Thursday, 10 March 2016

Ithaka Prize Finalist: The Evolution of the Brain, Past and Present

by Lucy Tyler

As he closed The Origin of Species (1859), Charles Darwin stated that: “In the distant future I see open fields for far more important researches. Psychology will be based on a new foundation, that of the necessary acquirement of each mental power and capacity by graduation.”

In doing so he claimed that our minds and mentalities had evolved and will continue to evolve. Just like other anatomy, our neuroanatomy is subject to evolution by the environment. Humans share 98% of their DNA with the great apes1, but how do our brain structures and functions compare? I question whether human superiority is a perceived quality or genuine attribute based on brain function and cognitive ability. What were the selection pressures that have shaped our neuroanatomy and give differentiation in cognitive ability between species? The extent to which the marked differentiation between humans is established by the interaction of cellular activity and genetics and also their environment, is a concept that feeds the nature versus nurture debate.  However I seek to find where genetics and the environment converge in exploration of the field of epigenetics. Moving away from the role of genetics, environmental stimuli are fundamental in human development when considering neuroplasticity, the remarkable property of the brain that means seemingly trivial exposures alter neuronal circuitry, creating inclinations and abilities. I am intrigued by the mechanism for neuroplasticity and how far it shapes an evolving individual throughout life. These changes to our neuronal configuration can be brought about by simple lifestyle choices. As well as several striking historical exhibitions of plasticity in human development, alterations occur in our neuronal networks continuously to which we have no access. We have such limited awareness of their implications despite their integral role in our quest to overcome brain dysfunction.

Intelligence can be considered a result of evolutionary change. The intelligence of the Homo sapiens, relative to the other species with whom it shares planet Earth, is the quality to which the superiority of man in conquering and thriving on the planet is often attributed.  Within the animal kingdom, as a taxonomic order, the primates are singled out as having great intelligence. I am defining intelligence as the ability to acquire and learn new skills and gain knowledge. We perceive primates and specifically humans to have great intelligence because of their ‘complex’ abilities giving rise to versatility in a changing environment as well as acquiring a multitude of skills throughout a lifetime. Using the belief that intelligence is what separates primates from other taxonomic orders, one can infer that the brain of the common ancestor was physiologically or structurally altered for that to be the case.

Suzana Herculano-Houzel, a research scientist at the Federal University of Rio de Janeiro sought to find out whether size has any relationship with intelligence and brain function. She devised a technique in which individual neurons were counted in a known volume of a sample of brain and the number scaled up with respect to the full brain volume. The results gave an accurate estimate of the proportion of brain matter that was neuron cells. Studying a range of rodents, she found a positive correlation between size and the number of neurons and furthermore with glial cells. An additional finding made was that individual neurons increased in size as the brain size increased. The results indicated that larger rodent brans had greater processing power. The fact that organisms with more neurons had larger neurons, appeared to support the assumption that brain size has significance in terms of the intelligence of the species. This is based on the idea that the more neurons there are in an organism’s brain, the greater the brain function and the organism can perform more complex cognitive activity. Greater regions of brain can be allocated to the control of particular functions, for example, the sense of smell, therefore containing a greater number of neurons. Alternatively, a greater number of neuronal territories can be established which enable more cognitive skills and abilities, thus ‘complexity’.

Upon extending this method to primate brains, Herculano-Houzel found that data from primate brains did not conform to the same observation. Despite larger brain size, neurones were not larger, facilitating a marked increase in the number of neurones per volume of brain.  The last primate brain from which data was collected was a human brain. The results fitted the general primate trend found previously. Perhaps this greater neuron density has allowed primates to have their intellectual superiority.

Intelligence might not be the best determinant to judge the way in which brains have evolved. A definition of intelligence applicable to different species and organisms is highly debated. There are some factors that we perceive as indicative of relative intelligence that as humans we cannot understand, for example language. As humans, we could argue that our own methods of communication are far superior to those of other species simply because we have no awareness of either the existence or meaning of potential language or means of communication. Moreover, in my own view, ‘cognitive superiority’ cannot exist when comparing organisms of a different species, as apparent differences in intelligence may arise from limitations of anatomy independent of neuronal function.

It is a relatively recently accepted theory that particular regions of the brain are not solely responsible for certain activities, and that neuronal circuitry is fundamental to the capability of performing cognitive tasks. By neuronal circuitry, I refer to the interaction between individual neurons, the efficiency by which it occurs and the number of networks possible. Lars Chittka from Queen Mary University of London is critical of the studies relating brain size and intelligence. He argues instead that it is neuronal circuitry that has greatest significance in determining differences between species. The basis for his belief stems from his study of bees. With a brain of only 1mm3, bees have the ability to build large nests, work cooperatively with other individuals in a community with a hierarchical arrangement. A study, documented by John Pearce in Animal Learning and Cognition, found that bees are capable of learning faster than some vertebrates including human infants. My interest is not to compare the level of intelligence of the two species but to emphasise the significance that a high level cognitive ability can be achieved by a small number of neurons. This suggests that efficiency and cellular activity along these neuronal pathways gives an organism its cognitive ability and is further evidence of the lack of causation between brain size and cognitive ability.

The way in which the Homo sapiens has colonised and undoubtedly established great superiority on planet earth indicates a divergence from the great apes, our closest living evolutionary relatives with whom we share the same taxonomic family. The final conclusion made by Herculano-Houzel written in The Journal of Comparative Neurology, vol 513 claims that the human brain is just “a linearly scaled-up primate brain”. Therefore the differences between structures of the brains of different species must be compared in order to find how Homo sapiens have acquired the cognition to accomplish its superiority. A research team from the University of Cambridge undertook a study of the variation in brain size and structure in 23 extinct and 37 existing species of primate. In their analysis of the way brain size has changed as body size evolved, no trend was found. Even along the lineages of evolutionary (phylogenetic) trees, no statistical significance was found between brain and body size. They concluded that the brains and bodies of primates evolved separately due to exposure to different selection pressures which caused there to be no correlation between the sizes2. Where human brains are structurally distinguishable from those of other primate species is by having a significantly larger neocortex.

The neocortex has been found to be the most recent evolutionary development of the human brain structure by anatomical comparison to the great apes. It is a structure that surrounds only mammalian brains. In mice the neocortex covers part of the top surface of the brain whereas in humans the neocortex covers the entirety of the outer surface3. Demonstrating that this cortical region has responsibility for several different cognitive activities, Oliver Sacks documents various instances of patients who have suffered damage to this outer cortical brain region and have acquired a range of symptoms. For example, one patient lost their ability to see in colour4. Another lost his ability to recognise objects and people5. Certain specific regions such as the motor, auditory and vision regions have been identified in the brains of some species. Of those identified, some areas have been found in some mammals but not others, suggesting evolution of such cognitive abilities in certain species. Abilities associated with ‘higher cognitive function’ have been identified and located in primates and not in other orders. In addition, areas conferring particular abilities have a more developed appearance in humans compared to other primates. Moreover, areas have been identified in humans that are non-existent in other primates.

