice lack growth hormone (GH), prolactin (PRL), and thyroid-stimulating hormone (TSH), live much longer than their normal siblings, and exhibit many symptoms of delayed aging. "Laron dwarf mice," produced by targeted disruption of the GH receptor/GH-binding protein gene (GHR-KO mice), are GH resistant and also live much longer than normal animals from the same line. Isolated GH deficiency in "little" mice is similarly associated with increased life span, provided that obesity is prevented by reducing fat content in the diet. Long-lived dwarf mice share many phenotypic characteristics with genetically normal (wild-type) animals subjected to prolonged caloric restriction (CR) but are not CR mimetics. We propose that mechanisms linking GH deficiency and GH resistance with delayed aging include reduced hepatic synthesis of insulin-like growth factor 1 (IGF-1), reduced secretion of insulin, increased hepatic sensitivity to insulin actions, reduced plasma glucose, reduced generation of reactive oxygen species, improved antioxidant defenses, increased resistance to oxidative stress, and reduced oxidative damage. The possible role of hypothyroidism, reduced body temperature, reduced adult body size, delayed puberty, and reduced fecundity in producing the long-lived phenotype of dwarf mice remains to be evaluated. An important role of IGF-1 and insulin in the control of mammalian longevity is consistent with the well-documented actions of homologous signaling pathways in invertebrates.

and

The endocrine regulation of aging by insulin-like signals
Tatar M, Bartke A, Antebi A.
Science, 2003. Feb 28;299(5611):1346-51.
Department of Ecology and Evolutionary Biology, Brown University, Providence, RI 02912, USA.
http://www.ncbi.nlm....pubmed/12610294
Abstract
Reduced signaling of insulin-like peptides increases the life-span of nematodes, flies, and rodents. In the nematode and the fly, secondary hormones downstream of insulin-like signaling appear to regulate aging.
In mammals, the order in which the hormones act is unresolved because insulin, insulin-like growth factor-1, growth hormone, and thyroid hormones are interdependent. In all species examined to date, endocrine manipulations can slow aging without concurrent costs in reproduction, but with inevitable increases in stress resistance. Despite the similarities among mammals and invertebrates in insulin-like
peptides and their signal cascade, more research is needed to determine whether these signals control aging in the same way in all the species by the same mechanism.






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