1. Spread of tau protein measured in brains of Alzheimer’s patients

    May 25, 2017 by Ashley

    From the Karolinska Institutet press release:

    In a new study presented in Molecular Psychiatry, researchers at Karolinska Institutet have measured how deposits of the pathological protein tau spread through the brain over the course of Alzheimer’s disease. Their results show that the size of the deposit and the speed of its spread differ from one individual to the next, and that large amounts of tau in the brain can be linked to episodic memory impairment.

    Already in a very early phase of Alzheimer’s disease there is an accumulation of tau in the brain cells, where its adverse effect on cell function causes memory impairment. It is therefore an attractive target for vaccine researchers. For the present study, Professor Agneta Nordberg at Karolinska Institutet’s Department of Neurobiology, Care Sciences and Society and her doctoral student Konstantinos Chiotis along with the rest of her team used PET brain imaging to measure the spread of tau deposits as well as the amyloid plaque associated with Alzheimer’s disease, and charted the energy metabolism of the brain cells. They then examined how these three parameters changed over the course of the disease.

    “There’s been an international race to measure tau spread, and we probably got there first,” says Professor Nordberg. “There are no previous reports on how tau deposits spread after 17 months into the disease. Our results can improve understanding of tau accumulation in Alzheimer’s disease, help ongoing research to quantify the effect of tau vaccines, and enable early diagnosis.”

    The study included 16 patients at different stages of Alzheimer’s disease from the memory unit at Karolinska Hospital in Huddinge. The patients were given a series of neurological memory tests and underwent PET scans at 17-month intervals. While all 16 participants had abundant amyloid plaque deposition in the brain, the size and speed of spread of their tau deposits differed significantly between individuals.

    “We also saw a strong direct correlation between size of deposit and episodic memory impairment,” continues Professor Nordberg. “This could explain why the disease progresses at such a varying rate from one patient to the other. That said, tau doesn’t seem to have much of an effect on the global general memory, which is more reasonably related to brain metabolism.”

    The study was conducted in collaboration with Uppsala University, where the PET scans were performed.


  2. Study finds ‘moral enhancement’ technologies neither feasible nor wise

    by Ashley

    From the North Carolina State University press release:

    A recent study by researchers at North Carolina State University and the Montreal Clinical Research Institute (IRCM) finds that “moral enhancement technologies” — which are discussed as ways of improving human behavior — are neither feasible nor wise, based on an assessment of existing research into these technologies.

    The idea behind moral enhancement technologies is to use biomedical techniques to make people more moral. For example, using drugs or surgical techniques to treat criminals who have exhibited moral defects.

    “There are existing ways that people have explored to manipulate morality, but the question we address in this paper is whether manipulating morality actually improves it,” says Veljko Dubljevic, lead author of the paper and an assistant professor of philosophy at NC State who studies the ethics of neuroscience and technology.

    Dubljevic and co-author Eric Racine of the IRCM reviewed the existing research on moral enhancement technologies that have been used in humans to assess the effects of these technologies and how they may apply in real-world circumstances.

    Specifically, the researchers looked at four types of pharmaceutical interventions and three neurostimulation techniques:

    • Oxytocin is a neuropeptide that plays a critical role in social cognition, bonding and affiliative behaviors, sometimes called “the moral molecule”;
    • Selective serotonin reuptake inhibitors (SSRIs) are often prescribed for depression, but have also been found to make people less aggressive;
    • Amphetamines, which some have argued can be used to enhance motivation to take action;
    • Beta blockers are often prescribed to treat high blood pressure, but have also been found to decrease implicit racist responses;
    • Transcranial magnetic stimulation (TMS) is a type of neurostimulation that has been used to treat depression, but has also been reported as changing the way people respond to moral dilemmas;
    • Transcranial direct current stimulation (TDCS) is an experimental form of neurostimulation that has also been reported as making people more utilitarian; and
    • Deep brain stimulation is a neurosurgical intervention that some have hypothesized as having the potential to enhance motivation.