In order to explain how humans have diverged from the great apes in terms of the neocortical size, two theories have been developed. Firstly, ecological theory is based on the selection pressure being food collection and the necessity for its efficiency in competition for resource with other species. A distinguishing factor in the comparison of species is the need to be selective versus the ability to have a wide range of food sources. The former requires an innate ability of which the organism is consciously unaware whereas the latter requires conscious thought and reasoning. To be able to obtain a wide range of food sources an organism must be cognitively adapted to do so as opposed to anatomically adapted. For example, having knowledge of a suitable or likely location requires spatial knowledge and sufficient memory or intuition to be able to navigate the way to it. To gain this wide range, the organism must be able to learn what substances are potentially poisonous, inedible or not beneficial. Greater creativity and cognition allows for different sources to be accessed when anatomy would not otherwise allow.  Using tools to obtain food implies a sophisticated form of cognition. Similarly hunting can require prediction and forethought of probable outcomes as well as co-operation, co-ordination and awareness of one’s own role within a group.  Ultimately having a wider range is an advantage to survival however this does not apply solely to primates. Other species such as lions hunt in a group. Lions however have a much smaller brain and neuron density than humans and some primates. In his article, Alan Camp speculates whether the factors raised in the ecological theory might apply to a greater extent to humans than other species. 

Alternatively, social theory focuses on the intellectual challenge of social interaction and its necessity. Camp argues that it offers a more plausible explanation of the way the primate brain has evolved and also how humans became differentiated from the great apes. The basis of social theory is balancing survival as an individual with the advantages of surviving in a group and how this balance changes in different situations. In this context, intelligence is acquired by solving social problems, such as knowing when to depend on a group or act independently, or knowing what to do in a co-operative effort and how to manipulate others to maximise chances of survival. Camp considers bees, elephants, dolphins, wolves, monkeys and the great apes as some of the most intelligent species, all of which have social lifestyles and depend to varying extents on group living. Social living creates cognitive challenges which require refined skills to solve. For example, signals must be sent, received and interpreted in the co-ordination and conduction of predation. Defence requires forethought, consideration and awareness of others in the group. Some groups of animals offer aid to each other, for example in cleaning, which is a demonstration of emotional intelligence. Many examples of behaviour in response to social challenges are documented in studies particularly of wild primates.

In The Thinking Ape Professor Richard Byrne reports an investigation in which tactical deception was observed among a group of baboons. Byrne observed a young baboon’s interaction with an adult female baboon who had found a large edible root. The young baboon gave a cry which attracted the attention of its mother. From the events that proceeded, Byrne inferred that the mother had made an assumption that the root was stolen from her son; she subsequently chased the adult away, allowing her son to eat the root. Although one cannot be certain of the cause or stimulus of the actions shown, a level of social intelligence was required in the response. Prediction was required from the young baboon as well as knowledge of the significance of that particular call to its mother. This cognition exhibited by the young baboon is an example of Machiavellian intelligence which is currently thought to be shown by a select number of species. In terms of natural selection this intelligence confers a more powerful survival advantage than that implied by the ecological theory.

The plausibility of each theory was measured by the correlation of a measured factor with the neocortical ratio - the ratio of the size of the neocortex to the size of the rest of the brain - of different species of primates. Byrne subsequently found no correlation between ecological factors but a positive correlation between the neocortex ratio and group size to which the organism belongs, in addition to other measures of social challenges such as tactical deception6. These findings therefore indicate a more likely explanation as to how Homo sapiens gained dominance and have evolved with greater intelligence. Nevertheless, I remain sceptical of how we define higher cognitive function. This is because I question the ability of the human species to impartially evaluate capabilities which they possess and find essential or relatable to their own methods of existence. However, the use of the neocortex ratio as opposed to simply neocortex size is important otherwise we continue to wrongly presume that a larger brain is a ‘better’ or higher functioning brain.

There are many other hypotheses for the reason or mechanism by which humans developed their cognitive superiority, including cerebellum size and the number of glial cells found in the brain. Albert Einstein was found to have more glia than other male controls used in an investigation2. This higher abundance of glial cells could have significance in determining what gives higher brain function and how it sets humans apart from other species.

The estimated ratio of neurones to glia with respect to occupied brain volume is 1:1. However there are significantly more glial cells than neurones due to their smaller size. In the nervous system there are many different types of cell which are categorised under the term ‘glial cells’. They are closely associated with neurones and perform a variety of different functions. Hence different subtypes of glia are found in the different areas of the nervous system.  There are two major types found in the central nervous system (CNS), astrocytes and oligodendrocytes.

Astrocytes are in greatest abundance and have been found to be involved in a number of different processes. One of the functions of astrocytes adjacent to capillaries is thought to be the protection of the CNS from toxic or undesirable substances circulating in the blood. Another type can form barriers or associations with synapses, where cell signalling between the glial cell and the nerve terminal modifies the nature of the synaptic transmission. Some glial cell receptors have pumping ion channels and intracellular enzymes as well as a high affinity for certain neurotransmitters. This helps to extract excess chemicals at the synapse.

Oligodendrocytes form the myelin sheath around nerve fibres, crucial to the conduction of action potentials and formation of neuronal networks. Sodium and potassium ion channels are located at the boundary between two segments of myelin, within the cell membrane around the axon. This creates a pathway where the potential for electrical conduction is interchanging, which creates electrical conduction significantly faster than along a non-myelinated axon of the same diameter. This particular feature most clearly implies an evolutionary feature that confers an advantage over an organism which does not possess it, perhaps explaining how improved cognitive function has developed in humans.

Thus, scientists believe that glia have an integral role in information processing. In the development of the brain in the early stages of life, glial cells are thought to be responsible for neuronal migration and the arrangement of neurone cells in the brain. This has been modelled as acting like a scaffold involving a complex signalling mechanism. In addition, the formation of axons and their diameter is guided by the interaction of glia. Findings from cell culture studies provide evidence that synapses are maintained and established by the signals transmitted from astrocytes. These signals and interactions also affect the efficiency of the transmission of the action potentials across the synapse.  Hence the implied importance of glia in the development of cognitive function or indeed dysfunction7.

