Neuroscience

Whites of Their Eyes: Study Finds Infants Respond to Social Cues...

Tue, 28 Oct 2014 21:36:24 -0400

Whites of Their Eyes: Study Finds Infants Respond to Social Cues From Sclera

Humans are the only primates with large, highly visible sclera – the white part of the eye.

The eye plays a significant role in the expressiveness of a face, and how much sclera is shown can indicate the emotions or behavioral attitudes of a person. Wide-open eyes, exposing a lot of white, indicate fear or surprise. A thinner slit of exposed eye, such as when smiling, expresses happiness or joy. Averted eyes, as well as direct eye contact, can mean several things. So the eye white, or how much of it is shown and at what angle, plays a role in the social and cooperative interactions among humans.

Adult humans are well-attuned to social cues involving the eye and use them, along with a great range of other facial and body features, to respond appropriately during social interactions. This sensitivity to eye cues is hard-wired into the brain of adults as they respond to social eye cues even without consciously seeing them.

But it is unclear whether the ability to unconsciously distinguish between different social cues indicated by the eyes exists early in development and can therefore be considered a key feature of the human social makeup.

A new University of Virginia and Max Planck Institute study, published online this week in the journal Proceedings of the National Academy of Sciences, finds that the ability to respond to eye cues apparently develops during infancy – at seven or so months.

“Our study provides developmental evidence for the notion that humans possess specific brain processes that allow them to automatically respond to eye cues,” said Tobias Grossmann, a University of Virginia developmental psychologist and one of the study’s authors.

Grossmann and his Max Planck Institute colleague Sarah Jessen used electroencephalography, or EEG, to measure the brain activity of 7-month-old infants while showing images of eyes wide open, narrowly opened, and with direct or averted gazes.

They found that the infants’ brains responded differently depending on the expression suggested by the eyes they viewed, which were shown absent of other facial features. They viewed the eye images for only 50 milliseconds – which is much less time than needed for an infant of this age to consciously perceive this kind of visual information.

“Their brains clearly responded to social cues conveyed through the eyes, indicating that even without conscious awareness, human infants are able to detect subtle social cues,” Grossmann said.

The infants’ brain responses displayed a different pattern to sclera depicting fearful expressions (wide-eyed) to non-fearful sclera. They also showed brain responses that differed when viewing direct gaze eyes compared to averted gaze.

“This demonstrates that, like adults, infants are sensitive to eye expressions of fear and direction of focus, and that these responses operate without conscious awareness,” Grossmann said. “The existence of such brain mechanisms in infants likely provides a vital foundation for the development of social interactive skills in humans.”

The infants in the study wore an EEG cap, like a small hat, which included sensors that could detect brain signals. Infants were sitting in the laps of their parents during the testing.

Researchers observe brain development in utero New investigation...

Tue, 28 Oct 2014 19:12:22 -0400

Researchers observe brain development in utero

New investigation methods using functional magnetic resonance tomography (fMRT) offer insights into fetal brain development. These “in vivo” observations will uncover different stages of the brain’s development. A research group at the Computational Imaging Research Lab from the MedUni Vienna has observed that parts of the brain that are later responsible for sight are already active at this stage.

To obtain insights into the development of the human brain in utero, the study group observed 32 fetuses from the 21st to 38th week of pregnancy (an average pregnancy lasts 40 weeks). The architecture of the brain is developed particularly during the middle trimester of pregnancy. Using functional magnetic resonance tomography, it was possible to measure activity and thereby gain information about the most important cortical and sub-cortical structures of the developing brain. During the period of the 26th to 29th week of pregnancy in particular, short-range neuronal connections developed especially actively, while in contrast to this, long-range nerve connections exhibited more linear growth during pregnancy. “It became apparent that the areas responsible for sensory perception are developed first and only then, around four weeks later, do the areas responsible for more complex, cognitive skills come along,” says first author Andras Jakab from the Computational Imaging Research Lab at the MedUni Vienna, explaining the results.

