Brain Evolution

Alzheimer's the evolutionary cost of better brains?

A recent genetics paper reports on evidence that changes in six genes involved in human brain development occurred around 50,000 to 200,000 years ago. These mutations may have helped increase the connectivity of our neurons, making us smarter. But these same genes are also implicated in Alzheimer's. Researchers speculate that the disorder is thus connected to our increased intelligence — the price we pay for having better brains. This is not inconsistent with a previous suggestion that the myelin ("white matter") sheathing our brain wiring was the key evolutionary change in making us unique, and that this myelin sheathing may also be the cause of our unique vulnerability to neurological disorders.

The study examined the genomes of 90 people with African, Asian, or European ancestry.

Genetics overlap found between Alzheimer's disease and cardiovascular risk factors

Data from genome-wide association studies of more than 200,000 individuals has revealed a genetic overlap between Alzheimer's disease and two significant cardiovascular disease risk factors: high levels of inflammatory C-reactive protein (CRP) and plasma lipids. The two identified genes (HS3ST1 and ECHDC3, on chromosomes 4 and 10) were not previously associated with Alzheimer's risk. However, the association of high plasma lipid levels and inflammation with Alzheimer's risk is supported by previous research.

The findings support the idea that inflammation and high blood lipids play a role in dementia risk, and may offer therapeutic targets.

How genetic changes lead to familial Alzheimer's disease

Variants in the presenilin-1 gene are the most common cause of inherited, early-onset Alzheimer's. Because presenilin is a component of gamma secretase, which cuts up amyloid precursor protein into Abeta40 and Abeta42 (the protein found in plaques), it's been thought that these presenilin-1 variants increase the activity of gamma secretase. However, attempts to stop Alzheimer's by using drugs to block gamma-secretase have so far been fruitless (indeed, counter-productive). Now a new mouse study has explained why: it appears that the presenilin-1 variants may in fact decrease, rather than increase, the activity of gamma-secretase. This suggests that the presenilin-1 variants are acting on other causes of Alzheimer's, and also suggests the possibility that restoring gamma-secretase, rather than blocking it, may be a more effective therapeutic strategy.

Mice genetically engineered for Alzheimer's are usually given dispositions for excessive amyloid plaques. However, it's becoming clear that Alzheimer's is more complex than a single cause. This may explain the signal failure of mouse models to provide treatments that work on humans. This research provides a different mouse model, which may help in the development of treatments.

Mining big data yields new Alzheimer's gene

Analysis of brain scans from the ENIGMA Consortium and genetic information from The Mouse Brain Library has revealed a new gene for Alzheimer's risk. The gene MGST3 regulates the size of the hippocampus.

The finding confirms the importance of hippocampal volume for maintaining memory and cognition, and supports the idea that “cognitive reserve” helps prevent age-related cognitive decline and dementia.

Gene involved in waste removal increases risk of Alzheimer's & other neurodegenerative disorders

Previous research has pointed to the gene TREM2 as a genetic risk factor for Alzheimer's disease. A recent study explains why variants in this gene might be associated with neurodegenerative disorders such as Alzheimer's, Parkinson's, ALS, and frontotemporal dementia.

It appears that the gene is involved in the microglia — the “cleaners” of the brain. Variants in the gene affect the recognition of waste products left behind by dead cells, reducing the amount of debris that the microglia can cope with.

The finding may point to a way of slowing the progression of these neurodegenerative diseases even when the disease is well established.

A new finding points to brain reorganization, rather than brain size, as the driver in primate brain evolution. Data from 17 anthropoid primate species (including humans) across 40 million years has found that around three quarters of differences between the brains of species of monkeys and apes are due to internal reorganization that is independent of size. The prefrontal cortex in particular appears to have played the biggest role in explaining the evolutionary changes in primate brains.

[3366] Smaers, J. B., & Soligo C.
(2013).  Brain reorganization, not relative brain size, primarily characterizes anthropoid brain evolution.
Proceedings of the Royal Society B: Biological Sciences. 280(1759), 

More evidence for the importance of glia, previously regarded as mere ‘support cells’ in the brain, comes from a mouse study — which also indicates the role of astrocytes in the evolution of the human brain. The study found that mice that received transplants of human glial progenitor cells learned much more quickly than normal mice.

The study follows on from recent findings that human astrocytes are very different from those found in mouse and rat brains. The study also points to one particular aspect of human astrocytes as being crucial: greater increases in the release of a cytokine called TNFa. When this was blocked, learning was reduced.

