The Economist recently published a video interview on pushing the limits of human ability in light of the 2012 London Olympic Games. Watch an interesting discussion on the limits of human ability and what it would take to surpass them.
The
Top Genetic Enhancements already done in mammals
Whether
we are talking about making people smarter or stronger or able to fly
or whatever, we are talking about making changes to the complex
systems that underpin human ability. Below is a quick canter through
the top genetic enhancements that have already been done in mammals
(and hence could presumably be done in humans).
1.
The Doogie Mouse. Better memory through over expression of NMR2B. A
very simple, yet good demonstration of how plastic our memory system
is. Since then several other ways of enhancing memory genetically
have been found, with slightly different effects on different types
of memory, forgetting and side effects.
Tan,
D. P., Q. Y. Liu, et al. (2006). "Enhancement of long-term
memory retention and short-term synaptic plasticity in cbl-b null
mice." Proceedings of the National Academy of Sciences of the
United States of America 103(13): 5125-5130.
2.
Color vision mice. Adding human photo pigment allows (at least
females) to see new colors. This is extra interesting since it shows
the brain can adapt to the signals from a new sense, at least when
growing up with it.
Gerald
H. Jacobs, Gary A. Williams, Hugh Cahill, Jeremy Nathans, Emergence
of Novel Color Vision in Mice Engineered to Express a Human Cone
Photopigment, Science 23 March 2007: Vol. 315. no. 5819, pp. 1723 -
1725
3.
Methuselah mice. By reducing growth hormone levels long-lived dwarf
mice can be produced. The current record holder survived 4 years 11
months and 3 weeks, while normal mice have a two year lifespan.
A.
Bartke, H. Brown-Borg, J. Mattison, B. Kinney, S. Hauck, C. Wright,
Prolonged longevity of hypopituitary dwarf mice. Exp. Gerontol. 36,
21-28 (2001) Bartke A, Brown-Borg H. Life extension in the dwarf
mouse. Curr Top Dev Biol. 2004;63:189-225.
4.
Monogamous voles. Normally non-monogamous voles can be turned
monogamous (and more social) by changing the vassopressin V1a
receptor.
Lim
M. M., Wang Z., Olazábal D. E., Ren X., Terwilliger E. F. and Young
L. J. 2004 Enhanced partner preference in a promiscuous species by
manipulating the expression of a single gene. Nature 429, 754–757.
5.
Regenerating MRL mice (OK, a case of accidental breeding rather than
genetic engineering, and it involves at least 20 genes). These mice
regenerate holes punched in their ears as well as some injuries to
heart muscle.
Schuelke
M, Wagner KR, Stolz LE, Hubner C, Riebel T, Komen W, Braun T., Tobin
JF, Lee SJ. Myostatin mutation associated with gross muscle
hypertrophy in a child. N Engl J Med 2004: 350: 2682–2688.
Lee
SJ (2007) Quadrupling Muscle Mass in Mice by Targeting TGF-ß
Signaling Pathways. PLoS ONE 2(8)
6.
The hard working monkeys. Work discipline through a blocked dopamine
D2 gene. Monkeys tend to slack off until they get close to a reward
they have to work for. If injected with a DNA construct that blocks
the D2 receptor they worked at an even rate. This is likely less a
case of workaholism and more a case of specific memory impairment for
how rewarding situations look. Still, adjusting the dopamine system
is likely to enable boosts of motivation.
Zheng
Liu, Barry J. Richmond, Elisabeth A. Murray, Richard C. Saunders,
Sara Steenrod, Barbara K. Stubblefield, Deidra M. Montague, and
Edward I. Ginns, DNA targeting of rhinal cortex D2 receptor protein
reversibly blocks learning of cues that predict reward, PNAS August
17, 2004 vol. 101 no. 33, 12336–12341
7.
Anticancer mice. These mice (the result of a lucky mutation) have
immune systems that kill cancer cells efficiently and can even help
other mice through blood transfusions.
Cui
Z, Willingham MC, Hicks AM, Alexander-Miller MA, Howard TD, Hawkins
GA, Miller MS, Weir HM, Du W, DeLong CJ. Spontaneous regression of
advanced cancer: identification of a unique genetically determined,
age-dependent trait in mice. Proc Natl Acad Sci U S A. 2003 May
27;100(11):6682-7.
Hicks
AM, Riedlinger G, Willingham MC, Alexander-Miller MA, Von Kap-Herr C,
Pettenati MJ, Sanders AM, Weir HM, Du W, Kim J, Simpson AJG, Old LG,
Cui Z. Transferable anticancer innate immunity in spontaneous
regression/complete resistance mice. PNAS E-published May 8, 2006.
8.
Antiobesity mice. These mice are protected from getting obese and
diabetic from their diet by their lack of acyl-CoA:diacylglycerol
acyltransferase 1 (DGAT1). Their fat tissue can even reduce obesity
and glucose buildup in other mice if transplanted. There are other
strains protected from obesity by lack of other proteins, and a
strain that have more adiponectin that put all excess fat into their
blubber, remaining healthy despite turning very obese.
Smith
SJ, et al. Obesity resistance and multiple mechanisms of triglyceride
synthesis in mice lacking DGAT. Nat. Genet. 2000;25:87–90
Chen
HC, et al. Increased insulin and leptin sensitivity in mice lacking
acyl CoA:diacylglylcerol acyltransferase 1. J. Clin. Invest.
2002;109:1049–1055. doi:10.1172/JCI200214672.
9.
Marathon mice. These mice have more expression of PPARδ in their
muscles, which makes them turn into type I (slow twitch) fibers that
work well for long-distance running. The mice have more endurance and
- even when not training - increased resistance to obesity.
Wang
YX, Zhang CL, Yu RT, Cho HK, Nelson MC, et al. (2004) Regulation of
Muscle Fiber Type and Running Endurance by PPARδ. PLoS Biol 2(10):
e294
So
what does this mean for the future
The
Geo-Trade Blog believes that our relationship with technology and how
it stretches our ability to perform in the world will be one of the
key areas of advance in the 21st Century. In fact, how we answer the
following questions will be key to determining the parameters: What
does the future, near and far, hold for humans? Is enhancement the
next stage of evolution? Should any limits be imposed? And if so,
how?