In another study, the study group led by Veronika Schöpf and Georg Langs was able to demonstrate for a correlation of eye movement and areas of the brain which are later responsible to process vision as early as the 30th to the 36th weeks of pregnancy. The fact that newborn babies first have to learn to “process” visual stimuli after birth is already known. It has now been possible to demonstrate that this important development starts even before birth. The research group investigated the relationship between eye movements and brain activity. Even at this stage of development, motor visual movement is linked to the areas in the visual cortex of the brain responsible for processing optical signals. “The relationship between eye movement and the responsible areas of the brain has therefore been demonstrated for the first time in utero”, explains first author Veronika Schöpf.

(Image caption: Three-dimensional reconstruction of a synapse in...

Tue, 28 Oct 2014 16:48:13 -0400

(Image caption: Three-dimensional reconstruction of a synapse in the mouse brain. Readily releasable fusionable synaptic vesicles (blue, around 45 millionths of a millimetre in diameter) are docked at the cell membrane. Credit: © MPI f. Experimental Medicine/ Benjamin H. Cooper)

Synapses always on the starting blocks

While neurons rapidly propagate information in their interior via electrical signals, they communicate with each other at special contact points known as the synapses. Chemical messenger substances, the neurotransmitters, are stored in vesicles at the synapses. When a synapse becomes active, some of these vesicles fuse with the cell membrane and release their contents. To ensure that valuable time is not lost, synapses always have some readily releasable vesicles on standby. With the help of high-resolution, three-dimensional electron microscopy, scientists at the Max Planck Institute of Experimental Medicine in Göttingen succeeded in demonstrating that these fusionable vesicles have a very special characteristic: they already have close contact with the cell membrane long before the actual fusion occurs. In addition, the research team also decoded the molecular machinery that facilitates the operation of this docking mechanism.

The fusion of the neurotransmitter vesicles with the cell membrane involves close cooperation between numerous protein components, which monitor each other and ensure that every single ‘participant’ is always in the right place. This is referred to as the fusion machinery and the comparison is an apt one: if a cogwheel in a clock mechanism is broken, the hands do not move. In a similar way, faulty or missing molecules impair synaptic operations.

In research studies carried out some years ago, Nils Brose and his colleague JeongSeop Rhee from the Max Planck Institute of Experimental Medicine in Göttingen already demonstrated that the transmission of information at the synapses in genetically modified mice, in which all known genes of the Munc13 or CAPS proteins had been switched off, is severely defective. Although the neurons of the genetically modified mice do not differ from those of healthy mice when examined under an optical microscope, if Munc13 is missing, the release of neurotransmitters actually grinds to a halt completely. Brose and Rhee’s findings showed that to be able to react immediately to signals at all times, each synapse must keep a small number of ‘readily releasable’ fusionable vesicles on standby.

But how do Munc13 and CAPS convert the vesicles to this kind of fusionable state? To answer this question, the Göttingen-based scientists studied the synaptic contacts in the minutest possible detail. To do this, neurobiologists Cordelia Imig and Ben Cooper, who have been working with Brose and Rhee for many years, used a high-pressure freezing process. This involves the rapid freezing of neurons in the brain tissue under high pressure so that no disruptive ice crystals are formed and the fine structure of the cells is particularly well conserved. The samples obtained in this way were then analysed using electron tomography. Using this method, electron microscope images of a structure are recorded from many different angles, in a similar way to the process used in medical computed tomography. The individual images can then be combined on the computer to give a high-resolution three-dimensional image – of a synapse in this case (see image).

“Our results showed that readily releasable vesicles in healthy synapses touch the cell membrane,” explains Cooper. “However, if Munc13 and CAPS proteins are missing, the vesicles do not reach the active zone and accumulate a few nanometres away from it.” To their astonishment, the researchers also observed that SNARE proteins, which collaborate with Munc13 and CAPS in the nerve endings, are also involved in this docking process. SNARE proteins are found in the cell and vesicle membranes of healthy synapses and control the fusion of the two membranes during neurotransmitter release. When a vesicle approaches the cell membrane, the individual SNARE molecules line up opposite each other like the sides of a zip and pull the membranes close to each other in this way. The vesicles await the starting gun for their fusion in this state – in the starting blocks, so to speak.