[3318] Han, X., Chen M., Wang F., Windrem M., Wang S., Shanz S., et al.
(2013).  Forebrain Engraftment by Human Glial Progenitor Cells Enhances Synaptic Plasticity and Learning in Adult Mice.
Cell Stem Cell. 12(3), 342 - 353.

Genetic comparisons have pinpointed a specific protein as crucial for brain size, both between and within species. Another shows how genetic regulation in the frontal lobes distinguishes the human brain from that of closely related species, and points to two genes in particular as critical.

The protein determining brain size

Comparison of genome sequences from humans and other animals has revealed what may be a crucial protein in the development of the human brain. The analysis found that humans have more than 270 copies of a protein called DUF1220 — more than any other animal studied — and that the number of copies in a species seems to match how close they are to us. Chimpanzees, for example, have 125, and gorillas 99, while marmosets have only 30, and mice just one.

Moreover, comparison of humans with microcephaly and macrocephaly reveals that those with microcephaly (“small brain”) have lower numbers of this protein than normal for humans, and those with macrocephaly (“large brain”) have higher numbers. Copy numbers of the protein were also correlated with gray matter volume in humans without these brain disorders.

In other words, evidence from three lines of inquiry converge on DUF1220 copy number being associated with brain size.

Differences in gene expression and connectivity

But the development of the human brain is not only about size. The human brain is more complex, more connected, than the brains of most other animals. Another genetic analysis has been comparing gene activity in humans, chimpanzees and rhesus macaques, using post-mortem brain tissue of three regions in particular – the frontal cortex, hippocampus and striatum.

Gene expression in the frontal lobe of humans showed a striking increase in molecular complexity, with much more elaborate regulation and connection. The biggest differences occurred in the expression of human genes involved in plasticity.

One gene in particular stood out as behaving differently in the human brain. This gene — called CLOCK, for obvious reasons — is thought to be the master regulator of our body’s clocks. The finding suggests it has influence beyond this role. Interestingly, this gene is often disrupted in mood disorders such as depression and bipolar syndrome.

A second important distinction was how many more connections there were in human brains among networks that included the language genes FOXP1 and FOXP2.

In comparison to all this, gene expression in the caudate nucleus was very similar across all three species.

The findings point to the role of learning (the genes involved in plasticity) and language in driving human brain evolution. They also highlight the need to find out more about the CLOCK gene.

Comparison of 99 chimpanzee brains ranging from 10-51 years of age with 87 human brains ranging from 22-88 years of age has revealed that, unlike the humans, chimpanzee brains showed no sign of shrinkage with age. But the answer may be simple: we live much longer. In the wild, chimps rarely live past 45, and although human brains start shrinking as early as 25 (as soon as they reach maturity, basically!), it doesn’t become significant until around 50.

The answer suggests one reason why humans are uniquely vulnerable to Alzheimer’s disease — it’s all down to our combination of large brain and long life. There are other animals that experience some cognitive impairment and brain atrophy as they age, but nothing as extreme as that found in humans (a 10-15% decline in volume over the life-span). (Elephants and whales have the same two attributes as humans — large brains and long lives — but we lack information on how their brains change with age.)

The problem may lie in the fact that our brains use so much more energy than chimps’ (being more than three times larger than theirs) and thus produce a great deal more damaging oxidation. Over a longer life-span, this accumulates until it significantly damages the brain.

If that’s true, it reinforces the value of a diet high in antioxidants.

[2500] Sherwood, C. C., Gordon A. D., Allen J. S., Phillips K. A., Erwin J. M., Hof P. R., et al.
(2011).  Aging of the cerebral cortex differs between humans and chimpanzees.
Proceedings of the National Academy of Sciences. 108(32), 13029 - 13034.

190-million-year-old fossil skulls of Morganucodon and Hadrocodium, two of the earliest known mammal species, has revealed that even at this early stage of mammalian evolution, mammals had larger brains than would be expected for their body size. High-resolution CT scans of the skulls have now shown that this increase in brain size can be attributed to an increase in those regions dealing with smell and touch (mammals have a uniquely well developed ability to sense touch through their fur).

Comparison of these fossils with seven fossils of early reptiles (close relatives of the first mammals), 27 other primitive mammals, and 270 living mammals, has further revealed that the size of the mammalian brain evolved in three major stages. First, an initial increase in the olfactory bulb and related areas (including the cerebellum) by 190 million years ago; then another jump in the size of these regions shortly after that time; and finally an increase in those regions that control neuromuscular coordination by integrating different senses by 65 million years ago.

