Our Brains are Hardwired for Language

People blog, they don’t lbog, and they schmooze, not mshooze. But why is this? Why are human languages so constrained? Can such restrictions unveil the basis of the uniquely human capacity for language?

A groundbreaking study published in PLOS ONE by Prof. Iris Berent of Northeastern University and researchers at Harvard Medical School shows the brains of individual speakers are sensitive to language universals. Syllables that are frequent across languages are recognized more readily than infrequent syllables. Simply put, this study shows that language universals are hardwired in the human brain.

LANGUAGE UNIVERSALS

Language universals have been the subject of intense research, but their basis remains elusive. Indeed, the similarities between human languages could result from a host of reasons that are tangential to the language system itself. Syllables like lbog, for instance, might be rare due to sheer historical forces, or because they are just harder to hear and articulate. A more interesting possibility, however, is that these facts could stem from the biology of the language system. Could the unpopularity of lbogs result from universal linguistic principles that are active in every human brain?

THE EXPERIMENT

To address this question, Dr. Berent and her colleagues examined the response of human brains to distinct syllable types—either ones that are frequent across languages (e.g., blif, bnif), or infrequent (e.g., bdif, lbif). In the experiment, participants heard one auditory stimulus at a time (e.g., lbif), and were then asked to determine whether the stimulus includes one syllable or two while their brain was simultaneously imaged.

Results showed the syllables that were infrequent and ill-formed, as determined by their linguistic structure, were harder for people to process. Remarkably, a similar pattern emerged in participants’ brain responses: worse-formed syllables (e.g., lbif) exerted different demands on the brain than syllables that are well-formed (e.g., blif).

UNIVERSALLY HARDWIRED BRAINS

The localization of these patterns in the brain further sheds light on their origin. If the difficulty in processing syllables like lbif were solely due to unfamiliarity, failure in their acoustic processing, and articulation, then such syllables are expected to only exact cost on regions of the brain associated with memory for familiar words, audition, and motor control. In contrast, if the dislike of lbif reflects its linguistic structure, then the syllable hierarchy is expected to engage traditional language areas in the brain.

While syllables like lbif did, in fact, tax auditory brain areas, they exerted no measurable costs with respect to either articulation or lexical processing. Instead, it was Broca’s area—a primary language center of the brain—that was sensitive to the syllable hierarchy.

These results show for the first time that the brains of individual speakers are sensitive to language universals: the brain responds differently to syllables that are frequent across languages (e.g., bnif) relative to syllables that are infrequent (e.g., lbif). This is a remarkable finding given that participants (English speakers) have never encountered most of those syllables before, and it shows that language universals are encoded in human brains.

The fact that the brain activity engaged Broca’s area—a traditional language area—suggests that this brain response might be due to a linguistic principle. This result opens up the possibility that human brains share common linguistic restrictions on the sound pattern of language.

FURTHER EVIDENCE

This proposal is further supported by a second study that recently appeared in the Proceedings of the National Academy of Science, also co-authored by Dr. Berent. This study shows that, like their adult counterparts, newborns are sensitive to the universal syllable hierarchy.

The findings from newborns are particularly striking because they have little to no experience with any such syllable. Together, these results demonstrate that the sound patterns of human language reflect shared linguistic constraints that are hardwired in the human brain already at birth.

Why your nose can be a pathfinder

When I was a child I used to sit in my grandfather’s workshop, playing with wood shavings. Freshly shaven wood has a distinct smell of childhood happiness, and whenever I get a whiff of that scent my brain immediately conjures up images of my grandfather at his working bench, the heat from the fireplace and the dog next to it.

Researchers at the Kavli Institute for Systems Neuroscience have recently discovered the process behind this phenomenon. The brain, it turns out, connects smells to memories through an associative process where neural networks are linked through synchronised brain waves of 20-40 Hz.

– We all know that smell is connected to memories, Kei Igarashi, lead author, explains.– We know that neurons in different brain regions need to oscillate in synchrony for these regions to speak effectively to each other. Still, the relationship between interregional coupling and formation of memory traces has remained poorly understood. So we designed a task to investigate how odour-place representation evolved in the entorhinal and hippocampal region, to figure out whether learning depends on coupling of oscillatory networks.