Dr Andrew Koob has researched the function of glial cells. The result of these studies is the hypothesis that astrocytes have a role in thought processes that occur in the cortex and neocortex. Along evolutionary lineages of phylogenetic trees, both the size and number of astrocytes increases. Humans have been found to have the greatest number of astrocytes of all the species studied. His research has also shown that astrocytes have a role in controlling blood flow to particular regions of the brain during particular activity. This enables particular neurones to gain oxygen, respire and carry out their function to transmit the action potentials necessary to stimulate responses. In an interview, Koob explains how astrocytes produce ‘calcium waves’. These waves are produced by ion pumping channels within the cell by active transport. Calcium then travels down cellular projections in its structure to reach and stimulate either, other astrocytes to do likewise or a neurone to fire a signal. According to Koob, scientists infer from these findings that calcium waves occurring in the cortex are responsible for the transmission process and occurrence of certain thoughts. Koob believes that these findings imply that glia have a role in creativity. He claims that dreams provide evidence of this. When exposed to an external stimulus such as a pin prick, a receptor transmits an action potential through sensory neurones to the CNS and brain where the signal is processed. The idea that one can have vivid dreams whilst not being exposed to any sensory input sending an impulse through sensory neurones is intriguing and inconsistent with this biomechanical model. According to Koob, astrocytes control and initiate neuronal behaviour and responses by releasing calcium waves. He claims that “Neuronal activity without astrocyte processing is a simple reflex”.

It could be argued that a dream is not a sensory experience but a thought process which requires no sensory input. Therefore sensory deprivation has no bearing on whether thought is stimulated or not. I question which neurones are stimulated to fire during thought or ‘day dream’ and whether glial cells have a role in this stimulus. If so, how does the metaphysical become translated into a chemical stimulus that is calcium waves and what induces a calcium wave. Koob explains that small concentrations of calcium can be and often are released randomly without cellular induction, causing calcium waves8.

From claims put forward by Koob one could formulate a theory to explain how different humans have different intelligence or affinities, for example why a musician might feel compelled to learn a particular instrument. Initially one would investigate the frequency, location and strength of randomly released calcium waves. Discoveries from the investigation of Einstein’s brain and its greater proportion of glial cells could validate such a study, especially since his brain was compared to those of adult male doctors with similar scientific motives in their pursuit of intelligence.  However, much literature on the subject of human development and evolution of the mind of the Homo sapiens refers to neuronal circuitry as being aided by glial cells, rather than vice versa.  I speculate whether it is glial cells that allow and control the formation of networks as the brain develops and whether their malfunction could be at least partially responsible for cognitive decline and degeneration we observe in dementia cases.

Evidently from analysis of evolutionary lineages, humans have gained more glial cells as they have gained more knowledge of the surroundings and how it is possible to manipulate the environment as well as other humans. What is changing in our brains now? Are we gaining glia or are we becoming wired more efficiently? Are there limits to the future development of the human brain and how far can our capabilities or future capabilities take us? Such questions are impossible to answer currently because of a lack of resources and evidence. This is inevitable when speculating about the future and especially about a relatively unknown subject area. However, the New Scientist published an article claiming that human brain evolution has reached its limit9. By modelling the information processing capacity of the human brain, researchers at the BT laboratories in Ipswich concluded that no significant improvement would be possible. The basis for their conclusion was that there is a fine balance between the size and number of neurone cells and the capillaries to which they are linked. It is recognised in the conclusion that brain size is irrelevant as an indicator of cognitive capability and instead looks to the number of neurones and synapses between them. Nevertheless, the writer refers to brain size and implies there is significance in the difference between the chimpanzee and human brain proportions.

One section of the research team was focused on the way in which the brain could process information more efficiently. Peter Cochrane claims that the brain could become larger but the heart would have to pump blood at a greater pressure to allow for more oxygen to reach the greater number of cells. In addition, Cochrane states that the axons would need to be wider to significantly improve “processing power”. This would require more myelin insulation which restricts room for the subsequent additional blood capillaries, which in turn reduce the space for the development of axons. In response to this research, Robert Barton, a lecturer at the University of Durham criticises the fact that “they assume that processing information involves the whole brain”. Other criticism stems from the apparent focus on brain size as opposed to efficiency and structural intricacies. I personally criticise the implication that a larger human brain has greater cognitive ability than a smaller one simply because the former has more neurones since this deems the average person of smaller stature to have lesser cognitive ability if their brain was proportionally sized. Barton also comments that the possibility of the evolution of new structures was not considered, nor the potential of existing structures to become more efficient and specialised. This article was published in 1997 and since then research has taken place regarding evolution of the brain, such as that I have cited. For example, more is now known about the existence of glial cells, which illustrates the tentative nature with which this topic should be considered and investigated since we are not currently aware of unknowns in terms of how its anatomy brings about a particular function.

Coming back to the example of Albert Einstein and his higher abundance of glial cells, I question not only whether he was ‘an anomaly’ in terms of his cognitive and creative ability to reason and have the intuition to form his theories; but also whether  genetics enables particular brain development  in some individuals and not others.  How did Einstein’s intellectual ability arise and in the same way how or why would a psychological disorder arise in one individual and not another?
The human genotype is the determinant for various anatomical functions as well as and dysfunctions, and is responsible for the diversity of functions possessed by different individuals. It is our neuroanatomy that determines how and where an action potential is transmitted or processed. The transmission of impulses across synapses can vary in efficiency by the nature of the receptors and their subsequent interaction with neurotransmitters. Other chemicals such as hormones can play a part in this process and its efficiency. Hormones are proteins and a single protein (or polypeptide) is encoded by a single gene. This is one way in which genetics could be influential in our brain development.

When considering the law, David Eagleman questions the ability to ‘blame’ an individual for a criminal act due to their brain’s development and lack of control over it. This leaves individuals to have different capacities to make “sound choices”. He emphasises that “we are not the ones driving the boat of our behaviour”. We cannot consciously access ‘who we are’ and where our ideas come from or how they are generated.  The initial chapters of Eagleman’s book Incognito, The Secret Lives of the Brain focus on how minute and insignificant the conscious self is when decisions are made and opinions created.  Eagleman gives great significance to genetics and presents data from the U.S. Department of Justice. These statistics are based in having identified a specific set of genes that would give a particular predisposition to committing the four given criminal acts. The number of cases in which the offender possesses the specific set of genes is given alongside the number which do not10.