The findings of the neurobiologists in Göttingen prove that Munc13, CAPS and SNARE proteins closely align the vesicle and cell membrane in the synapse, long before the signal for fusion is given. This is the only way that the fast and controlled transmission of information at the synapse can be guaranteed, thanks to which we can react specifically to information from our environment. “It had long been clear that synapses have to be extremely fast to carry out all of the many complex brain functions. Our study shows for the first time how this is managed at the molecular level and on the level of the synaptic vesicles,” says Brose. Because almost all of the protein components involved in this process also play a role in neurological and psychiatric diseases, the Göttingen-based scientists believe that their discovery will soon benefit medical research.

(Image caption: In the top image, cells from a mouse model of...

Tue, 28 Oct 2014 14:24:36 -0400

(Image caption: In the top image, cells from a mouse model of amyotrophic lateral sclerosis caused normal healthy brain cells (green) to die. But when scientists blocked an enzyme in the cells from the mouse model, more of the normal cells and their branches survived (bottom))

Heart drug may help treat ALS

Digoxin, a medication used in the treatment of heart failure, may be adaptable for the treatment of amyotrophic lateral sclerosis (ALS), a progressive, paralyzing disease, suggests new research at Washington University School of Medicine in St. Louis.

ALS, also known as Lou Gehrig’s disease, destroys the nerve cells that control muscles. This leads to loss of mobility, difficulty breathing and swallowing and eventually death. Riluzole, the sole medication approved to treat the disease, has only marginal benefits in patients.

But in a new study conducted in cell cultures and in mice, scientists showed that when they reduced the activity of an enzyme or limited cells’ ability to make copies of the enzyme, the disease’s destruction of nerve cells stopped. The enzyme maintains the proper balance of sodium and potassium in cells.

“We blocked the enzyme with digoxin,” said senior author Azad Bonni, MD, PhD. “This had a very strong effect, preventing the death of nerve cells that are normally killed in a cell culture model of ALS.”

The findings appear online Oct. 26 in Nature Neuroscience.

The results stemmed from Bonni’s studies of brain cells’ stress responses in a mouse model of ALS. The mice have a mutated version of a gene that causes an inherited form of the disease and develop many of the same symptoms seen in humans with ALS, including paralysis and death.

Efforts to monitor the activity of a stress response protein in the mice unexpectedly led the scientists to another protein: sodium-potassium ATPase. This enzyme ejects charged sodium particles from cells and takes in charged potassium particles, allowing cells to maintain an electrical charge across their outer membranes.

Maintenance of this charge is essential for the normal function of cells. The particular sodium-potassium ATPase highlighted by Bonni’s studies is found in nervous system cells called astrocytes. In the ALS mice, levels of the enzyme are higher than normal in astrocytes.

Bonni’s group found that the increase in sodium-potassium ATPase led the astrocytes to release harmful factors called inflammatory cytokines, which may kill motor neurons.

Recent studies have suggested that astrocytes may be crucial contributors to neurodegenerative disorders such as ALS, and Alzheimer’s, Huntington’s and Parkinson’s diseases. For example, placing astrocytes from ALS mice in culture dishes with healthy motor neurons causes the neurons to degenerate and die.

“Even though the neurons are normal, there’s something going on in the astrocytes that is harming the neurons,” said Bonni, the Edison Professor of Neurobiology and head of the Department of Anatomy and Neurobiology.

How this happens isn’t clear, but Bonni’s results suggest the sodium-potassium ATPase plays a key role. When he conducted the same experiment but blocked the enzyme in ALS astrocytes using digoxin, the normal motor nerve cells survived. Digoxin blocks the ability of sodium-potassium ATPase to eject sodium and bring in potassium.

In mice with the mutation for inherited ALS, those with only one copy of the gene for sodium-potassium ATPase survived an average of 20 days longer than those with two copies of the gene. When one copy of the gene is gone, cells make less of the enzyme.