Smell guides the way in maze
The researchers designed a maze for rats, where a rat would see a hole to poke its nose into. When poking into the hole, the rat was presented with one of two alternative smells. One smell told the rat that food would be found in the left food cup behind the rat. The other smell told it that there was food in the right cup. The rat would soon learn which smell would lead to a reward where. After three weeks of training, the rats chose correctly on more than 85% of the trials. In order to see what happened inside the brain during acquisition, 16–20 electrode pairs were inserted in the hippocampus and in different areas of the entorhinal cortex.

After the associations between smell and place were well established, the researchers could see a pattern of brain wave activity (the electrical signal from a large number of neurons) during retrieval.

Coherent brain activity evolves with learning
– Immediately after the rat is exposed to the smell there is a burst in activity of 20–40 Hz waves in a specific connection between an area in the entorhinal cortex, lateral entorhinal cortex (LEC), and an area in the hippocampus, distal CA1 (dCA1), while a similar strong response was not observed in other connections, Igarashi explains.

This coherence of 20–40 Hz activity in the LEC and dCA1 evolved in parallel with learning, with little coherence between these areas before training started. By the time the learning period was over, cells were phase locked to the oscillation and a large portion of the cells responded specifically to one or the other of the smell-odour pairs.

Long distance communication in brain mediated by waves
– This is not the first time we observe that the brain uses synchronised wave activity to establish network connections, Edvard Moser, director of the Kavli Institute for Systems Neuroscience says. – Both during encoding and retrieval of declarative memories there is an interaction between these areas mediated through gamma and theta oscillations. However, this is the first study to relate the development of a specific band of oscillations to memory performance in the hippocampus. Together, the evidence is now piling up and pointing in the direction of cortical oscillations as a general mechanism for mediating interactions among functionally specialised neurons in distributed brain circuits.

So, there you have it – the signals from your nose translate and connect to memories in an orchestrated symphony of signals in your head. Each of these memories connects to a location, pinpointed on your inner map. So when you feel a wave of reminiscence triggered by a fragrance, think about how waves created this connection in the first place.

Functional brain imaging reliably predicts which vegetative patients have potential to recover consciousness

A functional brain imaging technique known as positron emission tomography (PET) is a promising tool for determining which severely brain damaged individuals in vegetative states have the potential to recover consciousness, according to new research published in The Lancet.

It is the first time that researchers have tested the diagnostic accuracy of functional brain imaging techniques in clinical practice.

“Our findings suggest that PET imaging can reveal cognitive processes that aren’t visible through traditional bedside tests, and could substantially complement standard behavioural assessments to identify unresponsive or “vegetative” patients who have the potential for long-term recovery”, says study leader Professor Steven Laureys from the University of Liége in Belgium.

In severely brain-damaged individuals, judging the level of consciousness has proved challenging. Traditionally, bedside clinical examinations have been used to decide whether patients are in a minimally conscious state (MCS), in which there is some evidence of awareness and response to stimuli, or are in a vegetative state (VS) also known as unresponsive wakefulness syndrome, where there is neither, and the chance of recovery is much lower. But up to 40% of patients are misdiagnosed using these examinations.

“In patients with substantial cerebral oedema [swelling of the brain], prediction of outcome on the basis of standard clinical examination and structural brain imaging is probably little better than flipping a coin,” writes Jamie Sleigh from the University of Auckland, New Zealand, and Catherine Warnaby from the University of Oxford, UK, in a linked Comment.

The study assessed whether two new functional brain imaging techniques—PET with the imaging agent fluorodeoxyglucose (FDG) and functional MRI (fMRI) during mental imagery tasks—could distinguish between vegetative and MCS in 126 patients with severe brain injury (81 in a MCS, 41 in a VS, and four with locked-in syndrome—a behaviourally unresponsive but conscious control group) referred to the University Hospital of Liége, in Belgium, from across Europe. The researchers then compared their results with the well-established standardised Coma Recovery Scale–Revised (CSR-R) behavioural test, considered the most validated and sensitive method for discriminating very low awareness.