    “What we found is that, yes, many of these techniques do have some effects,” Dubljevic says. “But these techniques are all blunt instruments, rather than finely tuned technologies that could be helpful. So, moral enhancement is really a bad idea.

    “In short, moral enhancement is not feasible — and even if it were, history shows us that using science to in an attempt to manipulate morality is not wise,” Dubljevic says.

    The researchers found different problems for each of the pharmaceutical approaches.

    Oxytocin does promote trust, but only in the in-group,” Dubljevic notes. “And it can decrease cooperation with out-group members of society, such as racial minorities, and selectively promote ethnocentrism, favoritism, and parochialism.”

    The researchers also found that amphetamines boost motivation for all types of behavior, not just moral behavior. Moreover, there are significant risks of addiction associated with amphetamines. Beta blockers were found not only to decrease racism, but to blunt all emotional response which puts their usefulness into doubt. SSRIs reduce aggression, but have serious side-effects, including an increased risk of suicide.

    In addition to physical side effects, the researchers also found a common problem with using either TMS or TCDS technologies.

    “Even if we could find a way to make these technologies work consistently, there are significant questions about whether being more utilitarian in one’s decision-making actually makes one more moral,” Dubljevic says.

    Lastly, the researchers found no evidence that deep brain stimulation had any effect whatsoever on moral behavior.

    “Our goal here is to share a cautionary note with those who are discussing different techniques for moral enhancement,” Dubljevic says. “I am in favor of research that is done responsibly, but against dangerous social experiments.”


  3. Brain injury causes impulse control problems in rats

    May 24, 2017 by Ashley

    From the University of British Columbia press release:

    New research from the University of British Columbia confirms for the first time that even mild brain injury can result in impulse control problems in rats.

    The study, published in the Journal of Neurotrauma, also found that the impulsivity problems may be linked to levels of an inflammatory molecule in the brain, and suggest that targeting the molecule could be helpful for treatment.

    “Few studies have looked at whether traumatic brain injuries cause impulse control problems,” said the study’s lead author, Cole Vonder Haar, a former postdoctoral research fellow in the UBC department of psychology who is now an assistant professor at West Virginia University. “This is partly because people who experience a brain injury are sometimes risk-takers, making it difficult to know if impulsivity preceded the brain injury or was caused by it. But our study confirms for the first time that even a mild brain injury can cause impulse control problems.”

    For the study, researchers gave rats with brain injuries a reward test to measure impulsivity.

    Rats that were unable to wait for the delivery of a large reward, and instead preferred an immediate, but small reward, were considered more impulsive.

    The researchers found that impulsivity in the rats increased regardless of the severity of the brain injury. The impulsivity also persisted eight weeks after injury in animals with a mild injury, even after memory and motor function returned.

    “These findings have implications for how brain injury patients are treated and their progress is measured,” said Vonder Haar. “If physicians are only looking at memory or motor function, they wouldn’t notice that the patient is still being affected by the injury in terms of impulsivity.”

    After analyzing samples of frontal cortex brain tissue, the researchers also found a substantial increase in levels of an inflammatory molecule, known as interleukin-12, that correlated with levels of impulsivity. Interleukins are groups of proteins and molecules responsible for regulating the body’s immune system.

    The study builds on the researchers’ previous findings about the link between interleukin-12 and impulsivity.

    Catharine Winstanley, the study’s senior author and associate professor in the UBC department of psychology, said the findings are important because impulsivity is linked to addiction vulnerability.

    “Addiction can be a big problem for patients with traumatic brain injuries,” she said. “If we can target levels of interleukin-12, however, that could potentially provide a new treatment target to address impulsivity in these patients.”


  4. Study examines extent of neuronal loss in the brain during MS

    May 22, 2017 by Ashley

    From the Queen Mary University of London press release:

    A study by researchers from Queen Mary University of London establishes for the first time the extent of neuronal loss in the brain of a person with MS over their life, and finds that demyelination may not be as good an indicator of disease progression as previously thought.

    By dissecting and analysing brains from nine people with MS and seven healthy controls using gold standard techniques, they found that the mean number of neurons was 14.9 billion in MS versus 24.4 billion in controls — a 39% difference.