“The mice with only one copy of the sodium-potassium ATPase gene live longer and are more mobile,” Bonni said. “They’re not normal, but they can walk around and have more motor neurons in their spinal cords.”

Many important questions remain about whether and how inhibitors of the sodium-potassium ATPase enzyme might be used to slow progressive paralysis in ALS, but Bonni said the findings offer an exciting starting point for further studies.

Ultra-high-field MRI reveals language centres in the brain in...

Tue, 28 Oct 2014 12:01:06 -0400

Ultra-high-field MRI reveals language centres in the brain in much more detail

In a new investigation by the University Department of Neurology, it has been possible for the first time to demonstrate that the areas of the brain that are important for understanding language can be pinpointed much more accurately using ultra-high-field MRI (7 Tesla) than with conventional clinical MRI scanners. This helps to protect these areas more effectively during brain surgery and avoid accidentally damaging it.

Before brain surgery, it is important to precisely understand the areas of the brain required for language in order to avoid injuring them during the procedure. Their position can shift considerably, especially in patients with tumours or brain injuries. The brain’s flexibility also means that language centres can shift to other regions. If the areas responsible for language control and processing are injured during a brain operation, the patient can be left unable to communicate. In order to create a “map” of the language control centres prior to the operation, functional magnetic resonance imaging (fMRI) is used these days.

A multi-centre study from 2013 demonstrated the advantages of fMRI-assisted localisation of the motor centres in the brain. In a new investigation by the working group led by Roland Beisteiner (University Department of Neurology), it has been possible for the first time to demonstrate that the areas of the brain that are important for understanding language can be pinpointed even more accurately using ultra-high-field MRI (7 Tesla) than with conventional clinical MRI scanners. The focus lies on the two most important language centres in the brain known as Wernicke’s area (which controls the understanding of language) and Broca’s area (which controls the motor functions involved with speech).

The brain is scanned for activity while the patient is carrying out speech exercises. This allows the areas required for speech to be localised much more accurately than previously. “Ultra-high-field MR offers much greater sensitivity than classic MRI scanners”, explains Roland Beisteiner, “allowing even very weak signals to be recorded in areas that would otherwise have been missed.”

Activity in dendrites is critical in memory formation Why do we...

Mon, 27 Oct 2014 21:00:57 -0400

Activity in dendrites is critical in memory formation

Why do we remember some things and not others? In a unique imaging study, two Northwestern University researchers have discovered how neurons in the brain might allow some experiences to be remembered while others are forgotten. It turns out, if you want to remember something about your environment, you better involve your dendrites.

Using a high-resolution, one-of-a-kind microscope, Daniel A. Dombeck and Mark E. J. Sheffield peered into the brain of a living animal and saw exactly what was happening in individual neurons called place cells as the animal navigated a virtual reality maze.

The scientists found that, contrary to current thought, the activity of a neuron’s cell body and its dendrites can be different. They observed that when cell bodies were activated but the dendrites were not activated during an animal’s experience, a lasting memory of that experience was not formed by the neurons. This suggests that the cell body seems to represent ongoing experience, while dendrites, the treelike branches of a neuron, help to store that experience as a memory.

"There are a lot of theories on memory but very little data as to how individual neurons actually store information in a behaving animal," said Dombeck, assistant professor of neurobiology in the Weinberg College of Arts and Sciences and the study’s senior author. "Now we have uncovered signals in dendrites that we think are very important for learning and memory. Our findings could explain why some experiences are remembered and others are forgotten."

In the brain’s hippocampus, there are hundreds of thousands of place cells — neurons essential to the brain’s GPS system. Dombeck and Sheffield are the first to image the activity of individual dendrites in place cells.

Their findings contribute to our understanding of how the brain represents the world around it and also point to dendrites as a new potential target for therapeutics to combat memory deficits and debilitating diseases, such as Alzheimer’s disease (AD). Disruption to the brain’s GPS system is one of the first symptoms of AD, with many patients unable to find their way home. Understanding how place cells and their dendrites store these types of memories could help us find new ways to treat the disease.