Overall, FDG-PET was better than fMRI in distinguishing conscious from unconscious patients. Mental imagery fMRI was less sensitive at diagnosis of a MCS than FDG-PET (45% vs 93%), and had less agreement with behavioural CRS-R scores than FDG-PET (63% vs 85%). FDG-PET was about 74% accurate in predicting the extent of recovery within the next year, compared with 56% for fMRI.

Importantly, a third of the 36 patients diagnosed as behaviourally unresponsive on the CSR-R test who were scanned with FDG-PET showed brain activity consistent with the presence of some consciousness. Nine patients in this group subsequently recovered a reasonable level of consciousness.

According to Professor Laureys, “We confirm that a small but substantial proportion of behaviourally unresponsive patients retain brain activity compatible with awareness. Repeated testing with the CRS–R complemented with a cerebral FDG-PET examination provides a simple and reliable diagnostic tool with high sensitivity towards unresponsive but aware patients. fMRI during mental tasks might complement the assessment with information about preserved cognitive capability, but should not be the main or sole diagnostic imaging method.”

The authors point out that the study was done in a specialist unit focusing on the diagnostic neuroimaging of disorders of consciousness and therefore roll out might be more challenging in less specialist units.

Commenting on the study Jamie Sleigh and Catherine Warnaby add, “From these data, it would be hard to sustain a confident diagnosis of unresponsive wakefulness syndrome solely on behavioural grounds, without PET imaging for confirmation…[This] work serves as a signpost for future studies. Functional brain imaging is expensive and technically challenging, but it will almost certainly become cheaper and easier. In the future, we will probably look back in amazement at how we were ever able to practise without it.”

(Image caption: Blockade of p25 generation in the brain of an Alzheimer’s disease mouse model mitigates amyloid plaque buildup. Hippocampal slices from a seven-month-old 5XFAD mouse (left) or 5XFAD;p35KI mouse (right), alongside markers for Aβ (red) and activated astrocyte (green). Nuclei are shown in blue.)

Neuroscientists find that limiting a certain protein in the brain reverses Alzheimer’s symptoms in mice

Limiting a certain protein in the brain reverses Alzheimer’s symptoms in mice, report neuroscientists at MIT’s Picower Intitute for Learning and Memory.

Researchers found that the overproduction of the protein known as p25 may be the culprit behind the sticky protein-fragment clusters that build up in the brains of Alzheimer’s patients. The work, which was published in the April 10 issue of Cell, could provide a new drug target for the treatment of the disease that affects more than five million Americans, says Li-Huei Tsai, director of MIT’s Picower Institute for Learning and Memory and senior author of the paper.

Abnormal clusters of protein fragments, known as beta amyloid plaques, are believed to cause the cognitive impairments, cell death, and tissue loss associated with Alzheimer’s. The p25 protein had been tied to the creation and buildup of beta amyloids, but until now, p25’s role in Alzheimer’s pathology was not well understood.

“This protein appears to help maintain normal brain activity, but also is part of a feedback loop with beta amyloids. It generates the plaques which, in turn, boost levels of p25,” Tsai says.

Lead author of the paper is Jinsoo Seo, a postdoc associate at the Picower Institute.

The benefits of p25 generation

Elevated p25 levels in the brain have been documented upon exposure to neurotoxic stimuli such as oxidative stress and beta amyloids.

“In this study, for the first time we show that a variety of physiological neuronal activities generate p25 in the hippocampus, where memories are encoded in the brain,” Tsai says.

To delineate the precise roles of p25, Tsai’s lab generated a transgenic mouse model, which enabled researchers to prevent the production of p25 without altering other proteins with essential roles in brain development.

The researchers found that p25 is required for synaptic plasticity, the ability of brain connections to change over time; especially for the process called long-term depression (LTD) that selectively weakens sets of synapses and is associated with memory extinction.

Tsai’s team observed that the mice unable to generate p25 could learn new tasks and form memories normally; however, when the researchers began to address memory extinction, they soon noticed that the mice have difficulties with replacing older memories with newer ones.

Too much of a good thing

“This finding not only boosts our understanding of p25 in synaptic functions, but also explains the underlying mechanism of the inordinate synaptic depression observed in the Alzheimer’s brain,” Seo says.

“This finding led us to question whether the blockade of p25 generation could mitigate pathological phenotypes in the Alzheimer’s brain,” Tsai says.