It’s speculated that the initial increase in smell and touch was driven by early mammals being nocturnal — dinosaurs being active during the day.

[2301] Rowe, T. B., Macrini T. E., & Luo Z-X.
(2011).  Fossil Evidence on Origin of the Mammalian Brain.
Science. 332(6032), 955 - 957.

A comparison of the brain and body size of over 500 species of living and fossilised mammals has found that the brains of monkeys grew the most over 60 million years, followed by horses, dolphins, camels and dogs. Those with relatively bigger brains tend to live in stable social groups. The brains of more solitary mammals, such as cats, deer and rhino, grew much more slowly during the same period.

On the other hand, a new study comparing wasp brains over time has revealed that the mushroom bodies (neural clusters responsible for processing and remembering smells and sights) of parasitic wasps are consistently larger and more complex than those of nonparasitic wasps, which represent the very oldest form of wasp.

Previously, findings that social insects tend to have larger mushroom bodies than solitary ones have lead researchers to believe that the transition from solitary to social living was behind the larger brain regions. These new findings suggest that it is parasitism (which evolved 90 million years before social insects appear) that is behind the growth in size. That may be because well-developed mushroom bodies help parasitic wasps better locate hosts for their larvae.

Of course, this doesn’t rule out the possibility that sociality lead to another boost in size and complexity, and indeed the researchers suggest that these neurological developments may have been a crucial precursor for central place foraging. This behavior is widespread in this group of insects (the Aculeata), requires extensive spatial learning, and may have contributed to the various developments of social behavior. A comparison of the brains of social worker bees and those of parasitic wasps would be helpful.

I love cognitive studies on bees. The whole notion that those teeny-tiny brains are capable of the navigation and communication feats bees demonstrate is so wonderful. Now a new study finds that, just like us, aging bees find it hard to remember the location of a new home.

The study builds on early lab research that demonstrated that old bees find it harder to learn floral odors. In this new study, researchers trained bees to a new nest box while their former nest was closed off. Groups composed of mature and old bees were given several days in which to learn the new home location and to extinguish the bees' memory of their unusable former nest box. The new home was then disassembled, and groups of mixed-age bees were given three alternative nest locations to choose from (including the former nest box). Some old bees (those with symptoms of senescence) preferentially went to the former nest site, despite the experience that should have told them that it was unusable.

The findings demonstrate that memory problems and increasing inflexibility with age are not problems confined to mammals.

Analysis of the brain sizes of 197 marsupial and 457 placental mammals has found that marsupial mammals (e.g. kangaroos, possums), had relative brain sizes that are at least as big as placental mammals. Previous belief that marsupials have relatively smaller brains appears to be produced by the inclusion of the one outlier group — primates. In both placental and marsupial groups, big brains were correlated to length of maternal care (i.e. lactation). Basal metabolic rate (the energy an animal expends at rest), although correlated with brain size in placental mammals, did not correlate with marsupial brain size. Because brain tissue uses so much energy, it has been assumed that a high metabolism was a prerequisite for a big brain.

The new findings indicate that maternal investment is a more critical factor than metabolic rate. It may also be that primates have been especially advantaged by combining both methods of increasing brain size: fast growth in the womb with the help of the mother’s high metabolic rate (placental method), and slower but lengthy growth after birth with the help of extended lactation (marsupial method).

[1895] Weisbecker, V., & Goswami A.
(2010).  Brain size, life history, and metabolism at the marsupial/placental dichotomy.
Proceedings of the National Academy of Sciences. 107(37), 16216 - 16221.

For a long time, it has been assumed that mammals have different (better!) brains than other animals — partly because of the highly convoluted neocortex. Specifically, the mammalian neocortex features layers of cells (lamination) connected by radially arrayed columns of other cells, forming functional modules characterized by neuronal types and specific connections. Early studies of homologous regions in nonmammalian brains found no similar arrangement. Now new technology has revealed that a part of the chicken brain that handles auditory information is also composed of laminated layers of cells linked by narrow, radial columns of different types of cells with extensive interconnections that form microcircuits that are virtually identical to those found in the mammalian cortex. The finding suggests that the distinct structure of the mammalian neocortex has evolved from circuitry dating back at least 300 million years. The findings also indicate that mammalian and bird brains are more alike than we thought.

