Posts tagged neuroscience
Articles and news from the latest research reports.
How the Brain Remembers Pleasure and Its Implications for Addiction
Key details of the way nerve cells in the brain remember pleasure are revealed in a study by University of Alabama at Birmingham (UAB) researchers published today in the journal Nature Neuroscience. The molecular events that form such “reward memories” appear to differ from those created by drug addiction, despite the popular theory that addiction hijacks normal reward pathways.
Brain circuits have evolved to encourage behaviors proven to help our species survive by attaching pleasure to them. Eating rich food tastes good because it delivers energy and sex is desirable because it creates offspring. The same systems also connect in our mind’s environmental cues with actual pleasures to form reward memories.
This study in rats supports the idea that the mammalian brain features several memory types, each using different circuits, with memories accessed and integrated as needed. Ancient memory types include those that remind us what to fear, what to seek out (reward), how to move (motor memory) and navigate (place memory). More recent developments enable us to remember the year Columbus sailed and our wedding day.
“We believe reward memory may serve as a good model for understanding the molecular mechanisms behind many types of learning and memory,” said David Sweatt, Ph.D., chair of the UAB Department of Neurobiology, director of the Evelyn F. McKnight Brain Institute at UAB and corresponding author for the study. “Our results provide a leap in the field’s understanding of reward-learning mechanisms and promise to guide future attempts to solve related problems such as addiction and criminal behavior.”
The study is the first to illustrate that reward memories are created by chemical changes that influence known memory-related genes in nerve cells within a brain region called the ventral tegmental area, or VTA. Experiments that blocked those chemical changes — a mix of DNA methylation and demethylation — in the VTA prevented rats from forming new reward memories.
Methylation is the attachment of a methyl group (one carbon and three hydrogens) to a DNA chain at certain spots (cytosine bases). When methylation occurs near a gene or inside a gene sequence, it generally is thought to turn the gene off and its removal is thought to turn the gene on. This back-and-forth change affects gene expression without changing the code we inherit from our parents. Operating outside the genetic machinery proper, epigenetic changes enable each cell type to do its unique job and to react to its environment.
Furthermore, a stem cell in the womb that becomes bone or liver cells must “remember” its specialized nature and pass that identity to its descendants as they divide and multiply to form organs. This process requires genetic memory, which largely is driven by methylation. Note, most nerve cells do not divide and multiply as do other cells. They can’t, according to one theory, because they put their epigenetic mechanisms to work making actual memories.
Natural pleasure versus addiction
The brain’s pleasure center is known to proceed through nerve cells that signal using the neurochemical dopamine and generally is located in the VTA. Dopaminergic neurons exhibit a “remarkable capacity” to pass on pleasure signals. Unfortunately, the evolutionary processes that attached pleasure to advantageous behaviors also accidentally reinforced bad ones.
Addiction to all four major classes of abused drugs — psychostimulants, opiates, ethanol and nicotine — has been linked to increased dopamine transmission in the same parts of the brain associated with normal reward processing. Cues that predict both normal reward and effects of cocaine or alcohol also make dopamine nerve cells fire as do the experiences they recall. That had led to idea that drug addiction must take over normal reward-memory nerve pathways.
Along those lines, past research has argued that dopamine-producing neurons in the VTA — and in a region that receives downstream dopamine signals from the VTA called the nucleus accumbens (NAC) — both were involved in natural reward and drug-addiction-based memory formation. While that may true to some extent, this study revealed that blocking methylation in the VTA with a drug stopped the ability of rats to attach rewarding experiences to remembered cues but doing so in the NAC did not.
“We observed an important distinction, not in circuitry, but instead in the epigenetic regulation of that circuitry between natural reward responses and those that occur downstream with drugs of abuse or psychiatric illness,” said Jeremy Day, Ph.D., a post-doctoral scholar in Sweatt’s lab and first author for this study. “Although drug experiences may co-opt normal reward mechanisms to some extent, our results suggest they also may engage entirely separate epigenetic mechanisms that contribute only to addiction and that may explain its strength.”