The Northwestern study will be published Oct. 26 by the journal Nature.

Neuroscientist John O’Keefe discovered place cells in 1971 (and received this year’s Nobel Prize in physiology and medicine), but it is only in the last few years that scientists, such as Dombeck and Sheffield, have been able to image these neurons that represent a map of where we are in our environment.

In their study, Dombeck and Sheffield found dendrite signals that could explain how an animal can experience something without storing the experience as a memory.

They saw that dendrites are not always activated when the cell body is activated in a neuron. Signals produced in the dendrites (used to store information) and signals within the neuron cell body (used to compute and transmit information) can be either highly synchronized or desynchronized depending on how well the neurons remember different features of the maze.

Scientists have long believed that the neuronal tasks of computing and storing information are connected — when neurons compute information, they are also storing it, and vice versa. The Northwestern study provides evidence against this classic view of neuronal function.

"We experience events all the time, which must be represented in the brain by the activity of neurons, but not all these events can be recalled later," said Mark E. J. Sheffield, a postdoctoral fellow in Dombeck’s lab and first author of the study.

"A daily commute to work, for example, requires the activity of millions of neurons, but you would be hard pressed to remember what was happening halfway through your commute last Tuesday," Sheffield said. "How is it then that the neurons could be activated during the commute without storing that information in the brain? Now we may have an explanation for how this occurs."

Dombeck and Sheffield built their own laser scanning microscope that can image neurons on multiple planes. They then studied individual animals navigating (on a trackball) a virtual reality maze constructed using the video game Quake II.

Each lit-up structure seen in the images they took indicate a neuron firing action potentials. The activity of these neurons represents an animal’s experience of where it is in the environment, the researchers said. Whether the neurons store this experience or not appears to depend on the activity of the neurons’ dendrites.

(Image credit)

Just 30 minutes of exercise has benefits for the...

Mon, 27 Oct 2014 18:01:01 -0400

Just 30 minutes of exercise has benefits for the brain

University of Adelaide neuroscientists have discovered that just one session of aerobic exercise is enough to spark positive changes in the brain that could lead to improved memory and coordination of motor skills.

A study conducted by researchers in the University’s Robinson Research Institute has found changes in the brain that were likely to make it more “plastic” after only 30 minutes of vigorous exercise.

The study involved a small group of healthy people aged in their late 20s to early 30s who rode exercise bikes. They were monitored for changes in the brain immediately after the exercise and again 15 minutes later.

"We saw positive changes in the brain straight away, and these improvements were sustained 15 minutes after the exercise had ended," says research leader Associate Professor Michael Ridding.

"Plasticity in the brain is important for learning, memory and motor skill coordination. The more ‘plastic’ the brain becomes, the more it’s able to reorganise itself, modifying the number and strength of connections between nerve cells and different brain areas."

Associate Professor Ridding says past research has shown that regular physical activity can have positive effects on brain function and plasticity, but it was unknown whether a stand-alone session of exercise would also have similar positive effects.

"We now have evidence suggesting that it does," he says. "This exercise-related change in the brain may, in part, explain why physical activity has a positive effect on memory and higher-level functions."

Associate Professor Ridding says there is now mounting evidence that engaging in aerobic exercise positively influences brain function in many ways - at cellular and molecular levels, as well as in the brain’s architecture.

"Although this was a small sample group, it helps us to better understand the overall picture of how exercise influences the brain," he says.

"We know that plasticity is also important for recovery from brain damage, so this opens up potential therapeutic avenues for patients.

"Further research will be required to see what the possible long-term benefits could be for patients as well as healthy people."

Dietary Flavanols Reverse Age-Related Memory Decline Dietary...

Mon, 27 Oct 2014 15:00:49 -0400

Dietary Flavanols Reverse Age-Related Memory Decline

Dietary cocoa flavanols—naturally occurring bioactives found in cocoa—reversed age-related memory decline in healthy older adults, according to a study led by Columbia University Medical Center (CUMC) scientists. The study, published today in the advance online issue of Nature Neuroscience, provides the first direct evidence that one component of age-related memory decline in humans is caused by changes in a specific region of the brain and that this form of memory decline can be improved by a dietary intervention.

