amygdala A collection of bundles of neurons (nuclei) buried deep in the medial temporal lobes of the cerebral cortex, about the size and shape of a walnut. The amygdala are part of the limbic system and are involved in emotional processing and especially in the learning of emotionally salient associations. Aversive emotions, such as fear, are particularly dependent on the amygdala.
comparator theory An influential theory about the cognitive dysfunctions underlying schizophrenia. Introduced by Irwin Feinberg and substantially developed by Chris Frith, it proposes that delusions – especially delusions of control – originate in failures to distinguish properly between self-generated and externally caused sensations.
dementia The loss of cognitive ability to a point where it impairs the ability of a person to function. Memory loss is a defining feature but there are other impairments as well. There are many forms of dementia, of which the most well known is Alzheimer’s disease. Most instances of dementia are due to the degeneration of neural networks in the brain and are usually irreversible.
hippocampus A sea horse-shaped area found deep within the temporal lobes of the brain. This area is associated with the formation and consolidation of memories and also supports spatial navigation. Damage to the hippocampus can lead to severe amnesia, especially for episodic (autobiographical) memories.
olfactory system One of the most evolutionarily ancient parts of the brain. The olfactory system underpins the sense of smell and is less well-developed in humans than in many other animals. Signals from olfactory sensory neurons in the nose are conveyed to the olfactory bulb deep inside the brain. Olfaction and taste are distinct from the other senses in responding to chemical stimulation.
pheromones Chemical signals secreted by animals, which act as signals to others of the same species. Pheromones serve multiple purposes in social animals, including signalling alarm, fostering aggregation and helping navigation by marking out paths.
prefrontal cortex The most frontal part of the frontal lobes, the prefrontal cortex is associated with high-level cognitive functions, such as metacognition, complex planning and decision making, memory and social interactions. Collectively these operations are sometimes known as ‘executive functions’.
proprioceptive system Proprioception refers to the sense of the position of the various parts of the body and is distinct from both exteroception (the classical senses directed at the outside world) and interoception (the sense of the internal bodily state). Like other sensory pathways, the proprioceptive system involves a pathway from the sensory periphery through the thalamus and to dedicated parts of the cortex.
spatial memory A particular type of memory involving information about one’s location and orientation, necessary for finding one’s way around. Spatial memory depends on the hippocampus, in the medial temporal lobes. In rats, specific hippocampal neurons – place cells – activate only when the rat is in a particular place in its environment, giving rise to the notion of a ‘cognitive map’.
synapses The junctions between neurons, linking the axon of one to a dendrite of another. Synapses make sure that neurons are physically separate from each other so that the brain is not one continuous mesh. Communication across synapses can happen either chemically via neurotransmitters or electrically.
Neurogenesis populates the growing brain with neurons. Neuroplasticity adapts neurons and networks to the changing sensory environment. For much of the 20th century, the belief was that neurogenesis only takes place before birth and through early childhood, after which the brain’s structure was fixed. Today, we know that the brain is modified throughout our lives by neurogenesis. This changes the brain’s wiring diagram because the new neurons form new synapses that must be incorporated into existing networks. However, how neurogenesis is stimulated and its functional significance remains poorly understood. Neurogenesis in the adult hippocampus, a centre for the formation of spatial memory, is one exception. Here, neurogenesis may be stimulated by learning one’s way in a new environment. Once incorporated, the new hippocampal neurons and their synapses contribute to spatial memory functions and even cause the hippocampus to grow. The finding that taxi drivers have an enlarged hippocampus shows this link between exercising a brain function and growth of the region supporting that function. It is reassuring to know that the brain remains responsive and changeable throughout life. Exercise it and you can look forward to becoming both older (inevitably) and wiser (electively).
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Neurogenesis and neuroplasticity allow the brain to adapt to the different demands placed on it at different stages of life.