To investigate the molecular and epigenetic changes in the VTA, researchers took their cue from 19th century Russian physiologist Ivan Pavlov, who was the first to study the phenomenon of conditioning. By ringing a bell each day before giving his dogs food, Pavlov soon found that the dogs would salivate at the sound of the bell.
In this study, rats were trained to associate a sound tone with the availability of sugar pellets in their feed ports. This same animal model has been used to make most discoveries about how human dopamine neurons work since the 1990s, and most approved drugs that affect the dopamine system (e.g. L-Dopa for Parkinson’s) were tested in it before being cleared for human trials.
To separate the effects of memory-related brain changes from those arising from the pleasure of the eating itself, the rats were separated into three groups. Rats in the “CS+” rats got sugar pellets each time they heard a sound cue. The “CS–” group heard the sound the same number of times and received as many sugar pellets — but never together. A third tone-only group heard the sounds but never received sugar rewards.
Rats that always received sugar with the sound cue were found to poke their feed ports with their noses at least twice as often during this cue as control rats after three, 25-sound-cue sessions. Nose pokes are an established measure of the degree to which a rat has come to associate a cue with the memory of a tasty treat.
The team found that those CS+ rats (sugar paired with sound) that were better at forming reward memories had significantly higher expression of the genes Egr1 and Fos than control rats These genes are known to regulate memory in other brain regions by fine-tuning the signaling capacity of the connections between nerve cells. In a series of experiments, the team next revealed the methylation and demethylation pattern that drove the changes in gene expression seen as memories formed.
The study demonstrated that reward-related experiences caused both types of DNA methylation known to regulate gene expression.
One type involves attaching methyl groups to pieces of DNA called promoters, which reside immediately upstream of individual gene sequences (between genes), that tell the machinery that follows genetic instructions to “start reading here.” The attachment of a methyl group to a promoter generally interferes with this and silences a nearby gene. However, ancient organisms such as plants and insects have less methylation between their genes, and more of it within the coding regions of the genes themselves (within gene bodies). Such gene-body methylation has been shown to encourage rather than silence gene expression.
Specifically, the team reported that two sites in the promoter for Egr1 gene were demethylated during reward experiences and, to a greater degree, in rats that associated the sugar with the sound cue. Conversely, spots within the gene body of both Egr1 and Fos underwent methylation as reward memories formed.
“When designing therapeutic treatments for psychiatric illness, addictions or memory disorders, you must profoundly understand the function of the biological systems you’re working with,” Day said. “Our field has learned from experience that attempts to treat addiction with something that globally impairs normal reward perception or reward memories do not succeed. Our study suggests the possibility that future treatments could dial down drug addiction or mental illness without affecting normal rewards.”
(Image: Corbis)
Nicotine exposure gives baby rats addictive personalities
Results suggest explanation for why people exposed to nicotine in the womb are more likely to become smokers.
Exposure to nicotine in the womb increases the production of brain cells that stimulate appetite, leading to overconsumption of nicotine, alcohol and fatty foods in later life, according to a new study in rats.
Smoking during pregnancy is known to alter fetal brain development and increase the risk of premature birth, low birth weight and miscarriage. Prenatal exposure to nicotine also increases the likelihood of tobacco use and nicotine addiction in later life, but exactly how is unclear.
To understand the mechanisms behind this effect, Sarah Leibowitz, a behavioural neurobiologist at the Rockefeller University in New York, and her colleagues injected pregnant rats with small doses of nicotine — which the researchers say are comparable to the amount a pregnant woman would get from smoking one cigarette a day — and then examined the brains and behaviour of the offspring.
In a paper published in Journal of Neuroscience, they found that nicotine increased the production of specific types of neurons in the amygdala and hypothalamus. These cells produce orexin, enkephalin and melanin-concentrating hormone, neuropeptides that stimulate appetite and increase food intake.
Rats exposed to nicotine in the womb had more of these cells and produced more of the neuropeptides than those that were not, and this had long-term consequences on their behaviour. As adolescents, they not only self-administered more nicotine, but also ate more fat-rich food and drank more alcohol.
“These peptide systems stimulate food intake,” says Leibowitz, “but we found that they similarly increase the consumption of drugs and stimulate the brain’s reward mechanisms that promote addiction and substance abuse.”