[1637] Wang, Y., Brzozowska-Prechtl A., & Karten H. J.
(2010).  Laminar and columnar auditory cortex in avian brain.
Proceedings of the National Academy of Sciences. 107(28), 12676 - 12681.

The first comparison of the brain sizes of social and non-social individuals of the same species provides more support for the social brain hypothesis (we evolved our big brains to deal with social groups). The tropical sweat bee species, Megalopta genalis, have two sorts of queen: solitary ones, who themselves go out from the nest to forage for food, or social ones — who stay at home and sends out her daughters. Although even the social queens don't have bigger brains overall, the area associated with learning and memory (the mushroom body) was more developed in the social queens than in the solitary bees (and also the social daughters — suggesting dominance is also a factor).

Perhaps we should start thinking of language less as some specialized process and more as one approach to thought. A study involving native signers of American Sign Language (which has the helpful characteristic that subject-object relationships can be expressed in either of the two ways languages usually use: word order or inflection) has revealed that there are distinct regions of the brain that are used to process the two types of sentences: those in which word order determined the relationships between the sentence elements, and those in which inflection was providing the information. These brain regions are the ones designed to accomplish tasks that relate to the type of sentence they are trying to interpret. Word order sentences activated areas involved in working memory and lexical access, including the dorsolateral prefrontal cortex, the inferior frontal gyrus, the inferior parietal lobe, and the middle temporal gyrus. Inflectional sentences activated areas involved in building and analyzing combinatorial structure, including bilateral inferior frontal and anterior temporal regions as well as the basal ganglia and medial temporal/limbic areas. In other words, as an increasing body of evidence tells us, we process words in the same way as we do the concepts represented by the words; speaking (or reading) is, neutrally speaking, the same as doing.

[453] Newman, A. J., Supalla T., Hauser P., Newport E. L., & Bavelier D.
(2010).  Dissociating neural subsystems for grammar by contrasting word order and inflection.
Proceedings of the National Academy of Sciences. 107(16), 7539 - 7544.

Older news items (pre-2010) brought over from the old website

Humans aren’t the only ones to think about what they know

As we get smarter about designing experiments and working out how to ask the right questions, the gap between human and non-human cognition keeps closing. Now a rat study has found evidence that rats can think about whether they know something or not. The study involved offering rats rewards for classifying a brief tone as either short or long. A right answer led to a large food reward; a wrong one, nothing. But on some tests runs, before starting, the rats were given a chance to back out of the test, in which case they got a small reward anyway. In some of the tests, the signal lengths were very different, making the discrimination very easy. But in others the difference was a lot harder to discern. In such a case, if the rats realized they couldn’t be sure of the answer, they would be better to forego the test and get the small, but guaranteed prize. Which was what was found.

[387] Foote, A. L., & Crystal J. D.
(2007).  Metacognition in the Rat.
Current Biology. 17(6), 551 - 555.

Size of brain areas does matter -- but bigger isn't necessarily better

In a fascinating mouse study that overturns our simplistic notion that, when it comes to the brain, bigger is better, researchers have found that there is an optimal size for regions within the brain. The study found that if areas of the cortex involved in body sensations and motor control are either smaller or larger than normal, mice couldn’t run an obstacle course, keep from falling off a rotating rod, or perform other tactile and motor behaviors that require balance and coordination as well as mice with normal-sized areas could. It now seems that the best size in one that is best tuned to the context of the neural system within which that area functions — which is not really so surprising when you consider that every brain region acts as part of a network, in conjunction with other regions. This study builds upon a previous discovery by the same researchers, that a gene controls how the cortex in mice is divided during embryonic development into its functionally specialized areas. Different levels of the protein expressed by this gene changes the size of the sensorimotor areas of the cortex. It is known that significant variability in cortical area size exists in humans, and this may explain at least in part variability in human performance.

[334] Leingärtner, A., Thuret S., Kroll T. T., Chou S-J., Leasure L. J., Gage F. H., et al.
(2007).  Cortical area size dictates performance at modality-specific behaviors.
Proceedings of the National Academy of Sciences. 104(10), 4153 - 4158.