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Dominant male mice emit airborne chemical signals (pheromones) that stimulate neurogenesis in the olfactory bulb and hippocampus in the brain of female mice. The new neurons in the female’s brain influence her choice of mate, causing her to show a strong preference to mate with dominant males. Whether something similar occurs in the human brain remains to be seen. In man as in mouse, however, the olfactory bulb and hippocampus are sites of significant adult neurogenesis.
RELATED BRAINPOWER
3-SECOND BIOGRAPHY
JOSEPH ALTMAN
1925–
First to report neurogenesis in the adult mammalian brain in the 1960s, though his work was largely ignored at the time
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Michael O’Shea
The hippocampus, the brain’s GPS, can update and expand its route-finding program throughout adult life; good news for London’s cab drivers.
The premise behind brain training is that the brain is just like a muscle and that regular mental exercises can lead to general cognitive performance gains, as well as protection from atrophy. It sounds intuitive, but there is as yet almost no science to support this assumption. In fact, there is good evidence that brain training is pointless for most. For instance, one large-scale online study by Adrian Owen involved more than 11,000 participants between the ages of 18 and 60, who trained on various standard brain-training memory and reasoning tasks for six weeks. Although performance naturally improved on the tasks being trained, crucially there were no improvements on similar, but untrained tasks. This is probably because 21st-century adults lead complicated enough lives and so we are constantly ‘trained’ by the need to understand our PCs, smart phones and computer games, not to mention the Sudoku and crossword puzzles that so many of us enjoy. One recent lab-based training paradigm that has shown some promise, however, involves the tricky task of keeping in mind two different streams of information simultaneously. Not only did performance increase dramatically over the weeks of training on this fiendish exercise, but so did IQ, particularly for those who started in the lower IQ range.
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Keeping your brain trim and smart by mental exercise sounds sensible, but it isn’t well supported by the scientific evidence – at least not yet.
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Although normal adults barely benefit from brain training, there is tentative evidence that this practice aids a range of disorders, including ADHD, early Alzheimer’s disease and even schizophrenia. Why brain training works for these clinical populations is unclear, but it may be that some clinical symptoms arise from a particularly low working-memory capacity and brain training returns this to near normal levels, thus alleviating the more specific problems.
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NEUROGENESIS & NEUROPLASTICITY
3-SECOND BIOGRAPHY
ADRIAN OWEN
1966–
Demonstrated the limited use of standard brain training techniques
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Daniel Bor
A daily crossword workout may make you a champion cruciverbalist, but it won’t help you with quantum physics.
Who are you? You are different from other people – even genetically indistinguishable twins are not born identical. A complex network of environmental, genetic and developmental influences combines to shape the various parts that make up your body – with your brain being especially susceptible. These influences can even occur before birth – during pregnancy, a modification of the womb composition by alcohol, drugs or changes in diet can lead to major changes in behaviour and personality later in life. During normal development, people – and their brains – become receptive to a wide range of environmental influences, including, critically, those arising from relationships with other humans. These differences in brain development coincide with changes in the wiring of the neural networks and these changes lie at the heart of personality differences that neuroscience is just beginning to unravel. So far, the evidence suggests that how neurotic, extrovert or intelligent we are seems to be associated with size and shape of our brains and the activity in the different brain areas. For example, it is well known that the amygdala, a nut-sized brain structure, is a key player in processing fear. Interestingly, it is hyperactive in anxious people or the very phobic, and the higher the anxiety of the patient, the higher the amygdala activity when they see fearful faces.
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You are your brain. Your personality emerges from the interaction of different networks in the brain, shaped by your genes and personal history.
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One way to measure individual differences in brain structure relevant to personality is called ‘voxel-based morphology’, or VBM. VBM quantifies fine differences in brain volume between individuals, which can then be related to different facets of personality. For example, a recent study showed that brain volume in the ‘posterior superior temporal sulcus’ (pSTS) predicted the level of loneliness in a sample of people. Not yet an ‘explanation’ of loneliness, but the pSTS is linked to the processing of social cues, which seems very relevant.