As people age, they typically show some decline in cognitive abilities, including learning and remembering such things as the names of new acquaintances or where they parked the car or placed their keys. This normal age-related memory decline starts in early adulthood but usually does not have any noticeable impact on quality of life until people reach their fifties or sixties. Age-related memory decline is different from the often-devastating memory impairment that occurs with Alzheimer’s, in which a disease process damages and destroys neurons in various parts of the brain, including the memory circuits.

Previous work, including by the laboratory of senior author Scott A. Small, MD, had shown that changes in a specific part of the brain—the dentate gyrus—are associated with age-related memory decline. Until now, however, the evidence in humans showed only a correlational link, not a causal one. To see if the dentate gyrus is the source of age-related memory decline in humans, Dr. Small and his colleagues tested whether compounds called cocoa flavanols can improve the function of this brain region and improve memory. Flavanols extracted from cocoa beans had previously been found to improve neuronal connections in the dentate gyrus of mice.

Dr. Small is the Boris and Rose Katz Professor of Neurology (in the Taub Institute for Research on Alzheimer’s Disease and the Aging Brain, the Sergievsky Center, and the Departments of Radiology and Psychiatry) and director of the Alzheimer’s Disease Research Center in the Taub Institute at CUMC.

A cocoa flavanol-containing test drink prepared specifically for research purposes was produced by the food company Mars, Incorporated, which also partly supported the research, using a proprietary process to extract flavanols from cocoa beans. Most methods of processing cocoa remove many of the flavanols found in the raw plant.

In the CUMC study, 37 healthy volunteers, ages 50 to 69, were randomized to receive either a high-flavanol diet (900 mg of flavanols a day) or a low-flavanol diet (10 mg of flavanols a day) for three months. Brain imaging and memory tests were administered to each participant before and after the study. The brain imaging measured blood volume in the dentate gyrus, a measure of metabolism, and the memory test involved a 20-minute pattern-recognition exercise designed to evaluate a type of memory controlled by the dentate gyrus.

“When we imaged our research subjects’ brains, we found noticeable improvements in the function of the dentate gyrus in those who consumed the high-cocoa-flavanol drink,” said lead author Adam M. Brickman, PhD, associate professor of neuropsychology at the Taub Institute.

The high-flavanol group also performed significantly better on the memory test. “If a participant had the memory of a typical 60-year-old at the beginning of the study, after three months that person on average had the memory of a typical 30- or 40-year-old,” said Dr. Small. He cautioned, however, that the findings need to be replicated in a larger study—which he and his team plan to do.

Flavanols are also found naturally in tea leaves and in certain fruits and vegetables, but the overall amounts, as well as the specific forms and mixtures, vary widely.

The precise formulation used in the CUMC study has also been shown to improve cardiovascular health. Brigham and Women’s Hospital in Boston recently announced an NIH-funded study of 18,000 men and women to see whether flavanols can help prevent heart attacks and strokes.

The researchers point out that the product used in the study is not the same as chocolate, and they caution against an increase in chocolate consumption in an attempt to gain this effect.

Two innovations by the investigators made the study possible. One was a new information-processing tool that allows the imaging data to be presented in a single three-dimensional snapshot, rather than in numerous individual slices. The tool was developed in Dr. Small’s lab by Usman A. Khan, an MD-PhD student in the lab, and Frank A. Provenzano, a biomedical engineering graduate student at Columbia. The other innovation was a modification to a classic neuropsychological test, allowing the researchers to evaluate memory function specifically localized to the dentate gyrus. The revised test was developed by Drs. Brickman and Small.

Besides flavanols, exercise has been shown in previous studies, including those of Dr. Small, to improve memory and dentate gyrus function in younger people. In the current study, the researchers were unable to assess whether exercise had an effect on memory or on dentate gyrus activity. “Since we didn’t reach the intended VO2max (maximal oxygen uptake) target,” said Dr. Small, “we couldn’t evaluate whether exercise was beneficial in this context. This is not to say that exercise is not beneficial for cognition. It may be that older people need more intense exercise to reach VO2max levels that have therapeutic effects.”