Full text is available at

Neurons targeted by dementing illness may have evolved for complex social cognition

Special elongated nerve cells called spindle neurons, also known as Von Economo neurons (VENs), are found in two parts of the cerebral cortex known to be associated with social behavior, consciousness, and emotion (the anterior cingulate and fronto-insular cortex). They have only been found in humans and great apes, and, recently, whales. Because of this link with social behavior, and because these brain regions are targeted by frontotemporal dementia, a recent study investigated whether VENs play a role in this type of dementia that causes people to lose inhibition in social situations. Autopsies revealed that among FTD sufferers, the anterior cingulate cortex had a dramatic reduction in the number of VENs compared to controls. In contrast, Alzheimer's patients had only a small and statistically insignificant reduction.

[668] Seeley, W. W., Carlin D. A., Allman J. M., Macedo M. N., Bush C., Miller B. L., et al.
(2006).  Early frontotemporal dementia targets neurons unique to apes and humans.
Annals of Neurology. 60(6), 660 - 667.

A cognitive strategy shared by human infants and our great-ape kin

There are two basic strategies for remembering the location of something: either remembering the features of the item (it was a tree, a stone, etc.), or knowing the spatial placement (left, right, middle, etc.). All animal species tested so far seem to employ both strategies, but some species (e.g. fish, rats and dogs) have a preference for locational strategies, while others (e.g. toads, chickens and children) favor those which use distinctive features. A comparison of the cognitive strategies of humans, chimpanzees, bonobos, gorillas, and orangutans, has revealed that all non-human great apes and 1-year-old human infants prefer a locational strategy, even when an object strategy would be more efficient. This suggests that the common ancestor of all great apes enacted a similar strategy preference in employing spatial memory. However, 3-year-old human children in these circumstances chose the more efficient strategy.

[1007] Haun, D. B. M., Call J., Janzen G., & Levinson S. C.
(2006).  Evolutionary Psychology of Spatial Representations in the Hominidae.
Current Biology. 16(17), 1736 - 1740.

Genetic variations that may be key to the evolution of the human brain

It has been thought that most genetic variations between people and between species are due to small changes in the sequence of DNA lettering, but a new idea that’s becoming popular is that the number of copies of genes is an important source of variation that may be driving evolution. Comparison of the DNA sequences of humans, chimpanzees and monkeys, has now revealed that a gene that codes for a piece of protein called DUF1220 exists in 212 copies in humans, but only 37 in chimpanzees and 30 in monkeys. Mice and rats have only one. The protein is found in the heart, spleen, skeletal muscle, and small intestine, and particularly in brain regions associated with higher cognitive function.

[643] Popesco, M. C., MacLaren E. J., Hopkins J., Dumas L., Cox M., Meltesen L., et al.
(2006).  Human Lineage-Specific Amplification, Selection, and Neuronal Expression of DUF1220 Domains.
Science. 313(5791), 1304 - 1307.

An exploration of those 49 areas of the genome that have changed most between human and chimpanzee has revealed one area that's changed dramatically in a relatively short period of time. The gene is found only in mammals and birds, and hasn’t changed much in other animals — between a chimp and a chicken, there are only two differences in the 118 letters of DNA code that make up HAR1 (human accelerated region 1). But there are 18 differences in that one gene between human and chimp. That is a lot of change to happen in five million years. HAR1 is part of two overlapping genes -- both the rare RNA genes, not genes that code for proteins -- one of which (HAR1F) is active in nerve cells that appear early in embryonic development and play a critical role in the formation of the layered structure of the human cerebral cortex. The other also appears to be involved in cortical development.

[420] Siepel, A., Kern A. D., Dehay C., Igel H., Ares M., Vanderhaeghen P., et al.
(2006).  An RNA gene expressed during cortical development evolved rapidly in humans.
Nature. 443(7108), 167 - 172.

Avoiding predators may be the reason for our large brains

A study of predators in Africa and South America suggests a new theory for why we evolved big brains. Apparently predators prefer prey with smaller brains, suggesting that more smarts help you outwit your enemies. A popular theory has been that the complexities of being social pushed the increase in brain size, and it does seem that this is also a factor, but predation is probably behind this as well — living in a group protects against predators, because group mates help keep an eye out for danger. However, the study found that while predators did prefer less sociable prey, the strongest pattern was for predators to prefer prey with relatively small brains. The researchers suggest that the need for a larger brain was strengthened when our primate ancestors came down out of the trees, and entered a much more dangerous environment.