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3-SECOND BIOGRAPHIES
HANS EYSENCK
1916–97
Developed a theoretical framework about personality and the brain
RYOTA KANAI
1977–
Pioneer, with Geraint Rees, of linking neuroimaging to individual differences using VBM
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Tristan Bekinschtein
Macbeth was wrong. We are learning that there is, after all, an art to find the mind’s construction in the face. Sorry Shakespeare.
If you’re getting on in years, you might be complaining to your more sprightly friends and family, as you mix up their names, that your brain isn’t what it once was. Unfortunately, this is one example where science heavily reinforces our intuitions that the general ageing process is at least as brutal on our brains as the rest of our bodies. We start our lives after birth with a full complement of neurons, but the connections between them explode in number in the first 15 months or so of life and continue to sprout aggressively until we end our teenage years. However, very soon after this, in many ways our brain has already reached its peak and the only direction is down. Although certain brain regions decline faster than others, we lose on average approximately 10 per cent of our grey and white matter every decade of our adult lives. Mirroring this, our powers of reasoning, as measured by non-verbal IQ tests, peaks in our early 20s and declines steadily after this. And if that weren’t depressing enough, our long-lived brains end up in our last decades being particularly susceptible to various forms of disease, with Alzheimer’s disease the main concern. After the age of 65, Alzheimer’s is increasingly common and more than 40 per cent of those over 85 have it.
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One drawback of such a bright brain is its decline in later years, when the cortex thins and we become increasingly susceptible to dementia.
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One ray of hope comes from recent evidence to overturn the view that neurogenesis, the formation of new neurons, does not occur in adulthood. Neurogenesis has been observed in the olfactory bulb, responsible for smell, and the hippocampus, a critical region for memory formation. However, like everything else, neurogenesis rates slow as we age. A key question for future research is whether this process can be harnessed to fight Alzheimer’s and other age-related brain diseases.
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NEUROGENESIS & NEUROPLASTICITY
3-SECOND BIOGRAPHIES
ALOIS ALZHEIMER
1864–1915
Neuropathologist who discovered Alzheimer’s disease
JOHN MORRISON
1952–
Prominent modern neuroscientist specializing in the ageing brain
LISBETH MARNER
1974–
Neuropathologist who showed age-related white matter changes
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Daniel Bor
‘Old age ain’t no place for sissies’, according to Bette Davis, herself sampling H. L. Mencken. Of all the ages of man (and woman), the seventh is the cruellest.
Among the neurodegenerative diseases, Parkinson’s is second only to Alzheimer’s in its prevalence, with one per cent of people over 60 and four per cent of those over 80 affected. There is no cure and no known cause. Early signs that can anticipate diagnosis by several years include: loss of sense of smell, insomnia, constipation, depression and a tremor in one thumb. Later, shaking in both arms, slowness of movement, postural instability, rigidity, muscular weakness and stooped posture develop. Finally, about 20 per cent of people with the condition exhibit dementia. Parkinson’s involves progressive degeneration of particular neurons which, when healthy, release dopamine in other parts of the brain involved in movement control. This impairs the smooth execution of voluntary movement. Drugs can manage these symptoms and slow the disease’s progression. However, not all symptoms are easily explained by this mechanism. In advanced stages, when medication may become ineffective, deep brain stimulation (DBS), involving implanting a brain pacemaker, may be beneficial. A cure, based on stem cell transplantation or gene therapy research, remains a distant hope. Perhaps more immediate benefit resides in recognizing subtle signs that appear years before normal diagnosis. Introducing treatments at very early stages may prevent the progression of the disease.
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Parkinson’s is a debilitating prevalent disease affecting movement and mood, in which the brain’s dopamine-containing neurons degenerate and die. There is no known cause or cure.