Leibowitz notes that children whose mothers smoked during pregnancy are more likely to smoke themselves during adolescence and adulthood. Her team’s findings suggest a possible mechanism for that.
The use of nicotine patches or e-cigarettes during pregnancy could have a similar effect. “Whether given subcutaneously, as in our study, or via smoking or patches, the same amount of nicotine would still get into the brain to affect neuronal development and function,” Leibowitz says.
The results highlight the toxic effects of nicotine exposure on brain development, says George Koob, a neurobiologist at the Scripps Research Institute in La Jolla, California. He also adds that the study casts new light on the role of these neuropeptides in reward and motivation.
In earlier work, Leibowitz and her colleagues showed that rats exposed to fat and alcohol in the womb likewise overconsume these substances as adolescents. “Our studies make it very clear that neuronal development in utero is highly sensitive to these substances,” she says, “with each promoting their overconsumption and addictive-like behaviour in the offspring.”
She and her collaborators are now comparing the effects of nicotine, fat and alcohol to learn more about how this promotion occurs. They are also exploring ways to reverse the effects of prenatal exposure to these substances, thus preventing their overconsumption in later life, which could lead to addiction and obesity.
Russell Foster is a circadian neuroscientist: He studies the sleep cycles of the brain. And he asks: What do we know about sleep? Not a lot, it turns out, for something we do with one-third of our lives. In this talk, Foster shares three popular theories about why we sleep, busts some myths about how much sleep we need at different ages — and hints at some bold new uses of sleep as a predictor of mental health.
Russell Foster studies sleep and its role in our lives, examining how our perception of light influences our sleep-wake rhythms.
Brain Atrophy Seen in Patients With Diabetes
Brain atrophy rather than cerebrovascular lesions may explain the relationship between type 2 diabetes mellitus (T2DM) and cognitive impairment, according to a study published online Aug. 12 in Diabetes Care.
Chris Moran, M.B., B.Ch., from Monash University in Melbourne, Australia, and colleagues analyzed magnetic resonance imaging scans and cognitive tests in 350 participants with T2DM and 363 participants without T2DM. In a blinded fashion, cerebrovascular lesions (infarcts, microbleeds, and white matter hyperintensity [WMH] volume) and atrophy (gray matter, white matter, and hippocampal volumes) were evaluated.
The researchers found that T2DM was associated with significantly more cerebral infarcts and significantly lower total gray, white, and hippocampal volumes, but not with microbleeds or WMH. Gray matter loss was distributed mainly in medial temporal, anterior cingulate, and medial frontal lobe locations in patients with T2DM, while white matter loss was distributed in frontal and temporal regions. Independent of age, sex, education, and vascular risk factors, T2DM was associated with significantly poorer visuospatial construction, planning, visual memory, and speed. When adjusting for hippocampal and total gray volumes, the strength of these associations was cut by almost one-half, but was unchanged with adjustments for cerebrovascular lesions or white matter volume.
"Cortical atrophy in T2DM resembles patterns seen in preclinical Alzheimer’s disease," the authors write. "Neurodegeneration rather than cerebrovascular lesions may play a key role in T2DM-related cognitive impairment."
(Source: pri-med.com)
Depressed people have a more accurate perception of time
People with mild depression underestimate their talents. However, new research carried out researchers at the University of Limerick and the University of Hertfordshire shows that depressed people are more accurate when it comes to time estimation than their happier peers.
Depressed people often appear to distort the facts and view their lives more negatively than non-depressed people. Feelings of helplessness, hopelessness and worthlessness and of being out of control are some of the main symptoms of depression. For these people time seems to pass slowly and they will often use phrases such as “time seems to drag” to describe their experiences and their life. However, depressed people sometimes have a more accurate perception of reality than their happier friends and family who often look at life through rose-tinted glasses and hope for the best.
Dr Rachel Msetfi, senior lecturer in psychology, University of Limerick and one of the studies authors, said: “We found that depressed people tended to be more accurate when estimating time whereas non-depressed people tended to be less accurate. This finding, along with some of our other work, suggests that depression leads to more attention paid to time passing. Sometimes this might lead to a phenomenon known as ‘depressive realism’, though on other occasions time might seem to be moving more slowly than usual.”