In the mouse model of Alzheimer’s disease, inhibiting p25 production improved cognitive function, greatly reduced plaque formation and neuroinflammation, hallmark features of Alzheimer’s disease.

These results hold out the hope that a drug that regulates p25 could benefit Alzheimer’s disease patients by improving cognitive function and perhaps delaying the development of brain pathology, Tsai says.

Neuroscientists Find Brain Activity May Mark the Beginning of Memories

By tracking brain activity when an animal stops to look around its environment, neuroscientists at Johns Hopkins University believe they can mark the birth of a memory.

Using lab rats on a circular track, James Knierim, professor of neuroscience in the Zanvyl Krieger Mind/Brain Institute at Johns Hopkins, and a team of brain scientists, noticed that the rats frequently paused to inspect their environment with head movements as they ran. The scientists found that this behavior activated a place cell in their brain, which helps the animal construct a cognitive map, a pattern of activity in the brain that reflects the animal’s internal representation of its environment.

In a paper recently published in the journal Nature Neuroscience, the researchers state that when the rodents passed that same area of the track seconds later, place cells fired again, a neural acknowledgement that the moment has imprinted itself in the brain’s cognitive map in the hippocampus.

The hippocampus is the brain’s warehouse for long- and short-term processing of episodic memories, such as memories of a specific experience like a trip to Maine or a recent dinner. What no one knew was what happens in the hippocampus the moment an experience imprints itself as a memory.

“This is like seeing the brain form memory traces in real time,” said Knierim, senior author of the research. “Seeing for the first time the brain creating a spatial firing field tied to a specific behavioral experience suggests that the map can be updated rapidly and robustly to lay down a memory of that experience.”

A place cell is a type of neuron within the hippocampus that becomes active when an animal or human enters a particular place in its environment. The activation of the cells help create a spatial framework much like a map, that allows humans and animals to know where they are in any given location. Place cells can also act like neural flags that “mark” an experience on the map, like a pin that you drop on Google maps to mark the location of a restaurant.

“We believe that the spatial coordinates of the map are delivered to the hippocampus by one brain pathway, and the information about the things that populate the map, like the restaurant, are delivered by a separate pathway,” said Knierim. “When you experience a new item in the environment, the hippocampus combines these inputs to create a new spatial marker of that experience.”

In the experiments, researchers placed tiny wires in the brains of the rats to monitor when and where brain activity increased as they moved along the track in search of chocolate rewards. About every seven seconds, the rats stopped moving forward and turned their heads to the perimeter of the room as they investigated the different landmarks, a behavior called “head-scanning.”

“We found that many cells that were previously silent would suddenly start firing during a specific head-scanning event,” said Knierim. “On the very next lap around the track, many of these cells had a brand new place field at that exact same location and this place field remained usually for the rest of the laps. We believe that this new place field marks the site of the head scan and allows the brain to form a memory of what it was that the rat experienced during the head scan.”

Knierim said the formation and stability of place fields and the newly-activated place cells requires further study. The research is primarily intended to understand how memories are formed and retrieved under normal circumstances, but it could be applicable to learning more about people with brain trauma or hippocampal damage due to aging or Alzheimer’s.

“There are strong indications that humans and rats share the same spatial mapping functions of the hippocampus, and that these maps are intimately related to how we organize and store our memories of prior life events,” said Knierim. “Since the hippocampus and surrounding brain areas are the first parts of the brain affected in Alzheimer’s, we think that these studies may lend some insight into the severe memory loss that characterizes the early stages of this disease.”

(Image: Shutterstock)

Brain activity drives dynamic changes in neural fiber insulation

The brain is a wonderfully flexible and adaptive learning tool. For decades, researchers have known that this flexibility, called plasticity, comes from selective strengthening of well-used synapses — the connections between nerve cells.

Now, researchers at the Stanford University School of Medicine have demonstrated that brain plasticity also comes from another mechanism: activity-dependent changes in the cells that insulate neural fibers and make them more efficient. These cells form a specialized type of insulation called myelin.

“Myelin plasticity is a fascinating concept that may help to explain how the brain adapts in response to experience or training,” said Michelle Monje, MD, PhD, assistant professor of neurology and neurological sciences.