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Progress in Parkinson’s research is being made on several fronts. The prevention of neuron degeneration through the development of anticell death agents shows some promise, as does the gene therapy involving the use of viral carriers to introduce therapeutic genes into specific brain regions. Stem cell research in animals is another exciting area. Here, the aim is to replace dead and dying dopamine-producing neurons with new cells transplanted into motor centres in the brain.
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3-SECOND BIOGRAPHIES
JAMES PARKINSON
1755–1824
The first to thoroughly document the symptoms of shaking palsy (1817)
JEAN-MARTIN CHARCOT
1825–93
Proposed renaming the disease to honour the name of James Parkinson
ARVID CARLSSON
1923–
Established the crucial role of dopamine depletion in Parkinson’s
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Michael O’Shea
Parkinson’s disease gradually blots out the neurons responsible for motor co-ordination, producing the characteristic shaking motion and slow movements in people with the condition.
Ernest Rutherford split the atom in 1917. Forty years later, in work that had much the same seismic effect on his own field, Roger Sperry effectively ‘split’ the brain, revealing the functions, limitations, co-operation and differences of the two hemispheres and establishing the foundations for brain mapping and new theories of the mind.
Sperry started academic life as an English Literature student and all-round athlete at Oberlin College, Ohio. One of his ancillary courses was Introductory Psychology, and it soon became his overriding interest. After graduating with a BA, he took degrees in psychology and zoology (from the University of Chicago) going on to postdoctoral research at Harvard. After a spell as Associate Professor at Chicago – multi-tasking in the schools of anatomy, psychology and neurological diseases – he was poached by the California Institute of Technology, where he became Hixon Professor of Psychobiology until his retirement.
Sperry’s early research focused on brain circuitry and neural specificity. His elegant experiments indicated that nerves specific to certain activities (seeing or locomotion, for example) could not reroute themselves to reproduce their original function if they were transplanted; at least in these respects the mammalian nervous system seems hardwired and unable to modify or adapt itself. These discoveries provided strong evidence that the development of neural pathways occurred via intricate chemical codes under genetic control, a foundational idea within modern development neurobiology.
But it was while on an enforced sabbatical (he had been diagnosed with tuberculosis or TB) that Sperry began to think about the corpus callosum – the bridge that joins two hemispheres of the brain – a structure whose function no one really understood. ‘Splitting’ the brain by cutting through this structure proved to alleviate the symptoms of epilepsy without apparent impairment. Sperry’s work on ‘split-brain’ patients showed that the two hemispheres worked independently but in co-operation; without the linking crossover system of the corpus callosum, they behaved much like two separate brains in one head. This research spearheaded a string of discoveries about the lateralization of brain function – for example, that language is usually (but not always) lateralized to the left hemisphere. It also led him to speculate that ‘split-brain’ patients may, in fact, have two separate and simultaneously existing consciousnesses. Sperry’s work won him a share in the Nobel Prize for Physiology or Medicine in 1981. It also led him to speculate on a theory of mind (that consciousness is an emergent function of neural activity), which he considered to be his most important contribution to neurobiology.
Born in Hartford, Connecticut
1935
BA from Oberlin College, Ohio
1937
MA in Psychology
1941
PhD in Zoology from University of Chicago under Paul Weiss
1941–46
Fellowships at Harvard
1942
Worked at Yerkes Laboratory of Primate Biology
1942–45
Part of the OSRD Medical Research Unit on Nerve Injuries
1946
Associate Professor of Anatomy at University of Chicago
1949
Diagnosed with TB and sent to Adirondacks for treatment
1952–53
Associate Professor of Psychology at University of Chicago; Section Chief for Neurological Diseases and Blindness at the National Institute of Health
1954
Hixon Professor of Psychobiology at California Institute of Technology
1965
Published first of a series of papers proposing a new theory of mind
1972
California Scientist of the Year
1981
Awarded Nobel Prize (jointly) for Physiology or Medicine ‘for his discoveries concerning the functional specialization of the cerebral hemispheres’.
