Evolution and Human Brain Size
Like a specialist in any field, the neuroscientist
has many descriptive facts about the human brain readily available to him:
there are over 100 billion neurons in the human brain, it weighs 1400g (300g
accounting for the fluid displacement of the CSF), it consumes a staggering 20%
of the total body’s energy budget despite it only taking up 2% total body mass.
Regardless of these advances in knowledge, there is still current debate
regarding the evolution of the human brain and its size. As Carlson puts it,
“…the human brain is larger than that of any other large mammal when corrected
for body size—more than three times larger than that of a chimpanzee, our
closest relative. What types of genetic changes are required to produce a large
brain?” (Carlson, 82). The question, while interesting, is not new—Aristotle was
the first ‘empirical’ biologist to observe and wonder about this phenomenon now
termed encephalization.
The disproportionate size of our brain to our body in relation
to other species, and the way in which our brains developed so that they are
(so to speak) the outliers of the mammalian world is nothing short of
fascinating. So again, what types of genetic variations are needed to produce such an
unusually large brain size?
There are two primary explanations for this large brain
outlier phenomenon in the literature. First, Rakic (1995) suggests that human
brain size may possibly be a consequence of the ventricular zone size
increasing during symmetrical division of the progenitor cells. This is
Ockham’s razor indeed (the simplest answer is probably right). Brain size,
regardless of the species, is ultimately determined by the size of the ventricular
zone, since each symmetrical division doubles the amount of progenitor cells,
which in turn doubles the volume of the brain itself. Take, for instance, the
difference between a human brain and that of the rhesus monkey—the human brain
is 10 times larger. In this theory, at least three to four added symmetrical
divisions of progenitor cells would be required to account for this size
difference. In fact, symmetrical cell division lasts about 2 days longer in
humans, which gives ample time for further symmetrical divisions to occur. What’s
more, in humans, the period of division is longer too, which may account for
the fact that the human cortex is 15% thicker than our closest relatives.
Alternatively, Chenn and Walsh (2002) suggest that a
protein named β-catenin,
which researchers now know to be involved in regulating the size of the
cerebral cortex by controlling symmetrical cell division of progenitor cells, may
play a role in the regulation and
development of human brain size. Methodologically, the researchers employed a
genetic manipulation approach to increase levels of β-catenin in neuro
progenitor cells in mouse fetuses. Results indicated that the number of
progenitor cells increased significantly, and thus the mice grew larger brains
(and larger heads to house those big brains!). In fact, the cerebral cortex of
the mice grew so dramatically that it developed convolutions normally seen only
in more complex brains. The figure below provides an interesting comparison. Interestingly,
in a follow-up, replication study, Woodhead et al. (2006), found that disruption
of the β-catenin signals in the ventricular
zone led to the development of a significantly smaller cerebral cortex.
(Left: A normal mouse head. Right: the genetically engineered mouse head that produced excessive amounts of β-catenin)
One last theory is provided by Ana Navarrete et al. (2011). After discussing what they term the
traditional expensive-tissue hypothesis, the researchers dismiss it on the
simple grounds that the supporting empirical data are equivocal. The
expensive-tissue hypothesis suggests a trade-off between the size of the human
brain and the size of the human digestive tract. In the final analysis,
Navarrete et al. suggests that, “We propose that human encephalization was made
possible by a combination of stabilization of energy inputs and a redirection
of energy from locomotion, growth and reproduction.”
Regardless of the theory advanced, the encephalization of
the human brain, from the time of Aristotle until today, continues to be a
source of interest—one that, once again, highlights the uniqueness of the human
being.
References
(And recommended Readings)
Carlson, Neil R. (2009). Physiology of Behavior. New York, NY: Allyn & Bacon.
Chenn, A. & Walsh, C. (2002). Regulation of
Cerebral Cortical Size by control of cell cycle exit in neural precursors. Science,
297(5580), 365-369. Doi: 10.1126/science.1074192
de Winter, W., & Oxnard, C. E.
(2001). Evolutionary ratiations and convergences in the structural organization of mammalian brains. Nature, 409(6821), 710-714. doi: 10.1038/35055547
Koscik,
Timothy R. and Tranel, Daniel (2012). Brain evolution and human
neuropsychology:
The Inferential Brain Hypothesis. Journal of
the International Neuropsychological Society, 18(3), 394-401.
Navarrete,
Ana, van Schaik, Carel P., and Isler, Karin (2011). Energetics and the
evolution of human brain size. Nature,
480(7375), 91-93.
Woodhead, G., Mutch, C., Olson, E.,
and Chenn, A. (2006). Cell autonomous β-catenin signaling regulates cortical precursor proliferation. Journal of Neuroscience, 26, 12620-12630.
Prepared
by +Phillip Kuna for John G. Kuna, PsyD and Associates
(570)961-3361
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