In the study, volunteers, who were classified as mildly depressed or non-depressed, made estimates of the length of different time intervals of between two and sixty-five seconds. Overall, those volunteers who were mildly–depressed were more accurate in their time estimations.
Dr Msetfi noted that: “Time is a very important part of everyday experience, it flies when we are having fun or enjoying ourselves. One of the commonest experiences of depression is that people feel that time passes slowly and sometimes painfully. Our findings may help to shed a little light on how people with depression can be treated. People with depression are often encouraged to check themselves against reality, but maybe this timing skill can be harnessed to help in the treatment of mildly-depressed people. These findings may also link to successful mindfulness based treatments for depression which focus on encouraging present moment awareness.”
The paper, “Time perception and depressive realism: Judgement type, psychophysical functions and bias”, is published in PLOS ONE.
(Source: ul.ie)
Omega-3 removes ADHD symptoms
A new multidisciplinary study shows a clear connection between the intake of omega-3 fatty acids and a decline in ADHD symptoms in rats.
Researchers at the University of Oslo have observed the behaviour of rats and have analyzed biochemical processes in their brains. The results show a clear improvement in ADHD-related behaviour from supplements of omega-3 fatty acids, as well as a faster turnover of the signal substances dopamine, serotonin and glutamate in the nervous system. There are, however, clear sex differences: a better effect from omega-3 fatty acids is achieved in male rats than in female.
Unknown biology behind ADHD
Currently the psychiatric diagnosis ADHD (Attention Deficit/Hyperactivity Disorder) is purely based on behavioural criteria, while the molecular genetic background for the illness is largely unknown. The new findings indicate that ADHD has a biological component and that the intake of omega-3 may influence ADHD symptoms.
“In some research environments it is controversial to suggest that ADHD has something to do with biology. But we have without a doubt found molecular changes in the brain after rats with ADHD were given omega-3,” says Ivar Walaas, Professor of Biochemistry.
The fact that omega-3 can reduce ADHD behaviour in rats has also been indicated in previous international studies. What is unique about the study in question is a multidisciplinarity that has not previously been seen, with contributions from behavioural science in medicine as well as from psychology, nutritional science and biochemistry.
Hyperactive rats
The rats used in the study are called SHR rats – spontaneously hypertensive rats. Although this is primarily a common type of rat, random mutations in their genes have resulted in genetic damage that produces high blood pressure. It is therefore first and foremost blood-pressure researchers who have so far been interested in these rats.
However, the rats do not suffer from high blood pressure until they have reached puberty. Before that age they present totally different symptoms – namely hyperactivity, poor ability to concentrate and impulsiveness. It is exactly these three criteria that form the basis for making the ADHD diagnosis in humans. The animals also react to Ritalin, the central nervous system stimulant, in the same way as humans with ADHD: the hyperactive responses are stabilized. SHR rats are therefore increasingly used in research as a model for ADHD.
Supplements as early as the foetal stage
Researchers believe that omega-3 can have an effect from the very beginning of life. Omega-3 was therefore added to the food given to mother rats before they were impregnated, and this continued throughout their entire pregnancy and while they fed their young. The baby rats were also given omega-3 in their own food after they were separated from their mother at the age of 20 days. Another group of mother rats were given food that did not have omega-3 added, thus creating a control group of SHR offspring that had not been given these fatty acids at the foetal stage or later.
The researchers started to analyze the behaviour of the offspring some days after they were separated from the mother. They studied behaviour driven by reward as well as spontaneous behaviour. Substantial differences were noted for both types of behaviour between the rats that had been given the omega-3 supplement as foetuses and as baby rats and those that had not.
Rewards made male rats more concentrated
The reward-driven behaviour was such that the rats were allowed access to a drop of water each time they pressed an illuminated button. The ADHD rats that had not been given omega-3 could not concentrate on pressing the button, whereas the rats that had been brought up on omega-3 easily managed to hold their concentration for the seconds this takes and were able to enjoy a delicious drop of water as a reward.