1984
Retired but remained Emeritus Professor of Psychobiology at California Institute of Technology
1989
Awarded the National Medal of Science
1991
Lifetime Achievement Award, American Psychological Association
17 April 1994
Died in Pasadena, California
Approximately 0.7 per cent of the population will experience schizophrenia at some point in life. Contrary to some common beliefs, its main features are not split or multiple personalities, but a combination of ‘negative’ symptoms, including emotional flattening and lack of motivation, and ‘positive’ features, including perceptual hallucinations, false beliefs, paranoid delusions and disorganized thinking and speech. ‘Thought insertions’ – patients experiencing a lack of ownership of their own thoughts – can be among the most distressing symptoms. Although the brain basis of schizophrenia is not well understood, there are some promising theories. The comparator theory proposes that schizophrenic brains have problems distinguishing between self-generated and externally caused sensations. For instance, when we make a movement, our brain predicts the sensory consequences of the movement so that we experience the movement, as self-caused. If these predictions go awry, the brain may falsely attribute control to some external source, leading to a ‘delusion of control’. Recently, the theory has been extended to explain perceptual hallucinations, using the idea that perceptions are also based on predictions. This implies that schizophrenics, unlike most, should be able to tickle themselves, which turns out to be true.
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Schizophrenia involves perceptual hallucinations, false beliefs and thought insertions. These symptoms may arise from a failure to properly combine prior expectations with new sensory evidence.
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Several genes have now been associated with susceptibility to schizophrenia. One of them, COMT (catechol-O-methyltransferase), is involved in breaking down the neurotransmitter dopamine, involved in prediction-based learning. The identification of such genetic targets may open new avenues for diagnosis and treatment. However, there is no simple link between genes and mental states. Such conditions involve complex networks of genetic, developmental and psycho-social causes.
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VOLITION, INTENTION & ‘FREE WILL’
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EUGEN BLEULER
1857–1939
Swiss psychiatrist and contemporary of Freud, who coined the term schizophrenia
CHRIS FRITH
1942–
Pioneer in the neuroscience of schizophrenia
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Anil Seth
Most of us can differentiate between what we do and what comes at us from outside; schizophrenics have problems with this, so feel constantly under ambush from different parts of themselves.
The essence of meditation is to train oneself to be as aware as possible of as little as possible. Unlike brain training, meditation is increasingly being shown to have profound effects on thought, emotions and the brain. For instance, long-term meditators have a shrunken amygdala, a brain region associated with anxiety or fear, and an enlarged prefrontal cortex, associated with our highest forms of cognitive processing and intelligence. Long-term meditators also appear somewhat protected from dementia, which makes sense given that meditation causes brain regions linked to complex thought and memory to grow instead of shrink. Activity in the prefrontal cortex can also become more efficient through meditation, so that less activity is needed to perform optimally on a given task. In line with this, long-term meditation improves a range of attentional, working memory and spatial processing tasks. Perception also appears altered, with experienced meditators being able to detect fainter stimuli and being less susceptible to certain visual illusions. Meditation even reduces the need for sleep. Due to its stress-reducing properties, meditation is increasingly being used as a clinical tool, relieving symptoms of chronic pain, depression, anxiety, schizophrenia and other conditions.
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In the normal population, meditation has a profound effect on the brain, calms emotions, boosts cognition and can help treat a range of mental illnesses.
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One needn’t spend years in intensive meditation practice before any benefits are seen. One study found that just four meditation sessions were sufficient to increase working memory capacity. Another showed that five sessions increased performance on an attentional task that involved resolving conflict. At the same time, just five sessions are also needed to lessen a participant’s sense of anxiety, anger and tiredness.
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NEUROGENESIS & NEUROPLASTICITY
3-SECOND BIOGRAPHIES
JON KABAT-ZINN
1944–
Pioneer of applying meditation to clinical populations
SARA LAZAR
1965–
Carried out important studies linking meditation with brain changes
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Daniel Bor