The researchers’ findings are described in a paper published online April 10 in Science Express.

“The findings illustrate a form of neural plasticity based in myelin, and future work on the molecular mechanisms responsible may ultimately shed light on a broad range of neurological and psychiatric diseases,” said Monje, senior author of the paper. The lead authors of the study are Stanford postdoctoral scholar Erin Gibson, PhD, and graduate student David Purger.

Sending neural impulses quickly down a long nerve fiber requires insulation with myelin, which is formed by a cell called an oligodendrocyte that wraps itself around a neuron. Even small changes in the structure of this insulating sheath, such as changes in its thickness, can dramatically affect the speed of neural-impulse conduction. Demyelinating disorders, such as multiple sclerosis, attack these cells and degrade nerve transmission, especially over long distances.

Myelin-insulated nerve fibers make up the “white matter” of the brain, the vast tracts that connect one information-processing area of the brain to another. “If you think of the brain’s infrastructure as a city, the white matter is like the roads, highways and freeways that connect one place to another,” Monje said.

In the study, Monje and her colleagues showed that nerve activity prompts oligodendrocyte precursor cell proliferation and differentiation into myelin-forming oligodendrocytes. Neuronal activity also causes an increase in the thickness of the myelin sheaths within the active neural circuit, making signal transmission along the neural fiber more efficient. It’s much like a system for improving traffic flow along roadways that are heavily used, Monje said. And as with a transportation system, improving the routes that are most productive makes the whole system more efficient.

In recent years, researchers have seen clues that nerve cell activity could promote the growth of myelin insulation. There have been studies that showed a correlation between experience and myelin dynamics, and studies of isolated cells in a dish suggesting a relationship between neuronal activity and myelination. But there has been no way to show that neuronal activity directly causes myelin changes in an intact brain. “You can’t really implant an electrode in the brain to answer this question because the resulting injury changes the behavior of the cells,” Monje said.

The solution was a relatively new and radical technique called optogenetics. Scientists insert genes for a light-sensitive ion channel into a specific group of neurons. Those neurons can be made to fire when exposed to particular wavelengths of light. In the study, Monje and her colleagues used mice with light-sensitive ion channels in an area of their brains that controls movement. The scientists could then turn on and off certain movement behaviors in the mice by turning on and off the light. Because the light diffuses from a source placed at the surface of the brain down to the neurons being studied, there was no need to insert a probe directly next to the neurons, which would have created an injury.

By directly stimulating the neurons with light, the researchers were able to show it was the activation of the neurons that prompted the myelin-forming cells to respond.

Further research could reveal exactly how activity promotes oligodendrocyte-precursor-cell proliferation and maturation, as well as dynamic changes in myelin. Such a molecular understanding could help researchers develop therapeutic strategies that promote myelin repair in diseases in which myelin is degraded, such as multiple sclerosis, the leukodystrophies and spinal cord injury.

“Conversely, when growth of these cells is dysregulated, how does that contribute to disease?” Monje said. One particular area of interest for her is a childhood brain cancer called diffuse intrinsic pontine glioma. The cancer, which usually strikes children between 5 and 9 years old and is inevitably fatal, occurs when the brain myelination that normally takes place as kids become more physically coordinated goes awry, and the brain cells grow out of control.

Meditation as object of medical research

Mindfulness meditation produces personal experiences that are not readily interpretable by scientists who want to study its psychiatric benefits in the brain. At a conference near Boston April 5, 2014, Brown University researchers will describe how they’ve been able to integrate mindfulness experience with hard neuroscience data to advance more rigorous study.

Mindfulness is always personal and often spiritual, but the meditation experience does not have to be subjective. Advances in methodology are allowing researchers to integrate mindfulness experiences with brain imaging and neural signal data to form testable hypotheses about the science — and the reported mental health benefits — of the practice.

A team of Brown University researchers, led by junior Juan Santoyo, will present their research approach at 2:45 p.m on Saturday, April 5, 2014, at the 12th Annual International Scientific Conference of the Center for Mindfulness at the University of Massachusetts Medical School. Their methodology employs a structured coding of the reports meditators provide about their mental experiences. That can be rigorously correlated with quantitative neurophysiological measurements.