    The density of neurons in MS was smaller by 28%, and cortical volume by 26%, and they found that the whole brain was affected equally.

    Importantly, the number of neurons was strongly associated with the thickness of the cortex, which is something that can be measured by MRI. The decline in volume of the cortex could therefore be detected in vivo and be used to predict neuronal loss in patients or measure neurodegeneration during clinical trials.

    Lead researcher Klaus Schmierer said: “Given that we found no association between neuronal loss and demyelination, trying to detect demyelinating lesions in the cortex — an area of research strongly driven by the availability of high field MRI systems — may be of lesser importance than measuring cortical volume and getting on with early active treatment.”

    As cortical neuronal loss is responsible for cognitive and other functions, which occur early in MS, the researchers say that to avoid neurodegeneration, early treatment is key.


  5. Study suggests human sense of smell is stronger than we think

    May 19, 2017 by Ashley

    From the Rutgers University press release:

    When it comes to our sense of smell, we have been led to believe that animals win out over humans: No way can we compete with dogs and rodents, some of the best sniffers in the animal kingdom.

    But guess what? It’s a big myth. One that has survived for the last 150 years with no scientific proof, according to Rutgers University-New Brunswick neuroscientist John McGann, associate professor in the Department of Psychology, School of Arts and Sciences, in a paper published on May 12 in Science.

    McGann, who has been studying the olfactory system, or sense of smell, for the past 14 years, spent part of the last year reviewing existing research, examining data and delving into the historical writings that helped create the long-held misconception that human sense of smell was inferior because of the size of the olfactory bulb.

    “For so long people failed to stop and question this claim, even people who study the sense of smell for a living,” says McGann, who studies how the brain understands sensory stimuli using information gleaned from prior experience.

    “The fact is the sense of smell is just as good in humans as in other mammals, like rodents and dogs.” Humans can discriminate maybe one trillion different odors, he says, which is far more, than the claim by “folk wisdom and poorly sourced introductory psychology textbooks,” that insist humans could only detect about 10,000 different odors.

    McGann points to Paul Broca, a 19th century brain surgeon and anthropologist as the culprit for the falsehood that humans have an impoverished olfactory system — an assertion that, McGann says, even influenced Sigmund Freud to insist that this deficiency made humans susceptible to mental illness.

    “It has been a long cultural belief that in order to be a reasonable or rational person you could not be dominated by a sense of smell,” says McGann. “Smell was linked to earthly animalistic tendencies.” The truth about smell, McGann says, is that the human olfactory bulb, which sends signals to other areas of a very powerful human brain to help identify scents, is quite large and similar in the number of neurons to other mammals.

    The olfactory receptor neurons in the nose work by making physical contact with the molecules composing the odor, and they send this information back to that region of the brain.

    “We can detect and discriminate an extraordinary range of odors; we are more sensitive than rodents and dogs for some odors; we are capable of tracking odor trails; and our behavioral and affective states are influenced by our sense of smell,” McGann writes in Science.

    In Broco’s 1879 writings, he claimed that the smaller volume of the olfactory area compared to the rest of the brain meant that humans had free will and didn’t have to rely on smell to survive and stay alive like dogs and other mammals.

    In reality, McGann says, there is no support for the notion that a larger olfactory bulb increases sense of smell based solely on size and insists that the human sense of smell is just as good and that of animals.

    “Dogs may be better than humans at discriminating the urines on a fire hydrant and humans may be better than dogs at discriminating the odors of fine wine, but few such comparisons have actual experimental support,” McGann writes in Science.

    The idea that humans don’t have the same sense of smell abilities as animals flourished over the years based on some genetic studies which discovered that rats and mice have genes for about 1000 different kinds of receptors that are activated by odors, compared to humans, who only have about 400.

    “I think it has been too easy to get caught up in numbers,” says McGann. “We’ve created a confirmation bias by working off a held belief that humans have a poor sense of smell because of these lower numbers of receptors, which in reality is still an awful lot.”