Surprisingly enough, it was only male rats that showed an improvement in reward-driven behaviour. However, with regard to the rats’ spontaneous behavior, the same type of reduction in hyperactivity and attention difficulties was noted in both male and female rats that had been given the omega-3 supplement.
Changes in brain chemistry
Professor Walaas and his research group became involved in the study at this point in order to analyze the molecular processes in the rats’ brains.
The group analyzed the level of the chemical connections in the brain, the so-called neurotransmitters that transfer nerve impulses from one nerve cell to another. The researchers measured how much of the neurotransmitters such as dopamine, serotonin and glutamate was released and broken down within the nerve fibres. A key player in this work was Kine S. Dervola, PhD candidate, who reports clear sex differences in the turnover of the neurotransmitters – just as there had been in the reward-driven behaviour.
“We saw that the turnover of dopamine and serotonin took place much faster among the male rats that had been given omega-3 than among those that had not. For serotonin the turnover ratio was three times higher, and for dopamine it was just over two and a half times higher. These effects were not observed among the female rats. When we measured the turnover of glutamate, however, we saw that both sexes showed a small increase in turnover,” Ms Dervola tells us.
Transferrable to humans?
The researchers are cautious about drawing conclusions as to whether the results can be transferred to humans.
“In the first place there is of course a difference between rats and humans, and secondly the rats are sick at the outset. Thirdly the causes of ADHD in humans are in no way mapped sufficiently well. But the end result of what takes place in the brains of both rats and humans with ADHD is hyperactivity, poor ability to concentrate and impulsiveness,” says Professor Walaas, and concludes:
“Giving priority to basic research like this will greatly increase our detailed knowledge of ADHD.”
Reference:
Dervola, Kine-Susann Noren; Roberg, Bjørg Åse; Wøien, Grete; Bogen, Inger Lise; Sandvik, Torbjørn; Sagvolden, Terje; Drevon, Christian A, Espen B. Johansen and Sven Ivar Walaas (2012). Marine omega-3 polyunsaturated fatty acids induce sex-specific changes in reinforcer-controlled behavior and neurotransmitter metabolism in a spontaneously hypertensive rat model of ADHD. Behavioral and Brain Functions. ISSN 1744-9081. 8(56).
(Source: med.uio.no)
Receptor may aid spread of Alzheimer’s and Parkinson’s in brain
Scientists at Washington University School of Medicine in St. Louis have found a way that corrupted, disease-causing proteins spread in the brain, potentially contributing to Alzheimer’s disease, Parkinson’s disease and other brain-damaging disorders.
Image: An electron micrograph shows clumps of corrupted tau protein outside a nerve cell. Scientists have identified a receptor that lets these clumps into the cell, where the corruption can spread. Blocking this receptor with drugs may help treat Alzheimer’s, Parkinson’s and other disorders.
The research identifies a specific type of receptor and suggests that blocking it may aid treatment of theses illnesses. The receptors are called heparan sulfate proteoglycans (HSPGs).
“Many of the enzymes that create HSPGs or otherwise help them function are good targets for drug treatments,” said senior author Marc I. Diamond, MD, the David Clayson Professor of Neurology. “We ultimately should be able to hit these enzymes with drugs and potentially disrupt several neurodegenerative conditions.”
The study is available online in the Proceedings of the National Academy of Sciences.
Over the last decade, Diamond has gathered evidence that Alzheimer’s disease and other neurodegenerative diseases spread through the brain in a fashion similar to conditions such as mad cow disease, which are caused by misfolded proteins known as prions.
Proteins are long chains of amino acids that perform many basic biological functions. A protein’s abilities are partially determined by the way it folds into a 3-D shape. Prions are proteins that have become folded in a fashion that makes them harmful.
Prions spread across the brain by causing other copies of the same protein to misfold.
Among the most infamous prion diseases are mad cow disease, which rapidly destroys the brain in cows, and a similar, inherited condition in humans called Creutzfeldt-Jakob disease.
Diamond and his colleagues have shown that a part of nerve cells’ inner structure known as tau protein can misfold into a configuration called an amyloid. These corrupted versions of tau stick to each other in clumps within the cells. Like prions, the clumps spread from one cell to another, seeding further spread by causing copies of tau protein in the new cell to become amyloids.