 Since the data uses the average number of crimes committed annually, the reliability of the results will always be improving since the data set is increasing. Fluctuation in the in the number of cases that occur will not affect the results since this is not a factor measured. Conducting the chi –squared test on the data shows that genetics does have significance in inclination to commit crime because there is a less than 5% probability that the difference between results is due to chance.
To be critical of Eagleman’s use of data, as well as specifying the gene or genes involved, the groups should have been further broken down to know whether the cases used were carrying a particular genotype or a proportion of a number of possibilities. If the latter was the case then creating more groups showing the number of specific genes possessed by the group of criminals would better illustrate the likelihood of committing crime. To further validate this study, the number of people who possess the genes in the general population but have not committed a crime should be included; therefore the way genetics influences the probability of criminal action can be seen. However, simply investigating the possession of genes might not be sufficient to determine the extent of the role of genetics in our mental ‘fate’. Epigenetic changes that can alter the genotype inherited by an individual are generated throughout life according to environmental exposures. Therefore the role of the environment has implications for not only the evolution of the mind of an individual, but also their genotype.

Investigating the intricacies not considered by Eagleman, Laura Spinney published an article in the New Scientist questioning whether we start life with afflictions that occurred in our parents before our conception and which influence our likelihood of mental illness later in life. After the Israeli invasion of Lebanon in 1982 there was a high incidence of post-traumatic stress disorder (PTSD) among the returning Israeli soldiers. Upon analysing the data, epidemiologist Zahava Solomon found a significantly higher incidence among soldiers whose parents had survived the Holocaust. When she published her findings Solomon offered the explanation that children of Holocaust survivors had increased vulnerability due to having heard their parent’s accounts of their ordeals. Alternatively, the explanation offered by neuroscience suggests that vulnerability to PTSD existed before these patients were born. This hypothesis was initially devised by Rachel Yehuda, the head of the Traumatic Stress Studies Division of the Mount Sinai School of Medicine in New York City. Yehuda suggests that our epigenetic mechanisms dictate the vulnerability to the future occurrence of mental illness, whereby the environment doesn’t change the genes that are passed on to offspring; rather their genetic activity is changed. The field of neuro-epigenetics was initially researched by Yehuda when she opened a clinic for Holocaust survivors and their families. This allowed her to discover, similarly to Solomon, that the incidence of PTSD and mental illness was higher in the adult offspring of Holocaust survivors than in the general population. As part of the ‘fight or flight’ response, the pituitary gland releases adrenocorticotrophic hormone. This stimulates the adrenal glands to secrete adrenalin and noradrenalin. Cells of the heart, muscles and lungs have receptors for these hormones so are stimulated to act accordingly to the situation. After the situation the adrenal glands secrete the hormone cortisol which binds to glucocorticoid receptors found in the hippocampus to end the stress response. A lower level of cortisol would therefore increase the period of being in a state of stress. Incidence of PTSD is associated to low levels of cortisol. This was reflected in Yehuda’s findings when studying the hormone profiles of Holocaust survivors as well as their children; published in Psychoneuroendocrinology vol. 27. Furthermore, the worse the case of parental PTSD, the lower the cortisol level of the offspring. I would be curious to investigate whether siblings were affected similarly and whether both patents with PTSD caused a significantly lower offspring cortisol level than a subject with one parent with PTSD. I feel that these variables could give greater insight into the origin and significance of the consequences of epigenetic mechanisms.

Yehuda’s findings did not entirely show that the child’s stress response was formed by that of the parents because it could not discount Solomon’s hypothesis that the response is learned or copied. In addition insufficient information was known about the families investigated which could indicate whether parenting or family circumstances independent of historical events were at all influential in the stress response. I argue that other families with different historical circumstances should be included in the study to determine whether this epigenetic trend can be identified in association with other mental illnesses or circumstances.

Progressing from Yehuda’s study, Michael Meaney investigated the quality of parenting of female rats and the stress response of their offspring. The study, conducted at the McGill University in Montreal, showed that rats neglected in childhood had a prolonged stress response which was more volatile and were described as “hyper vigilant”. Meaney offered two implications of this lifestyle. Firstly, the neglected offspring suffered the consequences of the actions of their mothers, and secondly, the neglected offspring benefited from a greater chance of survival by their subsequent hypervigilance. The same research found fewer glucocorticoid receptors in their hippocampus than the rats with attentive mothers. This was the consequence of epigenetic changes altering the activity of the gene encoding the receptor. If there are less receptors, then a lower concentration of cortisol reaches the brain and the stress response remains active for longer.

In 2009, by studying the brain tissue of 24 suicide victims as well as their family history and circumstances growing up, Meaney found a reduced abundance of glucocorticoid receptors in the hippocampus in those who had suffered neglect. These findings were a strong indication to Yehuda that childhood experiences can alter brain development in terms of how the stress response develops. She then sought to determine when in human development these epigenetic mechanisms can have an effect. She studied 38 women who had been pregnant and had been at or near the World Trade Center at the time of the 9/11 attacks. Around 50% of the women had since developed PTSD, and Yehuda was able to monitor the cortisol levels of their children from a very early age. Of the group with PTSD, both mother and child at 9 months had lower cortisol levels compared to the other group. In contrast to Solomon’s and Yehuda’s initial study, the possibility of the effects of verbal accounts of experiences could be rejected because of the age of the offspring. However, the lower cortisol levels could have been caused by events that occurred within those first 9 months, therefore the point at which these epigenetic changes occur and the extent of their effect remains unknown.

Jonathan Seckl, a hormone specialist from the University of Edinburgh who worked alongside Yehuda in the 9/11 study, raises the issue that cortisol has a dual function. As well as diminishing a stress response it alters our metabolism to adapt to food supply. When there is a low abundance of food the liver is stimulated to break down stored protein for energy. Furthermore the kidneys are stimulated to retain a higher concentration of sodium.  This has implications for the study of survivors of concentration camps because of the malnourishment experienced as well as the trauma. When working with Yehuda, Seckl found a strong correlation between the age of Holocaust survivors at the time of their ordeal and the activity of enzymes that break down cortisol in the liver and kidneys. According to Seckl, the metabolism of the survivors was adapted in accordance to the malnutrition experienced. This quality was then inherited by their offspring through the epigenetic changes that subsequently occurred. He claims that this could have resulted in prevalence of PTSD as a ‘side effect’ or alternatively, the result of being conditioned to a dangerous environment where survival was impaired, which was likewise proposed by Meaney. Thus the hypothesis that PTSD as a mental illness arises from past experiences altering epigenetics could be rejected.

The research group led by Meaney also observed that neglected rats that were fostered by a more attentive mother in their first week of life developed a diminished stress response compared to other neglected rats from the same litter. This provokes the nature versus nurture argument. How far the brain evolution of an individual during their lifetime is predetermined by their genetics is a complex question to answer but the role of the environment is being increasingly cited in neuroscience research when considering the remarkable plastic property of the brain. Indeed, according to Yehuda “this is about how nurture transforms nature”11.