    The problem with this continuing myth, McGann says, is that smell is much more important than we think. It strongly influences human behavior, elicits memories and emotions, and shapes perceptions.

    Our sense of smell plays a major, sometimes unconscious, role in how we perceive and interact with others, select a mate, and helps us decide what we like to eat. And when it comes to handling traumatic experiences, smell can be a trigger in activating PTSD.

    While smell can begin to deteriorate as part of the aging process, McGann says, physicians should be more concerned when a patient begins to lose the ability to detect odors and not just retreat back to the misconception that humans’ sense of smell is inferior.

    “Some research suggests that losing the sense of smell may be the start of memory problems and diseases like Alzheimer’s and Parkinson’s,” says McGann. “One hope is that the medical world will begin to understand the importance of smell and that losing it is a big deal.”


  6. Study expands understanding of how the brain encodes fear memory

    by Ashley

    From the UC Riverside press release:

    Research published by scientists at the University of California, Riverside on “fear memory” could lead to the development of therapies that reduce the effects of post-traumatic stress disorder (PTSD).

    To survive in a dynamic environment, animals develop adaptive fear responses to dangerous situations, requiring coordinated neural activity in the hippocampus, medial prefrontal cortex (mPFC), and amygdala – three brain areas connected to one another. A disruption of this process leads to maladaptive generalized fear in PTSD, which affects 7 percent of the U.S. population.

    Jun-Hyeong Cho, an assistant professor of cell biology and neuroscience and Woong Bin Kim, a postdoctoral researcher in Cho’s lab, have now found that a population of hippocampal neurons project to both the amygdala and the mPFC, and that it is these neurons that efficiently convey information to these two brain areas to encode and retrieve fear memory for a context associated with an aversive event.

    The study, which appeared in the May 10 print issue of the Journal of Neuroscience, is the first to quantify these “double-projecting” hippocampal neurons and explain how they convey contextual information more efficiently for fear responses, compared to hippocampal neurons that project only to either the mPFC or the amygdala.

    “This study, done using a mouse model, expands our understanding of how associative fear memory for a relevant context is encoded in the brain,” said Cho, the lead author of the study and a member of the UCR School of Medicine’s Center for Glial-Neuronal Interactions, “and could inform the development of novel therapeutics to reduce pathological fear in PTSD.”

    To visualize the double-projecting hippocampal neurons, Cho and Kim used a tracing method in which hippocampal neurons that project to different brain areas were labeled with fluorescence proteins with different colors. The pair also developed a novel approach of electrophysiological recordings and optogenetics to examine how exactly the double-projecting neurons connected to the mPFC and amygdala. (These experimental approaches can be used to examine other brain areas that project to multiple targets.)

    “We were surprised to find that as much as 17 percent of hippocampal neurons that projected to the amygdala or the mPFC were, in fact, double-projecting neurons,” Cho said. “Although previous studies demonstrated the existence of double-projecting hippocampal neurons, neuroscientists largely ignored them when studying the role of neural pathways between the hippocampus, amygdala and mPFC in contextual fear learning.”

    Cho explained that the acquisition (encoding) and retrieval of contextual fear memory requires coordinated neural activity in the hippocampus, amygdala and mPFC. The hippocampus encodes context cues, the amygdala stores associations between a context and an aversive event, and the mPFC signals whether a defensive response is appropriate in the present context.

    Context is broadly defined as the set of circumstances around an event. In contextual fear conditioning, experimental subjects are placed in an emotionally neutral context (such as a room) and presented an aversive stimulus (such as an electrical shock). Then, they learn to associate the context with the aversive event, and show fear responses (such as freezing behavior) when placed subsequently in that context.

    “Our study suggests that double-projecting hippocampal neurons can facilitate synchronized neural activity in the mPFC and amygdala that is implicated in learned fear,” he said. “It is by modulating the activity of the mPFC and basal amygdala that these double-projecting hippocampal neurons contribute to the acquisition and retrieval of fear memory for a context associated with an aversive event.”

    Cho also explained that multiple projections from single neurons appear to be a general feature of the neural circuits in the brain and could promote synchronized neural activity and long-term changes in the efficiency of neural communication.