“In the neuroscience of mindfulness and meditation, one of the problems that we’ve had is not understanding the practices from the inside out,” said co-presenter Catherine Kerr, assistant professor (research) of family medicine and director of translational neuroscience in Brown’s Contemplative Studies Initiative. “What we’ve really needed are better mechanisms for generating testable hypotheses – clinically relevant and experience-relevant hypotheses.”

Now researchers are gaining the tools to trace experiences described by meditators to specific activity in the brain.

“We’re going to [discuss] how this is applicable as a general tool for the development of targeted mental health treatments,” Santoyo said. “We can explore how certain experiences line up with certain patterns of brain activity. We know certain patterns of brain activity are associated with certain psychiatric disorders.”

Structuring the spiritual

At the conference, the team will frame these broad implications with what might seem like a small distinction: whether meditators focus on their sensations of breathing in their nose or in their belly. The two meditation techniques hail from different East Asian traditions. Carefully coded experience data gathered by Santoyo, Kerr, and Harold Roth, professor of religious studies at Brown, show that the two techniques produced significantly different mental states in student meditators.

“We found that when students focused on the breath in the belly their descriptions of experience focused on attention to specific somatic areas and body sensations,” the researchers wrote in their conference abstract. “When students described practice experiences related to a focus on the nose during meditation, they tended to describe a quality of mind, specifically how their attention ‘felt’ when they sensed it.”

The ability to distill a rigorous distinction between the experiences came not only from randomly assigning meditating students to two groups – one focused on the nose and one focused on the belly – but also by employing two independent coders to perform standardized analyses of the journal entries the students made immediately after meditating.

This kind of structured coding of self-reported personal experience is called “grounded theory methodology.” Santoyo’s application of it to meditation allows for the formation of hypotheses.

For example, Kerr said, “Based on the predominantly somatic descriptions of mindfulness experience offered by the belly-focused group, we would expect there to be more ongoing, resting-state functional connectivity in this group across different parts of a large brain region called the insula that encodes visceral, somatic sensations and also provides a readout of the emotional aspects of so-called ‘gut feelings’.”

Unifying experience and the brain

The next step is to correlate the coded experiences data with data from the brain itself. A team of researchers led by Kathleen Garrison at Yale University, including Santoyo and Kerr, did just that in a paper in Frontiers in Human Neuroscience in August 2013. The team worked with deeply experienced meditators to correlate the mental states they described during mindfulness with simultaneous activity in the posterior cingulate cortex (PCC). They measured that with real-time functional magnetic resonance imaging.

They found that when meditators of several different traditions reported feelings of “effortless doing” and “undistracted awareness” during their meditation, their PCC showed little activity, but when they reported that they felt distracted and had to work at mindfulness, their PCC was significantly more active. Given the chance to observe real-time feedback on their PCC activity, some meditators were even able to control the levels of activity there.

“You can observe both of these phenomena together and discover how they are co-determining one another,” Santoyo said. “Within 10 one-minute sessions they were able to develop certain strategies to evoke a certain experience and use it to drive the signal.”

Toward therapies

A theme of the conference, and a key motivator in Santoyo and Kerr’s research, is connecting such research to tangible medical benefits. Meditators have long espoused such benefits, but support from neuroscience and psychiatry has been considerably more recent.

In a February 2013 paper in Frontiers in Human Neuroscience, Kerr and colleagues proposed that much like the meditators could control activity in the PCC, mindfulness practitioners may gain enhanced control over sensory cortical alpha rhythms. Those brain waves help regulate how the brain processes and filters sensations, including pain, and memories such as depressive cognitions.

Santoyo, whose family emigrated from Colombia when he was a child, became inspired to investigate the potential of mindfulness to aid mental health beginning in high school. Growing up in Cambridge and Somerville, Mass., he observed the psychiatric difficulties of the area’s homeless population. He also encountered them while working in food service at Cambridge hospital.

“In low-income communities you always see a lot of untreated mental health disorders,” said Santoyo, who meditates regularly and helps to lead a mindfulness group at Brown. He is pursuing a degree in neuroscience and contemplative science. “The perspective of contemplative theory is that we learn about the mind by observing experience, not just to tickle our fancy but to learn how to heal the mind.”