The extent to which our brain and mind development is dictated by our genotype is very limited when the plasticity of the brain is taken into account. I question how far genetics predisposes our minds to become what they are since an attribute of the brain known as plasticity allows the brain of an individual to evolve and adapt during their lifetime. A prime example of this was written about by Susan Greenfield in The Private Life of the Brain who documented the case of a six year old child in Italy. He suffered a small curable infection in one eye before he was a year old. Consequently his eye was bandaged (unnecessarily). The bandage was worn during a ‘critical period’ when neuronal pathways would have been forming to sufficiently connect the eye to the brain. The child developed normal sight in the unobstructed eye because connection could be formed in response to the light stimuli that were received. Brain scans revealed that the territory that the connection between the bandaged eye and the brain would be expected to occupy had been used by the other eye. Subsequently when his bandage was removed, the boy remained blind in that eye since. This patient exhibited blindness which was non-congenital but had evolved due to his environment12. A prominent example of plasticity is shown in the development of a human from birth. American neuroscientist Michael Merzenich has conducted studies on various mammalian species and how their development is helped or hindered by various environmental exposures. Any physical changes to the brain of the subject were monitored. His studies revealed two significant periods of time in brain development and its plastic nature. The first is known as the ‘Critical Period’ in which “basic processing machinery” is set up where no learning action or trial is necessary for mechanisms to be established but exposure to a particular factor is necessary. The neuroanatomy is prepared to become selective. Merzenich gives the example of sound as the environmental  factor, whereby if a young brain is reared exposed to ‘meaningless’ or unimportant sound, that sound is made artificially important. The same would likewise occur during exposure to valuable sound such as spoken language for a child. In the case of both the valuable and invaluable exposure, Merzenich claims that neuroanatomy gives each factor a distinct representation according to its significance during the lifetime of the individual, for example for a repertoire of sounds. In addition, Merzenich claims that if a baby were raised continuously exposed to the meaningless noise of a “moderately loud ceiling fan”, its brain would become developed to be “a master processor” for that sound, subsequently impairing its ability to process valuable sound exposure as it develops. Merzenich therefore uses this observation to explain why some children are less adept than others at learning a new language, for example, or at recognising musical tone or melody.

In the second period of plasticity, the brain now acts selectively so the anatomy and biochemistry is refined according to behavioural input such as whether the individual is rewarded for an action or skill by success or significance to the individual. According to the research conducted by Merzenich, this second epoch occurs from late in the first year of life13.

Having referred to a distribution of neuronal territory, many experimental accounts do not specify whether it is the number of individual neurons, synapses, their efficiency, abundance of neurotransmitters, glial cells or the number of potential connections that has significance in brain plasticity and development. When Greenfield writes of studies of kittens conditioned to lift and lower a particular paw during a number of daily sessions, a “denser pattern of connections” can be identified between brain cells in the same brain regions concerned with this activity compared to kittens that have not selectively been conditioned. These studies imply that plasticity alters the number of neuronal circuits.

Therefore as the brain develops, greater connectivity is established throughout it so that different areas of the brain can be connected and interact. The efficiency and quality of the interaction could be improved by a more direct circuit which can be refined over time by plasticity or the activation or abundance of glial cells. This means that information gathered by multiple different senses can be used to generate a response. I speculate whether this is the mechanism by which different perspectives occur. In addition the different territories of nerves that contribute to a single action or perspective can increase in efficiency to different extents, allowing more subtle and refined actions to occur (or cause some areas to be more dominant). For example a violinist becomes more adept at the fingerings for particular notes by knowing how the notes should sound, how it feels, whereas a trumpet player can improve by becoming more fluent in the change in their embouchure position when playing different notes. In The Private Life of the Brain, Greenfield states that the brain is personalised by the arrangements of neuronal connections and regards this as the “aspect of the physical brain that actually is the mind.” Associations and configurations change and shift during a lifetime, by responding to environmental exposures. She highlights that as plasticity occurs, exposures are no longer independent occurrences but certain combinations can stimulate connections caused by a previous experience. Visual signals for example are intercepted and conducted by other pathways stemming from junctions in the network the signal takes to the cortex. These junctions provide associations between different groups of neurons, so information from the environment can be used elsewhere. According to Greenfield, the visual signals are also transmitted in the opposite direction back to their origin so the information can be used to modify or strengthen the way an incoming signal is transmitted.

The nature and mechanisms for brain plasticity have implications for the ecological and social theories mentioned previously. A more complex brain will have a greater capacity for many different neuronal configurations to be formed giving more connections in a network. Greenfield explains this referring to the length of childhood. She claims that a longer ‘childhood’ will enable more connections to be established reflecting the generic cognitive requirement for the species and the animal’s immediate environment, in addition to the specific and individual past experiences. A more complex brain is developed by the environment thus exhibiting more plasticity. Greenfield gives the example of a goldfish, whose environment and lifestyle would not stimulate such great a change in its neuronal circuitry as it would in a primate. In animals such as the goldfish, there is limited learning that can occur from experience, therefore according to Greenfield, they would be “at the dictates of their genes”.

I criticise Greenfield’s use of the term ‘childhood’ since it implies that plasticity of the brain is restricted to childhood, which has a vague definition and has a limit. Furthermore, the studies conducted by Merzenich found that plasticity occurs in the brain throughout life in the second epoch.

This definition of neuroplasticity means that it is enabled by the development of new synaptic connections, greater synaptic efficiency and an element of selectivity by neurotransmitters; hence the interchangeable use of the terms synaptic plasticity and neuroplasticity. Canadian psychologist Donald Hebb created a hypothesis attempting to explain the mechanism for plasticity as long ago as 1949.
When an axon of cell A is near enough to excite a cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’s efficiency, as one of the cells firing B, is increased.(The Organization of Behaviour, 1949)

A pair of cells develops a relationship, the strength of which is determined by how much they have fired together before. Throughout life select neuronal pathways become stronger relative to others and new pathways are formed in a network. By practising an activity and carrying it out repeatedly, one is exercising these pathways and strengthening them. For example when learning to play a musical instrument or the notes in a composition, the relevant neurones are stimulated to repeatedly fire until they reach a critical threshold whereby the connections physically change. It is currently thought that the change is brought about by the activation of proteins. Cyclic adenosine monophosphate response element binding protein (CREB) is one such protein.  For the critical threshold to occur, CREB must be activated to migrate from its peripheral situation to the nucleus of the neurone. In the nucleus CREB binds to particular sections of DNA (or gene), causing these genes to be expressed, encoding specific proteins. The activity of these proteins leads to new stronger synaptic connections forming between two particular neurones. In this way, regular transmission through a particular pathway – long term potentiation - creates a stronger synaptic connection, whereas long term depression of a particular synapse makes it weaker14.