    The study came about when, a few years ago, Cho and Kim were selectively labeling and stimulating hippocampal neurons that project to the mPFC, and examining how this manipulation affects fear memory formation in mice. When they carefully examined the brain tissue, they found that labeled hippocampal neurons also projected to the amygdala.

    “We initially thought there was something wrong with our experiments,” Kim, the postdoctoral researcher, said. “But, when we repeated the experiments, the same pattern was observed consistently. We realized that this could be an exciting finding that may account for how contextual information is processed and conveyed between brain areas for the formation of fear memory for the context associated with an aversive event.”

    Next, to better understand the role of double-projecting hippocampal neurons in fear learning and memory, Cho and Kim plan to selectively silence these neurons and examine how this manipulation impacts the formation of fear memory for a context associated with an aversive event.


  7. How shifts in excitation-inhibition balance may lead to psychiatric disorders

    May 18, 2017 by Ashley

    From the Elsevier press release:

    In a special issue of Biological Psychiatry titled “Cortical Excitation-Inhibition Balance and Dysfunction in Psychiatric Disorders,” guest editors Dr. Alan Anticevic and Dr. John Murray, both of Yale University, bring together seven reviews that highlight advancements in understanding the balance of excitatory and inhibitory signaling in the brain, and what might happen when it goes awry.

    Alterations in excitation/inhibition (E/I) balance constitute an emerging theme in clinical neuroscience, wrote Anticevic and Dr. John Lisman of Brandeis University in a commentary accompanying the special issue. The effects of E/I imbalance stretch across diagnostic boundaries, as indicated by the variety of psychiatric disorders addressed in the reviews, including schizophrenia, autism spectrum disorder, major depressive disorder, and bipolar disorder.

    Presenting both human and animal studies, the reviews summarize research on the developmental aspects of E/I regulation and how alterations in circuit stability and compensatory mechanisms with negative effects may emerge when the E/I balance tips. In particular, multiple reviews frame the disturbances in the E/I balance around altered glutamate synaptic development — the excitatory arm of the E/I balance — and present hypotheses for how those developmental alterations may lead to impaired structural and functional circuitry in the brain. A case is made for the need for a combination of approaches, including computational neuroscience, imaging, pharmacological, and genetic studies, in addition to consideration of the coregulation of excitation and inhibition (rather than focusing on the neurotransmitter systems independently) to explain the role of E/I imbalance in psychiatric disorders.

    The collection of reviews not only collate findings aimed at improving our understanding of how these developmental changes and potential negative consequences arise, but also explore how to restore E/I balance. Restoration aims to alleviate the subsequent dysfunctional neural activity that manifests as clinical symptoms, such as impaired working memory in schizophrenia. This is explored, for example, through pharmacological manipulation of glutamate modulation on E/I circuitry.

    The special issue is “Cortical Excitation-Inhibition Balance and Dysfunction in Psychiatric Disorders”, Biological Psychiatry, volume 81, issue 10 (May 2017), published by Elsevier.


  8. Neuronal targets to restore movement in Parkinson’s disease model

    by Ashley

    From the Carnegie Mellon University press release:

    Researchers working in the lab of Carnegie Mellon University neuroscientist Aryn Gittis, have identified two groups of neurons that can be turned on and off to alleviate the movement-related symptoms of Parkinson’s disease. The activation of these cells in the basal ganglia relieves symptoms for much longer than current therapies, like deep brain stimulation and pharmaceuticals.

    The study, completed in a mouse model of Parkinson’s, used optogenetics to better understand the neural circuitry involved in Parkinson’s disease, and could provide the basis for new experimental treatment protocols. The findings, published by researchers from Carnegie Mellon, the University of Pittsburgh and the joint CMU/Pitt Center for the Neural Basis of Cognition (CNBC) are available as an Advance Online Publication on Nature Neuroscience‘s website.

    Parkinson’s disease is caused when the dopamine neurons that feed into the brain’s basal ganglia die and cause the basal ganglia to stop working, preventing the body from initiating voluntary movement. The basal ganglia is the main clinical target for treating Parkinson’s disease, but currently used therapies do not offer long-term solutions.