In the new study, first author Brandon Holmes, an MD/PhD student, showed that HSPGs are essential for binding, internalizing and spreading clumps of tau. When he genetically disabled or chemically modified the HSPGs in cell cultures and in a mouse model, clumps of tau could not enter cells, thus inhibiting the spread of misfolded tau from cell to cell.
Holmes also found that HSPGs are essential for the cell-to-cell spread of corrupted forms of alpha-synuclein, a protein linked to Parkinson’s disease.
“This suggests that it may one day be possible to unify our understanding and treatment of two or more broad classes of neurodegenerative disease,” Diamond said.
“We’re now sorting through about 15 genes to determine which are the most essential for HSPGs’ interaction with tau,” Holmes said. “That will tell us which proteins to target with new drug treatments.”
(Source: news.wustl.edu)
First to measure the concerted activity of a neuronal circuit
Neurobiologists from the Friedrich Miescher Institute for Biomedical Research have been the first to measure the concerted activity of a neuronal circuit in the retina as it extracts information about a moving object. With their novel and powerful approach they can now not only visualize networks of neurons but can also measure functional aspects. These insights are direly needed for a better understanding of the processes in the brain in health and disease.
For many decades electrophysiology and genetics have been the main tools in the toolbox of approaches to study individual neurons in the central nervous system to understand perception and behavior. In the last five years however, neurobiology has been riding a wave of technological advances that brought unprecedented insights: Optogenetics and genetically encoded activity sensors has allowed scientists to control and measure the activity of clearly defined neurons; the application of rabies viruses enabled the visualization of networks of interconnected nerve cells. What was still missing, was the link between neural circuit and monitoring of activity.
Scientists from the Friedrich Miescher Institute for Biomedical Research have now been the first to measure the concerted activity of a neuronal circuit in the retina as it extracts information about the movement of an object.
In a world defined through eyesight, it is crucial to be able to discern whether something moves towards us, moves away or moves next to us. It comes as no surprise then that in the retina several parallel neuronal circuits are reserved for the extraction of information about movement and that most of them are dedicated to the analysis of the direction of motion.
As they report online in Neuron, Keisuke Yonehara and Karl Farrow, two Postdoctoral Fellows in Botond Roska’s team at the FMI, have now been able to monitor the activity of all circuit elements in a motion sensitive retinal circuit at once, and pinpoint the site, at a subcellular level, where the information about the direction of the movement becomes encoded. To achieve this, they used genetically altered rabies viruses expressing calcium sensors developed by the laboratory of Klaus Conzelmann in Munich. The special property of rabies viruses is that they move across connected neurons and therefore are able to deliver the sensors to all circuit elements within a defined neuronal circuit. Simultaneous two-photon imaging allowed them then to monitor activity in every part of the neuronal circuit at once, even in subcellular compartments, such as axons, synapses and dendrites.
"We are extremely thrilled that with this new method, which combines the power of genetically altered rabies viruses with very powerful two-photon microscopy, we are now able to link circuit architecture with activity and ultimately function," comments Yonehara. "We have illustrated the power of the method for a better understanding of the perception of movement and are convinced that the method will allow us to reach a better understanding of many processes in the retina and in other parts of the brain."
(Source: medicalxpress.com)
Art preserves skills despite onset of vascular dementia in ‘remarkable’ case of a Canadian sculptor
The ability to draw spontaneously as well as from memory may be preserved in the brains of artists long after the deleterious effects of vascular dementia have diminished their capacity to complete simple, everyday tasks, according to a new study by physicians at St. Michael’s Hospital.
The finding, scheduled to be released today in the Canadian Journal of Neurological Sciences, looked at the last few years of the late Mary Hecht, an internationally renowned sculptor, who was able to draw spur-of-the moment and detailed sketches of faces and figures, including from memory, despite an advanced case of vascular dementia.
"Art opens the mind," said Dr. Luis Fornazzari, neurological consultant at St. Michael’s Hospital’s Memory Clinic and lead author of the paper. "Mary Hecht was a remarkable example of how artistic abilities are preserved in spite of the degeneration of the brain and a loss in the more mundane, day-to-day memory functions."