In the Science journal, Michael Brecht and Dietmar Schmitz explain the difficulty of experimentally demonstrating links between cognitive behaviour and such plasticity. Currently studies have been unable to recognise specific locations of synapses involved in and changed by particular experiences in the human brain. This is because the stimulation of a single ‘experience’ can’t be physiologically replicated in brain tissue due to the complexity and nature of the plastic brain. In addition, results obtained from a brain slice preparation can’t be proven to reflect changes in neuroanatomy or cognitive behaviour from an ‘experience’. However, Brecht and Schmitz write of a model system of the rodent cortex to demonstrate whether an experience can be represented by identifiable physical change in a synapse.

Rodents’ whiskers pick up sensory inputs, consequently a signal is sent through specific and known groups of neurones.  In order to be able to more easily detect evidence of rapid synaptic strengthening in response to experience, all whiskers but one were removed from the rodents used. When the whisker is displaced an action potential conveys a signal causing potentiation of the relevant synapses. If this stimulation is long term or frequent, the activated glutamate (NMDA) neurotransmitter receptors become saturated. These findings showed that there was a limit to the synaptic strengthening that could occur thus potentially limiting any possible learning. In the same study, researchers used pharmacology to block the NMDA receptors, as if they were saturated. This caused restoration of potentiation across the synapses because different glutamate receptors were activated to receive the neurotransmitter. The NMDA receptor triggers the calcium concentration in the proceeding neuron to increase which enhances the signal transmission as it progresses through the pathway. New glutamate receptors are also produced in the membrane at the synapse which can add to the calcium release and further increase the transmission efficiency. Brecht and Schmitz speculate that the apparent phases of synaptic strengthening reflect the phases in memory and learning. These phases of memory are characterised by the significance or relevance of the ‘experience’15. For example, being able to play a sequence of notes on the piano using  sheet music versus being able to play fluently without the music, having practised.   
Memory tests are often carried out to measure cognitive ability. Memory is indicative of brain function due to the evident role of synaptic strength, efficiency and plasticity in enhanced learning which allows for it. One interpretation of Susan Greenfield’s reference to the length of “childhood” and neuroplasticity is that many people experience deterioration of their capability to remember as they age. Memory loss is certainly prevalent in many developed countries due to an increase in life expectancy. Consequently, perhaps there is a third epoch to add to those established by Merzenich.

The mechanism of brain plasticity increases in complexity with the implication of metaplasticity. Professor Wickliffe Abraham of the University of Otago, New Zealand explains metaplasticity as how “various intercellular signalling molecules can trigger lasting changes in the ability of synapses to express plasticity”16. Therefore, how neuroplasticity itself occurs is altered according to when and to what extent it should occur by the current condition of the brain.

The concept of metaplasticity could offer an explanation of why the brain degenerates and cognitive function deteriorates despite plasticity being possible, in addition to why the brain is unable to repair itself.
During a conference in 2004 Michael Merzenich claimed that “What we've done in our personal evolutions is build up a large repertoire of specific skills and abilities that are specific to our own individual histories. And in fact they result in a wonderful differentiation in humankind.” There are therefore many ways in which the environment can cause the brain to evolve in a lifetime to varying extents. The case of the Italian boy becoming blind is quite a profound exhibition of plasticity. The degree of plasticity brought about by bilingualism is an issue raised by Catherine de Lange writing in the New Scientist. De Lange is herself bilingual and quotes a study carried out by neuroscientist Laura Ann Pettito. The study used functional near-infrared spectroscopy (fNIRS) to measure the neuronal activity of monolingual and bilingual babies generated by exposure to unfamiliar languages.  fNIRS imaging monitors the change in concentrations and saturation of haemoglobin in the brain. If a particular network of neurones is stimulated to fire, the blood supply to those cells increases and is identifiable on the images. For both groups of babies within their first year any language could become meaningful, consistent with the theory of Merzenich’s first great epoch of plasticity. However for the monolingual babies, this stage ended around their first birthday and attentiveness was focused exclusively to the language they were most familiar with - their mother tongue. This was marked by a decrease in neuronal activity. On the contrary, the bilingual babies were found to have increased neuronal activity at the age of one year. At the same time, both groups of children reached the same milestone stages associated with speech and language at a similar age. Development is subsequently enhanced because more networks and associations between neuronal pathways can form. Psychologist Ellen Bialystok claims this shows that bilingual children are superior in the ‘executive system’ of the brain. This ‘system’ is thought to include many cognitive skills, for example allowing people to refine their focus and block out what is meaningless or irrelevant, such as the meaningless noise example provided by Merzenich. Stronger synaptic connections and an enhanced ‘executive system’ are thought to provide resilience against cognitive decline.  In 2007 Bialystok published data collected from 184 dementia patients. Half of the patients were bilingual, and experienced a delay of four years for the prevalence of dementia symptoms to reach that of the monolingual patients. Similarly in 2010 the same research group found a delay of five years in the progression of symptoms in bilingual Alzheimer’s patients amongst a group of 200 patients. Bialystok claims that occupation and education were taken into account and the results were still found to be valid17.

There are many ways in which plasticity has benefits for prolonged cognitive function, one of which is bought about by physical exercise. In Biological Sciences Review Nancy Rawlings claims that “Physical exercise induces brain plasticity”. Since the studies of Henry Molaison, the role of the hippocampus has been found to be integral to learning and the creation of memories. A study cited by Rawlings found that the size of the hippocampus is larger in those with a greater level of cardiovascular fitness. After a period of regular aerobic exercise the hippocampi of participants had increased in size more than those of participants partaking in stretching exercises. Furthermore the density of neurones and glia in the frontal and temporal lobes increased with fitness. As people age, their hippocampus becomes smaller and this is associated with Alzheimer’s disease and other causes of the deterioration of memory retention.  Similarly to bilingualism, it is thought that this apparent effect of exercise on the hippocampus could delay the progression of memory loss.  The participants in this study showed an improvement in their performance in memory tests after the period of increased aerobic exercise, suggesting that a larger hippocampus is beneficial and has significance.