    “A major limitation of Parkinson’s disease treatments is that they provide transient relief of symptoms. Symptoms can return rapidly if a drug dose is missed or if deep brain stimulation is discontinued,” said Gittis, assistant professor of biological sciences in the Mellon College of Science and member of Carnegie Mellon’s BrainHub neuroscience initiative and the CNBC. “There is no existing therapeutic strategy for long lasting relief of movement disorders associated with Parkinson’s.”

    To better understand how the neurons in the basal ganglia behave in Parkinson’s, Gittis and colleagues looked at the inner circuitry of the basal ganglia. They chose to study one of the structures that makes up that region of the brain, a nucleus called the external globus pallidus (GPe). The GPe is known to contribute to suppressing motor pathways in the basal ganglia, but little is known about the individual types of neurons present in the GPe, their role in Parkinson’s disease or their therapeutic potential.

    The research group used optogenetics, a technique that turns genetically tagged cells on and off with light. They targeted two cell types in a mouse model for Parkinson’s disease: PV-GPe neurons and Lhx6-GPe neurons. They found that by elevating the activity of PV-GPe neurons over the activity of the Lhx6-GPe neurons, they were able to stop aberrant neuronal behavior in the basal ganglia and restore movement in the mouse model for at least four hours — significantly longer than current treatments.

    While optogenetics is used only in animal models, Gittis said she believes their findings could create a new, more effective deep brain stimulation protocol.


  9. Men and women show equal ability at recognizing faces

    May 16, 2017 by Ashley

    From the Penn State press release:

    Despite conventional wisdom that suggests women are better than men at facial recognition, Penn State psychologists found no difference between men and women in their ability to recognize faces and categorize facial expressions.

    In the study, the researchers used behavioral tests, as well as neuroimaging, to investigate whether there is an influence of biological sex on facial recognition, according to Suzy Scherf, assistant professor of psychology and neuroscience.

    “There has been common lore in the behavioral literature that women do better than men in many types of face-processing tasks, such as face recognition and detecting and categorizing facial expressions, although, when you look in the empirical literature, the findings are not so clear cut,” said Scherf. “I went into this work fully expecting to see an effect of biological sex on the part of the observer in facial recognition — and we did not find any. And we looked really hard.”

    Scherf said that facial recognition is one of the most important skills people use to navigate social interactions. It is also a key motivation for certain types of behavior, as well.

    “Within 30 milliseconds of looking at a face, you can figure out the age, the sex, whether you know the person or not, whether the person is trustworthy, whether they’re competent, attractive, warm, caring — we can make categorizations on faces that fast,” said Scherf. “And some of that is highly coordinated with our behavioral decisions of what we are going to do following those attributions and decisions. For example, Do I want to vote for this person? Do I want to have a conversation with this person? Where do I fit in the status hierarchy? A lot of what we do is dictated by the information we get from faces.”

    Scherf added that the importance of facial recognition for both sexes underlines the logic of why men and women should have equal facial recognition abilities.

    “Faces are just as important for men, you can argue, as they are for women,” said Scherf. “Men get all the same cues from faces that women do.”

    According to Scherf, the researchers did not find any evidence of another commonly held belief that women could recognize faces of their own biological sex more easily than the other, also referred to as “own gender bias.”

    The researchers, who report their findings in eNeuro (available online), used a common face recognition task called the Cambridge Face Memory Test, which measures whether a person can identify a male face out of a line up of three faces. They also created their own female version of the memory test. Because of previous concerns of an own gender bias in women, the Cambridge Face Memory Test features only male faces.

    “We couldn’t test the own gender bias without a female version of this test,” said Scherf, who worked with Daniel B. Elbich and Natalie V. Motta-Mena, both graduate students in psychology.

    In a second test, they scanned the brains of participants in an MRI machine while the subjects watched a series of short video clips of unfamiliar faces, famous faces, common objects and navigational scenes, such as a clip of the Earth from outer space; and in a separate task as they recognized specific faces.