Hecht, who died in April 2013 at 81, had been diagnosed with vascular dementia and was wheelchair-bound due to previous strokes. Despite her vast knowledge of art and personal talent, she was unable to draw the correct time on a clock, name certain animals or remember any of the words she was asked to recall.
But she quickly sketched an accurate portrait of a research student from the Memory Clinic. And she was able to draw a free-hand sketch of a lying Buddha figurine and reproduce it from memory a few minutes later. To the great delight of St. Michael’s doctors, Hecht also drew an accurate sketch of famed cellist Mstislav Rostropovich after she learned of his death earlier that day on the radio.
While she was drawing and showing medical staff her own creations, Hecht spoke eloquently and without hesitation about art.
"This is the most exceptional example of the degree of preservation of artistic skills we’ve seen in our clinic," said Dr. Corinne Fischer, director at St. Michael’s Hospital’s Memory Clinic and another of the paper’s authors. "As well, most of the other studies that have been done in this area looked at other kinds of dementia such as Alzheimer’s disease or frontal temporal dementia, while this is a case of cognitive reserve in a patient with fairly advanced vascular dementia."
Dr. Fornazzari previously wrote a paper detailing a musician who, despite declining health because of Alzheimer’s disease, could still play the piano and learn new music. As well, in October 2011, Dr. Fischer and colleagues looked at bilingual patients with Alzheimer’s and discovered they had twice as much cognitive reserve as their unilingual counterparts.
Educators should take a page from these results and encourage schools to teach the arts – whether sculpture, painting or music – rather than cutting back on them, said Dr. Fornazzari. “Art should be taught to everyone. It’s better than many medications and is as important as mathematics or history.”
Both physicians want to lead a larger study of artists with neurological illnesses to further explore the importance of art and cognitive brain capacity.
Human Brains Are Hardwired for Empathy, Friendship, Study Shows
Perhaps one of the most defining features of humanity is our capacity for empathy – the ability to put ourselves in others’ shoes. A new University of Virginia study strongly suggests that we are hardwired to empathize because we closely associate people who are close to us – friends, spouses, lovers – with our very selves.
“With familiarity, other people become part of ourselves,” said James Coan, a U.Va. psychology professor in the College of Arts & Sciences who used functional magnetic resonance imaging brain scans to find that people closely correlate people to whom they are attached to themselves. The study appears in the August issue of the journal Social Cognitive and Affective Neuroscience.
“Our self comes to include the people we feel close to,” Coan said.
In other words, our self-identity is largely based on whom we know and empathize with.
Coan and his U.Va. colleagues conducted the study with 22 young adult participants who underwent fMRI scans of their brains during experiments to monitor brain activity while under threat of receiving mild electrical shocks to themselves or to a friend or stranger.
The researchers found, as they expected, that regions of the brain responsible for threat response – the anterior insula, putamen and supramarginal gyrus – became active under threat of shock to the self. In the case of threat of shock to a stranger, the brain in those regions displayed little activity. However when the threat of shock was to a friend, the brain activity of the participant became essentially identical to the activity displayed under threat to the self.
“The correlation between self and friend was remarkably similar,” Coan said. “The finding shows the brain’s remarkable capacity to model self to others; that people close to us become a part of ourselves, and that is not just metaphor or poetry, it’s very real. Literally we are under threat when a friend is under threat. But not so when a stranger is under threat.”
Coan said this likely is because humans need to have friends and allies who they can side with and see as being the same as themselves. And as people spend more time together, they become more similar.
“It’s essentially a breakdown of self and other; our self comes to include the people we become close to,” Coan said. “If a friend is under threat, it becomes the same as if we ourselves are under threat. We can understand the pain or difficulty they may be going through in the same way we understand our own pain.”
This likely is the source of empathy, and part of the evolutionary process, Coan reasons.
“A threat to ourselves is a threat to our resources,” he said. “Threats can take things away from us. But when we develop friendships, people we can trust and rely on who in essence become we, then our resources are expanded, we gain. Your goal becomes my goal. It’s a part of our survivability.”
People need friends, Coan added, like “one hand needs another to clap.”