[1325] Shultz, S., & Dunbar R. I. M.
(2006).  Chimpanzee and felid diet composition is influenced by prey brain size.
Biology Letters. 2(4), 505 - 508.,,1835615,00.html

Bigger brains associated with domain-general intelligence

Analysis of hundreds of studies testing the cognitive abilities of non-human primates provides support for a general intelligence, and confirms that the great apes are more intelligent than monkeys and prosimians. Individual studies have always been criticized for not clearly ensuring that one species wasn’t out-performing another simply because the particular testing situation was more suited to them. However, by looking at so many varied tests, the researchers have overcome this criticism. Although there were a few cases where one species performed better than another one in one task and reversed places in a different task, overall, some species truly outperformed others. The smartest species were clearly the great apes — orangutans, chimpanzees, and gorillas. Moreover, there was no evidence that any species performed especially well within a particular paradigm, contradicting the theory that species differences in intelligence only exist for narrow, specialized skills. Instead, the results argue that some species possess a broad, domain-general type of intelligence that allows them to succeed in a variety of situations.

Deaner, R.O., van Schaik, C.P. & Johnson, V. 2006. Do some taxa have better domain-general cognition than others? A meta-analysis of nonhuman primate studies. Evolutionary Psychology, 4, 149-196.

Full-text available at

Asymmetrical brains let fish multitask

A fish study provides support for a theory that lateralized brains allow animals to better handle multiple activities, explaining why vertebrate brains evolved to function asymmetrically. The minnow study found that nonlateralized minnows were as good as those bred to be lateralized (enabling it to favor one or other eye) at catching shrimp. However, when the minnows also had to look out for a sunfish (a minnow predator), the nonlateralized minnows took nearly twice as long to catch 10 shrimp as the lateralized fish.

[737] Dadda, M., & Bisazza A.
(2006).  Does brain asymmetry allow efficient performance of simultaneous tasks?.
Animal Behaviour. 72(3), 523 - 529.

Primates take weather into account when searching for fruits

In recent times, a popular hypothesis for why primates, and especially humans, have more strongly developed cognitive skills than other mammals, is that they result from the need for complex social skills. There is quite a lot of support for this argument. But it is not the only possibility and a recent study has looked at an alternative: that it evolved to deal with ecological problems, such as foraging for food. Researchers followed a group of wild gray-cheeked mangabeys from dawn to dusk over 210 days in their natural rainforest habitat, obtaining an almost complete record of their foraging decisions in relation to their preferred food, figs. The findings are consistent with the idea that monkeys make foraging decisions on the basis of episodic ("event-based") memories of whether or not a tree previously carried fruit, combined with knowledge of recent and present weather conditions and a more generalized understanding of the relationship between temperature and solar radiation and the maturation rate of fruit and insect larvae.

[493] Janmaat, K., Byrne R., & Zuberbuhler K.
(2006).  Primates Take Weather into Account when Searching for Fruits.
Current Biology. 16(12), 1232 - 1237.

'Perception' gene tracked humanity's evolution

A gene thought to influence perception and susceptibility to drug dependence is expressed more readily in human beings than in other primates, and this difference coincides with the evolution of our species. The gene encodes prodynorphin, an opium-like protein implicated in the anticipation and experience of pain, social attachment and bonding, as well as learning and memory. Although the protein prodynorphin is identical in humans and chimps, in the gene's promoter sequence (that controls how much of the protein is expressed) some 10% is different (this compares to the overall 1 to 1.5% difference between human and chimpanzee genes). There is high genetic variation in the prodynorphin promoter among humans, but not among other primates. Variants have been tentatively linked to schizophrenia, cocaine addiction, and epilepsy. The report supports a growing consensus among evolutionary anthropologists that hominid divergence from the other great apes was fueled not by the origin of new genes, but by the quickening (or slowing) of the expression of existing genes.

[732] Rockman, M. V., Hahn M. W., Soranzo N., Zimprich F., Goldstein D. B., & Wray G. A.
(2005).  Ancient and Recent Positive Selection Transformed Opioid cis-Regulation in Humans.
PLoS Biol. 3(12), e387 - e387.

Full text available at

Human brains still evolving

Two genes active in the brain — Microcephalin and ASPM — have now been sequenced. Both regulate brain size. The sequencing has revealed a distinctive mutation in both genes, both of which change the protein the gene codes for. For the Microcephalin gene, the mutation is now in the brains of about 70% of humans, and half of this group carry completely identical versions of the gene, suggesting the mutation arose recently (between 60,000 and 14,000 years ago) and spread quickly through the human species due to selection pressure, rather than accumulating random changes through neutral genetic drift. The new variant of ASPM appeared in humans even more recently — somewhere between 14,000 and 500 years ago — and is already present in about a quarter of people alive today.