In this particular study, the method of measuring and comparing cardiovascular fitness of participants is fairly sound. Participants carried out a “VO2 max” test. The test consisted of measuring the maximum oxygen consumption over time during exercise of maximised intensity. This maximum consumption was found using a progressive exercise assessment whereby the intensity of exercise is increased until the oxygen consumption reaches a steady volume. This assessment allowed for a quantitative measurement of cardiovascular fitness. Results can therefore be analysed for statistical significance. However, the way in which exercise is deemed to induce plasticity and what aspects of neurones and glia are altered remains unspecified. Rawlings herself offers several potential explanations. These include alterations to the structure of existing neurones, so that new connections form new neuronal networks. Another possibility is the production of more glia which would enable more efficient transmission of signals. During aerobic exercise, the blood supply reaching the brain increases which enables more oxygen to reach cells and therefore allows several metabolic processes to occur with greater efficiency and effect. Within nerve fibres the strength and efficiency of signals has been found to increase with fitness. Although Rawlings does not specify how evidence of this has been collected or evaluated, she offers the theory that either increased myelination, a change in the number of fibres within a pathway and their diameter, or a combination of these factors might have significance in this mechanism18.

It could be argued that the changes classified as plasticity that are ‘induced’ by exercise are not of the same nature as the changes brought about by traits such as bilingualism. This is because the aspect of exercise investigated for its effect in this case was not a sensory phenomenon that would be experienced differently be different people, rather it was an objective processes altering anatomy that caused this observed ‘plasticity’, or rather, ‘improved cognitive function’.
As claimed by Michael Merzenich, plasticity caused by the environment and a sensory response to it has created an impressive and seemingly infinite array of personalities. However, I argue that some of these can be grouped, not by the response and effect plasticity has given to create personality but the environmental exposure - the stimulus. When curiosity prompts an individual to investigate their own ailments or the incidence of a particular health disorder, they might find several statistics quoting the relative likelihood of the prevalence of a particular disease. For example, the MS Society offers the following statistics on the incidence of multiple sclerosis:  geographically, the distribution of MS cases increases with distance from the equator. In the UK MS has highest prevalence in Scotland. Lastly, despite MS having greatest distribution in Australia and Canada, the Maoris and Inuit tribes situated in these countries respectively have the lowest prevalence of the disease19.  Perhaps it is plasticity giving variation in neuro-physiology between two populations as a response to exposure to factors. This could result in an increased likelihood of having a disease.

Neuroplasticity allows a damaged brain to recover by conscious or unconscious stimulation. Greenfield gives the example of coma victims beginning to recover and finally responding to speech or music. It is often sound that provides this stimulation for the reasons shown by Merzenich in his theories surrounding the development of new-borns. The recovery of stroke victims is very similar. The plasticity of the brain is relied upon to establish new connections to replace what was lost by the incident and means that patients can often make a near complete recovery. Susan Greenfield recounts when her father suffered a stroke and recovered over the course of a year. More strikingly, neuroanatomist Jill Bolte Taylor was able to, study her own brain “from the inside out”. She tells of the fact that “in the course of four hours, I watched my brain completely deteriorate in its ability to process all information” and “I essentially became an infant in a woman’s body”. However she was able to make a complete recovery. In this recovery she noticed that the distribution of her cognitive function between the two hemispheres had shifted. The damage occurred in her left hemisphere, consequently due to plasticity, new pathways were established to replace the lost ones and a greater proportion of these would have been located in the right hemisphere simply because there were more existing pathways remaining after the stroke.  She claims to be more aware of a shift between the two hemispheres and an enhanced or biased role of the right side to compromise the damage suffered20. Not all stroke patients make a complete recovery. One stroke victim named Julia who was featured on a BBC documentary, recovered to the extent that she fully regained her bilingualism.  However she was unable to name objects despite knowing what they are and being able to identify their qualities21.

Henry Molaison was not a stroke patient but demonstrated that plasticity enables recovery from brain damage even at an old age. The hippocampus is a part of the brain that, as a result of this occurrence, scientists now know is associated with the creation of new memories and specifically conscious memory. Consequently at the age of 27, Henry lost the ability to remember events 30 seconds after they had occurred having had his hippocampus surgically removed. He could however remember events leading up to the operation in 1953. Researcher Suzanne Corkin, a researcher, prominent in the study of Henry, recalls him fondly telling her of his childhood and he was capable of recalling past significant events clearly, for example the Wall Street Crash22.  Many scientists conducted experiments on Henry hoping to discover more about how memories form and the extent of the role of the hippocampus in the creation of new memories. One experimental task involved Henry looking in a mirror showing the image of a piece of paper with the outline of a shape that was in front of him. He had to look in the mirror and draw around the shape outline on the page. This was carried out over a number of days, by the end of which Henry had greatly improved at his proficiency at the task, despite his lack of recollection of having ever done it before.

This indicated to researchers that we not only have memories which we can consciously access but also memory and the ability to learn unconsciously which does not involve the hippocampus. Henry was forming new memories, however these were not memories that could be consciously accessed23.

“My father’s brain could not replace the neurones he had lost, but gradually the ones that remained were able to take on the functions of their deceased colleagues. Even in old age, brain plasticity can occur. The brain, or, rather its internal circuitry, is constantly restless. ”

In 1960, poet Pedro Bach-y-Rita suffered a debilitating stroke which left him unable to control his movements, walk or communicate verbally. Until then little was known of the plastic property of the brain so the prospect for any recovery was bleak. However Pedro’s eldest son, George began an exercise regime in an attempt to restore his father’s brain function. Since he couldn’t walk Pedro was encouraged to crawl. When sufficient progression was seen, George then made sure that Pedro undertook everyday activities at home such as washing up; when dishes were broken due to Pedro’s lack of muscle control and coordination, George replaced them with metal ones. This effort was maintained for three years, after which Pedro could return to work and even climb mountains. After his death, Pedro’s son Paul, a neurologist, attended his autopsy. Paul’s hypothesis was that since his father had made such a recovery, the area of tissue damage was fairly small. On the contrary, results from the autopsy showed that nearly 97% of the nerves connecting the spinal cord and the cortex were destroyed in the stroke. Paul then began to speculate whether the brain had reorganised itself as it relearnt different skills. Paul’s research began to focus on the extent to which a damaged brain could be restored by plasticity. He was sure that the blind could be taught to see by using a different sense. He began investigating the sense of touch- “The brain is able to use information coming from the skin as if it were coming from the eyes” Paul Bach-y-Rita. 