Genes exhibit different behaviours in different stages of development

Mon, 27 Oct 2014 12:01:07 -0400

The effect that genes have on our brain depends on our age. These are the findings of a group of...

The pleasure of learning new words From our very first years, we...

Sun, 26 Oct 2014 18:00:52 -0400

The pleasure of learning new words

From our very first years, we are intrinsically motivated to learn new words and their meanings. First language acquisition occurs within a permanent emotional interaction between parents and children. However, the exact mechanism behind the human drive to acquire communicative linguistic skills is yet to be established.

In a study published in the journal Current Biology, researchers from the University of Barcelona (UB), the Bellvitge Biomedical Research Institute (IDIBELL) and the Otto von Guericke University Magdeburg (Germany) have experimentally proved that human adult word learning exhibit activation not only of cortical language regions but also of the ventral striatum, a core region of reward processing. Results confirm that the motivation to learn is preserved throughout the lifespan, helping adults to acquire a second language.

Researchers determined that the reward region that is activated is the same that answers to a wide range of stimuli, including food, sex, drugs or game. “The main objective of the study was to know to what extent language learning activates subcortical reward and motivational systems”, explains Pablo Ripollés, PhD student at UB-IDIBELL and first author of the article. “Moreover, the fact that language could be favoured by this type of circuitries is an interesting hypothesis from an evolutionary point of view”, points out the expert.

According to Antoni Rodríguez Fornells, UB lecturer and ICREA researcher at IDIBELL, “the language region has been traditionally located at an apparently encapsulated cortical structure which has never been related to reward circuitries, which are considered much older from an evolutionary perspective”. “The study —he adds— questions whether language only comes from cortical evolution or structured mechanisms and suggests that emotions may influence language acquisition processes”.

Subcortical areas are closely related to those that help to store information. Therefore, those facts or pieces of information that awake an emotion are more easily to remember and learn.

Motivation for learning a second language

By using diffusion tensor imaging, UB-IDIBELL researchers reconstructed the white matter pathways that link brain regions in each participant. Experts were able to correlate the number of new words learnt by each person during the experiment with a low myelin index, a measure of structure integrity. Results proved that subjects who presented higher myelin concentrations in the structures that carry information to the ventral striatum —in other words, those that are best connected to the reward area— were able to learn more words.

“Results provide a neural substrate of the influence that reward and motivation circuitries may have in learning words from context”, affirms Josep Marco Pallarès, UB-IDIBELL researcher. The activation of these circuitries during word learning suggests future research lines aimed at stimulating reward regions to improve language learning in patients with linguistic problems.

The fact that non-linguistic subcortical mechanisms, which are much older from an evolutionary perspective, work together with language cortical regions —which appeared latter— suggests new language theories trying to explain how reward mechanisms have influenced and supported one of our primal urges: the desire to acquire language and to communicate.

Experiment with words and gambling

Researchers carried out an experiment with thirty-six adults who participated in two magnetic resonance sessions. On the first one, functional magnetic resonance was used to measure participants’ brain activity while they perform two different tasks. This technique enables to detect accurately what brain regions are active while a person is performing a certain activity. In the first task, participants must learn the meaning of some new words from context in two different sentences. For instance, subjects saw on a screen the sentences: “Every Sunday the grandmother went to the jedin” and “The man was buried in the jedin”. Considering both sentences, participants could learn that the word jedin means “graveyard”. Then, participants completed two runs of a standard-event-related money gambling task.

The experiment revealed that when subjects inferred and memorized the meaning of a new word, brain activity in the ventral striatum was increased. Indeed, the same ventral striatum activation was observed when earning money in gambling. Therefore, to learn the meaning of a new word activates reward and motivational circuitries like in gambling activities. Moreover, it was observed that word learning produce an increase of brain activity synchronization between the ventral striatum and cortical language regions.