It’s a long path, perhaps, but Santoyo and his collaborators are walking it with progress.

Positive, negative thinkers’ brains revealed

The ability to stay positive when times get tough – and, conversely, of being negative – may be hardwired in the brain, finds new research led by a Michigan State University psychologist.

The study, which appears in the Journal of Abnormal Psychology, is the first to provide biological evidence validating the idea that there are, in fact, positive and negative people in the world.

“It’s the first time we’ve been able to find a brain marker that really distinguishes negative thinkers from positive thinkers,” said Jason Moser, lead investigator and assistant professor of psychology.

For the study, 71 female participants were shown graphic images and asked to put a positive spin on them while their brain activity was recorded. Participants were shown a masked man holding a knife to a woman’s throat, for example, and told one potential outcome was the woman breaking free and escaping.

The participants were surveyed beforehand to establish who tended to think positively and who thought negatively or worried. Sure enough, the brain reading of the positive thinkers was much less active than that of the worriers during the experiment.

“The worriers actually showed a paradoxical backfiring effect in their brains when asked to decrease their negative emotions,” Moser said. “This suggests they have a really hard time putting a positive spin on difficult situations and actually make their negative emotions worse even when they are asked to think positively.”

The study focused on women because they are twice as likely as men to suffer from anxiety related problems and previously reported sex differences in brain structure and function could have obscured the results.

Moser said the findings have implications in the way negative thinkers approach difficult situations.

“You can’t just tell your friend to think positively or to not worry – that’s probably not going to help them,” he said. “So you need to take another tack and perhaps ask them to think about the problem in a different way, to use different strategies.”

Negative thinkers could also practice thinking positively, although Moser suspects it would take a lot of time and effort to even start to make a difference.

Some innate preferences shape the sound of words from birth

Languages are learned, it’s true, but are there also innate bases in the structure of language that precede experience? Linguists have noticed that, despite the huge variability of human languages, here are some preferences in the sound of words that can be found across languages. So they wonder whether this reflects the existence of a universal, innate biological basis of language. A SISSA study provides evidence to support this hypothesis, demonstrating that certain preferences in the sound of words are already active in newborn infants.

Take the sound “bl”: how many words starting with that sound can you think of? Blouse, blue, bland… Now try with “lb”: how many can you find? None in English and Italian, and even in other languages such words either don’t exist or are extremely rare. Human languages offer several examples of this kind, and this indicates that in forming words we tend to prefer certain sound combinations to others, irrespective of which language we speak. The fact that this occurs across languages has prompted linguists to hypothesize the existence of biological bases of language (in born and universal) which precede language learning in humans. Finding evidence to support his hypothesis is, however, far from easy and the debate between the proponents of this view and those who believe that language is merely the result of learning is still open. But proof supporting the “universalist” hypothesis has now been provided by a new study conducted by a research team of the International School for Advanced Studies (SISSA) in Trieste and just published in the journal PNAS.

David Gomez, a SISSA research scientist working under the supervision of Jacques Mehler and first author of the paper, and his coworkers decided to observe the brain activity of newborns. “In fact, if it is possible to demonstrate that these preferences are already present within days from birth, when the newborn baby is still unable to speak and presumably has very limited language knowledge, then we can infer that there is an inborn bias that prefers certain words to others”, comments Gomez.

“To monitor the newborns’ brain activity we used a non-invasive technique, i.e., functional near-infrared spectroscopy”, explains Marina Nespor, a SISSA neuroscientist who participated in the study. During the experiments the newborns would listen to words starting with normally “preferred” sounds (like “bl”) and others with  uncommon sounds (“lb”). “What we found was that the newborns’ brains reacted in a significantly different manner to the two types of sound” continues Nespor.

“The brain regions that are activated while the newborns are listening react differently in the two cases”, comments Gomez, “and reflect the preferences observed across languages, as well as the behavioural responses recorded in similar experiments carried out in adults”. “It’s difficult to imagine what languages would sound like if humans didn’t share a common knowledge base”, concludes Gomez. “We are lucky that this common base exists. This way, our children are born with an ability to distinguish words from “non-words” ever since birth, regardless of which language they will then go on to learn”.