[381] Evans, P. D., Gilbert S. L., Mekel-Bobrov N., Vallender E. J., Anderson J. R., Vaez-Azizi L. M., et al.
(2005).  Microcephalin, a Gene Regulating Brain Size, Continues to Evolve Adaptively in Humans.
Science. 309(5741), 1717 - 1720.

[684] Mekel-Bobrov, N., Gilbert S. L., Evans P. D., Vallender E. J., Anderson J. R., Hudson R. R., et al.
(2005).  Ongoing Adaptive Evolution of ASPM, a Brain Size Determinant in Homo sapiens.
Science. 309(5741), 1720 - 1722.

New light on speech evolution in humans

A new monkey study challenges thinking that speech developed as a result of new structures that evolved in the human brain. A distinct brain region that controls jaw movements in macaque monkeys has been found in the same area and with the same anatomical characteristics as Broca's area. The discovery suggests that this area of the brain evolved originally to perform high-order control over the mouth and the jaw, and that as humans evolved this area came to control the movements necessary for speech.

[1333] Petrides, M., Cadoret G., & Mackey S.
(2005).  Orofacial somatomotor responses in the macaque monkey homologue of Broca's area.
Nature. 435(7046), 1235 - 1238.

Primitive brain learns faster than the "thinking" part of our brain

A study of monkeys has revealed that a primitive region of the brain known as the basal ganglia learns rules first, then “trains” the prefrontal cortex, which learns more slowly. The findings turn our thinking about how rules are learned on its head — it has been assumed that the smarter areas of our brain work things out; instead it seems that primitive brain structures might be driving even our most high-level learning.

[722] Pasupathy, A., & Miller E. K.
(2005).  Different time courses of learning-related activity in the prefrontal cortex and striatum.
Nature. 433(7028), 873 - 876.

Another clue to the evolution of the human brain

A new study suggests that the birth of a gene that fueled neurotransmission may have been a key advance in the evolution of the hominoid brain. GLUD2, a gene gene involved in glutamate metabolism, is found in humans and apes, but not in Old World monkeys, indicating that the gene appeared after monkeys and hominoids went their separate ways (some 23 million years ago), but before the gibbon lineage split from humans and great apes around 18 million years ago. Over time, GLUD2 acquired two amino acid changes that increased glutamate flux, possibly enhancing cognitive function in the hominoid brain.

[1277] Burki, F., & Kaessmann H.
(2004).  Birth and adaptive evolution of a hominoid gene that supports high neurotransmitter flux.
Nat Genet. 36(10), 1061 - 1063.

More support for social skill theory of brain evolution

Why do we have such large brains? Brains are very costly — they require a lot of energy. Gaining credence in recent years has been the idea that the advantage of our brain has been through the complex social skills it allows. Evidence supporting this has come from a study of records of primates deceiving each other for personal gain. The bigger the neocortex, it seems, the more likely a primate is to practice deception. The researchers gathered instances of deception across 18 species of primate and found no link with overall brain size, but a clear match between devious deeds and neocortex volume.

[838] Byrne, R. W., & Corp N.
(2004).  Neocortex size predicts deception rate in primates..
Proceedings of the Royal Society B: Biological Sciences. 271(1549), 1693 - 1699.,12978,1250723,00.html

More complex brain may have pre-dated Homo genus

New research supports Raymond Dart’s suggestion (in 1925) that the human brain started evolving its unique characteristics much earlier than has previously been supposed. One of the differences between human and ape brains is the position of the primary visual striate cortex (PVC), an area of the brain devoted exclusively to vision. In the ape brain, this is situated further forward than it is in human brains, making the PVC larger. It has been claimed that the PVC only decreased in size once the brain had grown substantially in size – when big-brained Homo (the hominid group that includes humans) appeared around 2.4 million years ago. However, new examination of an endocast of the brain of an Australopithecus africanus (Australopithecines pre-dated Homo, and their brains were similar in size to those of chimpanzees) has found evidence of a decreased PVC. This suggests an increase in the region lying in front of the PVC - the posterior parietal cerebral cortex, which is associated in humans with a variety of complex behaviors such as the appreciation of objects and their qualities, facial recognition and social communication.

[1379] Holloway, R. L., Clarke R. J., & Tobias P. V.
(2004).  Posterior lunate sulcus in Australopithecus africanus: was Dart right?.
Comptes Rendus Palevol. 3(4), 287 - 293.