    After the tests, the scans of neural activity happening in areas known for facial recognition — as well as other types of visual recognition — were statistically identical for both men and women.

    Participants were carefully selected for the study because certain conditions can affect facial recognition.

    “In order to enroll someone in our study, we went through a careful screening procedure to make sure that people did not have a history of neurological or psychiatric disorders in themselves, or in their first-degree relatives,” said Scherf. “This is important because in nearly all the affective disorders — depression, anxiety, schizophrenia, bipolar — face processing is disrupted.”

    The researchers also screened out participants with concussions, which can disrupt patterns of brain activation and function, Scherf added.

    Scherf, who also studies adolescents and pubertal development, began to investigate biological sex differences to further her own understanding of what sex differences — if any — exist in sexually mature men and women, compared to adolescents.

    The Social Science Research Institute and the National Science Foundation supported this work.


  10. Review highlights why animals have evolved to favor one side of the brain

    by Ashley

    From the Cell Press press release:

    Most left-handers can rattle off a list of their eminent comrades-in-arms: Oprah Winfrey, Albert Einstein, and Barack Obama, just to name three, but they may want to add on cockatoos, “southpaw” squirrels, and some house cats. “Handed-ness” or left-right asymmetry is prevalent throughout the animal kingdom, including in pigeons and zebrafish. But why do people and animals naturally favor one side over the other, and what does it teach us about the brain’s inner workings? Researchers explore these questions in a Review published April 19 in Neuron.

    “Studying asymmetry can provide the most basic blueprints for how the brain is organized,” says lead author Onur Güntürkün, of the Institute of Cognitive Neuroscience at Ruhr-University Bochum, in Germany. “It gives us an unprecedented window into the wiring of the early, developing brain that ultimately determines the fate of the adult brain.” Because asymmetry is not limited to human brains, a number of animal models have emerged that can help unravel both the genetic and epigenetic foundations for the phenomenon of lateralization.

    Güntürkün says that brain lateralization serves three purposes. The first of those is perceptual specialization: the more complex a task, the more it helps to have a specialized area for performing that task. For example, in most people, the right side of the brain focuses on recognizing faces, while the left side is responsible for identifying letters and words.

    The next area is motor specialization, which brings us to the southpaw. “What you do with your hands is a miracle of biological evolution,” he says. “We are the master of our hands, and by funneling this training to one hemisphere of our brains, we can become more proficient at that kind of dexterity.” Natural selection likely provided an advantage that resulted in a proportion of the population — about 10% — favoring the opposite hand. The thing that connects the two is parallel processing, which enables us to do two things that use different parts of the brain at the same time.

    Brain asymmetry is present in many vertebrates and invertebrates. “It is, in fact, an invention of nature, which evolved because many animals have the same needs for specialization that we do,” says Güntürkün, who is also currently a visiting fellow at the Stellenbosch Institute for Advanced Study in South Africa. Studies have shown that birds, like chickens, use one eye to distinguish grain from pebbles on the ground while at the same time using the other eye to keep watch for predators overhead.

    Research on pigeons has shown that this specialization often is a function of environmental influences. When a pigeon chick develops in the shell, its right eye turns toward the outside, leaving its left eye to face its body. When the right eye is exposed to light coming through the shell, it triggers a series of neuronal changes that allow the two eyes to ultimately have different jobs.

    A zebrafish model of lateralization, meanwhile, has enabled researchers to delve into the genetic aspects of asymmetrical development. Studies of important developmental pathways, including the Nodal signaling pathway, are uncovering details about how, very early in an embryo’s development, the cilia act to shuffle gene products to one side of the brain or the other. By manipulating the genes in Nodal and other pathways, researchers can study the effects of these developmental changes on zebrafish behaviors.

    Güntürkün says that this research can provide insight into the effects of asymmetry on brain conditions in humans. “There are almost no disorders of the human brain that are not linked to brain asymmetries,” he says. “If we understand the ontogeny of lateralization, we can make a great leap to see how brain wiring early in the developmental process may go wrong in these pathological cases.”