“A chimpanzee’s ability to learn is drastically reduced upon reaching maturity. But baby chimps will eagerly mimic a human caretaker – sticking out their tongues, opening their mouth wide, or making their best effort at a kissy face.” (Geoff, 2009)A newborn creature will spend much time exploring its environment. As it comes to know its surroundings, it no longer has to acquire new information at the same rate. It loses its ability to learn.
We humans are different. We never grow up. As adults, we retain this infant-like mental plasticity, much in the same way as a child’s tolerance for milk persists into adulthood in dairy-farming societies.
Geneticists are now a step closer to understanding this evolutionary change. A team led by David Kingsley of Stanford has shown that ancestral humans lost a key piece of DNA that switches on GADD45G, a gene that stifles growth of brain tissue. In non-humans, this gene regulator slows down the growth of brain tissue:
The GADD45G regulator was active in layers of the brain where cells that ultimately form the cortex are born. Specifically, in mice and chimps, GADD45G suppresses the development of brain regions which in humans are involved in higher cognitive functions like conscious thought and language."
Completely losing GADD45G would be like losing the brakes," says Kingsley. That happens in pituitary tumours when the regulator fails and cells grow without restraint, but in healthy humans the regulatory change would have only decreased activity in specific brain areas, causing them to grow larger. (Coghlan, 2011; see also McLean et al., 2011)
This kind of genetic change may largely explain how the brain progressively expanded in ancestral humans. And this evolution did not stop with the advent of Homo sapiens. Human populations today vary at several gene loci that regulate brain growth: ASPM, MCPH1, CDK5RAP2, and CENPJ. At these loci, the most recent alleles likewise seem to favor brain growth by allowing each cortical column of neurons to expand outward over a longer period of time. Interestingly, the main result does not seem to be higher IQ, but rather some other, still unknown, enhancement of mental capacity (Frost, 2008; Montgomery & Mundy, 2010; Rimol et al., 2010; Wang et al., 2008).
Differences in mental capacity should thus steadily increase from infancy to adulthood. This is an important point. If young children perform equally well on a mental task, it is often assumed that later differences must be due to differences in the learning environment.
References
Coghlan, A. (2011). Key to humanity is in missing DNA, New Scientist, March 9http://www.newscientist.com/article/mg20928033.500-key-to-humanity-is-in-missing-dna.html
Frost, P. (2008). The spread of alphabetical writing may have favored the latest variant of the ASPM gene, Medical Hypotheses, 70, 17-20.
Geoff. (2009). Chimpanzees and Neoteny, March 30.
http://www.gmilburn.ca/2009/03/30/chimpanzees-and-neoteny/
http://www.gmilburn.ca/2009/03/30/chimpanzees-and-neoteny/
McLean, C., Reno, P., Pollen, A., Bassan, A., Capellini, T., Guenther, C., Indjeian, V., Lim, X., Menke, D., Schaar, B., Wenger, A., Bejerano, G., & Kingsley, D. (2011). Human-specific loss of regulatory DNA and the evolution of human-specific traits, Nature, 471 (7337), 216-219 DOI: 10.1038/nature09774
Montgomery, S.H. and N.I. Mundy. (2010). Brain Evolution : Microcephaly genes weigh in, Current Biology, 20(5), R244
Rimol, L.M., I. Agartz, S. Djurovic, A.A. Brown, J.C. Roddey, A.K. Kähler, M. Mattingsdal, L. Athanasiu, A.H. Joyner, N.J. Schork, et al. for the Alzheimer’s Disease Neuroimaging Initiative (2010). Sex-dependent association of common variants of microcephaly genes with brain structure. Proceedings of the National Academy of Science. USA, 107, 384–388.
Wang, J.K., Li, Y., and Su, B. (2008). A common SNP of MCPH1 is associated with cranial volume variation in Chinese population. Human Molecular Genetics, 17, 1329–1335.