Consequently Paul constructed a chair with vibrating pins where a person’s back is. An image taken by a camera is then converted into a pattern or outline of vibrations felt on the subjects back. This device proved fairly successful as blind patients were able to identify objects placed in front of them. Nevertheless Bach-y-Rita’s colleagues remained critical and unconvinced that plasticity could lead to the blind regaining ‘sight’. Bach-y-Rita’s chair would only work on subjects who were not congenitally blind, because the outline or pattern of vibrations would not correspond to any shape of significance. Where the device was successful was when the subject could remember the shape of particular objects. Despite the scepticism, his research continued at the University of Wisconsin and in 2011, the year of Bach-y-Rita’s death, the first prototype for another device was completed. This new device called the BrainPort uses the sense of touch on the tongue. It currently has four hundred electrodes which are placed on the tongue and provide the stimulation. Gradually different degrees of stimulation can be felt and responded to, which correspond to different levels of light picked up from a camera and each electrode acts as a pixel of the image. Patients can be trained to recognise different shapes such as horizontal or vertical lines. Subsequent studies have used scanning to confirm that action potentials fired when this device is used, travel through the visual cortex of the brain despite the patient being unable to see visually21.

Having established how restless the human brain is, to focus on development potential rather than ‘intelligence’ can be argued as more valid. The basis for this is the lack of real definition of ‘intelligence’, especially within the human race because of the role of neuroplasticity and an environment and social experience that is significantly less generic than that of other species.  This can lead us to question how much the environment would need to change for an opportunity of another ‘evolutionary step’ to arise, perhaps towards the brain being able to repair itself. However even with our current cortical state, neuroplasticity has compellingly allowed us to overcome inabilities or conditions by manipulation and conditioning. This concept gives great prospects for stroke victims and even those suffering with blindness. It also can raise awareness of the potential to delay mental deterioration with ageing. Perhaps the concept of neuroplasticity will increase wariness of the use and overuse of pharmacology and the way it can impair development and alter mental activity which is beyond our conscious access.

The way in which perceived trivia can alter our neuronal connections has implications on a personal level.  These could lead to the questioning of the human condition and the extent or existence of free will. Free will is a topic considered extensively by David Eagleman who argues that the conscious self is minimalistic relative to the rest of the workings of the brain due to neuroplasticity. Our inclinations and motives are formed by past experience, hence he argues that there is a limit to the ‘choices’ we have. This idea extends to the extent to which blame can be given to a particular individual. Legal theory is based upon the fact that humans are all equal and have the same capability of moral decision making. According to Eagleman, “People are not created equal.” As examined, genetics, epigenetics, neuronal network development and plasticity create a diversity of capacities of reason and tendency towards opinions and actions. It is already recognised that an adolescent has different drives to an adult, for example because of the difference in the biochemistry of hormones. On this basis, how individuals are convicted and subsequently punished ought to be personalised, but without mental condition becoming an excuse. This could help to significantly reduce the re-offending rate. Indeed, Eagleman states that:

”With different genes and experience, people can be as different on the inside as they are on the outside. As neuroscience improves, we will have a better ability to understand people along a spectrum, rather than in crude binary categories. And this will allow us to tailor sentencing and rehabilitation for the individual rather than maintain that pretence that all brains respond to the same incentives and deserve the same punishments.” 

I argue whether the role of the conscience is so insignificant that individuals are unable to knowingly change their own neuronal circuitry and whether different people would have different capacities to make alterations. Therefore, is our potential and brain development dictated solely by plasticity and thus what is the extent of the placement, role and abundance of glial cells? What meant that Einstein could find his theories whereas his fellow scholars did not? Neuroplasticity does not currently give a direct answer to such questions, however we do know that neuroplasticity allows, among many other things, for people to be persuaded and change perspective, for example to accept the theories of Einstein or Darwin despite societal pressure. Likewise on the topic of legal theory, research surrounding neuroplasticity has implications worldwide and could be considered integral to the current state of lifestyles, politics and internal relations. Unresolved and long term conflicts such as those in the Middle East are illustrations of how the environment shapes an individual and their perspective or opinion. The subsequent actions can be interpreted as extremism by one party and morally acceptable or beneficial for another. The research carried out by Rachel Yehuda on epigenetics and consequential inherited predisposition to poor mental health, stems from such conflict events. For example, the consequences of the Syrian conflict on the numerous fleeing refugees and migrants could have huge implications for mental health and provision for their treatment. Equally though, this predisposition could be altered for the better by the plastic brain changing if migration is successful.

The way in which individuals develop in themselves is strongly influenced by parenting. Attitudes, potentials and inclinations are shaped by exposures and surroundings, even down to the intricacies of ‘meaningless noise’ studied by Michael Merzenich. Furthermore the possible impact of this on epigenetics is somewhat unknown at the time. The ubiquitous dwindling of perseverance in some subjects and not others throughout compulsory education due to lack of belief in a certain degree of success, is purely the approach of attitude and not due to lack of mental and neuronal capacity. The concept of neuroplasticity is evidence of this. ‘I am not a mathematical person’ is a common but incorrect student statement, which should be corrected to ‘I could be a mathematical person’. The process of becoming may not be instant and its length will vary between individuals but it is possible.

Therefore, what is intelligence? Is it purely a mind-set or what we are becoming as our brains evolve over time? By asking such questions, we might have reached the “distant future” referred to by Charles Darwin as he closed The Origin of Species. However there is an infinite future open for exploration of these unanswered questions of lifetime brain development.

2.       New Scientist, It’s Not What You’ve Got, volume 207, No 2771, page 38-41
4.       An Anthropologist on Mars, 1995, Oliver Sacks
5.       The Man Who Mistook His Wife for a Hat, 1985, Oliver Sacks
6.        Psychology Review, The Evolution of Human Intelligence, volume 8, No 1, September 2001
7.       The International Journal of Biochemistry and Cell Biology, 2004,  Cells in Focus: Glial Cells, Kristjan R. Jessen (University College London)
9.       New Scientist, Science: The End of The Road for Brain Evolution, 25th January 1997
10.   Incognito, The Secret Lives of the Brain, 2011, David Eagleman
11.   New Scientist, Born Scared, volume 208 No 2788 page 47-49
12.   The Private Life of the Brain, 2000, Susan Greenfield
14.   The Rough Guide to the Brain, Barry J. Gibb
15.   Science, New series volume 319, No 5859, January 2008, page 39-40,  Rules of Plasticity, Michael Brecht and Dietmar Schmitz
17.   New Scientist, Bilingual Brain Boost Two Tongues, Two Brains, Catherine DeLange (
18.   Biological Sciences Review, volume 27, No 3, February 2015, Exercise and the Brain, Nancy Rawlings
21.   BBC, The Brain: A Secret History ( 2015
23.   BMJ, volume 338, No 7696, March 21st 2009, page 716

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