Gene may be key to evolution of larger human brain

Researchers have now identified a gene that appears to have played a significant role in the expansion of the human brain's cerebral cortex. The gene is called the Abnormal Spindle-Like Microcephaly Associated (ASPM) gene, and dysfunction in this gene is linked to human microcephaly — a severe reduction in the size of the cerebral cortex. Comparison of the gene sequence in humans with that of 6 other primates (progressively less related to humans) revealed that the ASPM gene showed clear evidence of changes accelerated by evolutionary pressure in the lineage leading to humans, and the acceleration was most prominent in recent human evolution after humans diverged from chimpanzees (our closest primate relative) some five million years ago. A massive population-wide genetic change in the gene seems to have occurred in the human lineage every 300,000 to 400,000 years since then, with the last such change occurring between 200,000 and 500,000 years ago. Such strong evidence of evolutionary change is most unusual. No such change was found when other (non-primate) mammals were investigated.

[1199] Evans, P. D., Anderson J. R., Vallender E. J., Gilbert S. L., Malcom C. M., Dorus S., et al.
(2004).  Adaptive evolution of ASPM, a major determinant of cerebral cortical size in humans.
Hum. Mol. Genet.. 13(5), 489 - 494.

Evolution of the mammalian brain

Two recent studies cast light on the evolution of the mammalian brain. A study of the brains of cetaceans, has found that that the cortex of a killer whale is dramatically more “folded” than that of an Amazon River dolphin (the deep and complex folding, or gyrification, of the cortex surface is what allows the human brain to have far more informational capacity than would be expected from its mass). The whales’ brain was particularly convoluted in the area of the corpus callosum, the main “bridge” between the hemispheres. In other comparative study of mammalian brains, it was found that the larger the brain, the larger the mean diameter of the axons. Axons were also less densely packed and more heavily myelinated. Across all species studied, fast cross-brain conduction times were maintained at 1-2 milliseconds.

Research presented at the 2003 annual meeting of the Society for Neuroscience, held November 8–12 in New Orleans, LA

Human frontal cortex not proportionately larger compared to great apes

Humans are widely considered to have a disproportionately large frontal cortex compared to other animals, and the disparity in cognitive capabilities is partly attributed to this difference. However, a comparison of the relative size of the frontal cortex in humans versus other great apes reveals that human frontal cortices are not disproportionately large in comparison to those of the great apes. The authors suggest that the human advantage may be due to differences in individual cortical areas and to a richer interconnectivity, rather than an overall size difference.

[955] Semendeferi, K., Lu A., Schenker N., & Damasio H.
(2002).  Humans and great apes share a large frontal cortex.
Nat Neurosci. 5(3), 272 - 276.

Living in large groups could give you a better memory

A study into the brains of songbirds found that birds living in large groups have more new neurons and probably a better memory than those living alone. Does this have relevance for humans? We don't know yet, but it has been observed that social animals such as elephants tend to have better memories than loners.

[774] Lipkind, D., Nottebohm F., Rado R., & Barnea A.
(2002).  Social change affects the survival of new neurons in the forebrain of adult songbirds.
Behavioural Brain Research. 133(1), 31 - 43.

Manipulating a signaling protein in a developing mouse brain caused radical changes in the cortex and may provide a clue about how the cerebral cortex changes in evolution

Using a newly developed technique, University of Chicago researchers have manipulated one of the signaling proteins in the developing mouse brain and found such manipulations cause radical changes in the cortex. Fibroblast Growth Factor 8 (FGF8), a member of a family of signaling proteins involved in forming other structures in the embryo, is normally found near the front of the developing cortex. Using a new microsurgical technique, the researchers were able to manipulate the amount and position of this signaling protein in the embryo and look for changes in the cortical pattern much later. The researchers increased the amount of the signaling protein in its normal position, decreased it by inserting a gene for a receptor able to soak up the protein, or expressed it in a new position. Each manipulation profoundly affected cortical area pattern. "Most dramatic, when a new source of the signaling protein was generated close to the back of the embryonic cortex, the whole program changed." The generation of a new cortical area by a molecular manipulation has not been seen before and may provide a clue about how the cerebral cortex changes in evolution. One way that evolution seems to generate more functionally complex brains is by adding new areas to the cortex.

[498] Fukuchi-Shimogori, T., & Grove E. A.
(2001).  Neocortex Patterning by the Secreted Signaling Molecule FGF8.
Science. 294(5544), 1071 - 1074.