(Image caption: During development, nerve cells (shown in blue,...

Sun, 26 Oct 2014 12:01:06 -0400

(Image caption: During development, nerve cells (shown in blue, green, violet and yellow) extend their axons to target leg muscles. If the EphA4 receptors of the growing nerve cells no longer encounter freely accessible ephrins, the axons of many nerve cells (violet) are no longer able to find their partner cells. Credit: © MPI of Neurobiology / Gatto)

Neurons in a forest of signposts

Our ability to move relies on the correct formation of connections between different nerve cells and between nerve and muscle cells. Growing axons of nerve cells are guided to their targets by signposts expressed on the surface of other cells. Very prominent are “do not enter” signs that push axons away. Cell culture studies suggest that protein-cutting enzymes (proteases) remove these signs as soon as they are recognized by the growing axons. In this way, the “bond of recognition” between the axon and the sign is quickly broken, and the axons are more easily guided in a new direction. Scientists from the Max Planck Institute of Neurobiology in Martinsried and the Institut de Recherches Cliniques de Montréal have now shown that proteases indeed control the navigation of growing axons. However, contrary to the current belief, they do so by regulating the number of existing signs. Without proteases, the signposts would be masked and the axons would grow in the wrong direction. These findings clarified how cells form connections during development and may also improve our understanding of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS).

The human brain consists of about 100 billion nerve cells. During embryonic development each of these cells connects with other cells by means of a long extension, known as axon. Some axons need to navigate long distances through the body to find their correct targets, for example from the spinal cord down to the foot. Only if all these connections are correctly established we can perform basic and fine-tuned movements, such as walking or playing the piano.

It is therefore essential that each nerve cell finds its correct target. But how does an axon navigate and find the appropriate partner cells among billions of other possible targets? “We have now identified a few dozen guidance molecules and their receptors that help axons orient themselves,” says Rüdiger Klein, Director at the Max Planck Institute of Neurobiology. “However, these few receptor-guidance molecule pairs need to control a very large number of navigational decisions. Therefore, there must be some mechanisms to amplify and modulate the effects of these protein pairs”.

Cutting for speed?

Over the last decade, Rüdiger Klein and his team have been studying how nerve cells find their way during development. They are focusing on “do not enter” signs, e.g. ephrin guidance molecules and their Eph receptors. Ephrins and Eph receptors, being present on almost all cell surfaces: on axons as well as on cells in the surrounding tissues, help the growing axons to explore their surroundings and locate their partner cells.

As an axon travels through the body, it docks again and again to other cells via the ephrin/Eph system. This triggers cellular processes, in one or both cells, that eventually cause the connection to be severed and the cells to repel each other, preventing the axon to grow in the wrong direction. It has been hypothesised that this cellular repulsion is accelerated by proteases. Proteases are enzymes that cut Eph receptors and/or ephrins, thus by severing the Eph/ephrin bond between two opposing cells they might expedite the repulsion process. “In this way, proteases could contribute to changes in the guidance process – but this has not yet been experimentally proven.” says Rüdiger Klein.

Not faster, but better

To address this question, the neurobiologists studied how proteases affect the rate of cellular repulsion controlled by EphA4 receptors and ephrins. “Although the experiments in cell culture initially appeared to confirm the theory, we discovered something quite different in living organisms,” states Rüdiger Klein. Contrary to expectations, cellular repulsion proceeded with undiminished accuracy in animals whose axons expressed EphA4 receptors resistant to protease severing. On the other hand, in animals whose axons and muscles expressed EphA4 receptors resistant to protease cutting many axons grew in the wrong direction. Because no cutting occurred, more and more functional EphA4 receptors accumulated on cell surfaces of the leg tissues. This accumulation caused EphA4 receptors to bind to the ephrins on the same cell surface, a phenomena termed as “masking”. Consequently, the ephrins could no longer act as “do not enter” signs for the growing axons. Thus, axons, being no longer repelled, are misguided in a “no entry zone” and are unable to find their correct targets.

These results show that the cleavage of Eph receptors by proteases does not, as expected, accelerate the repulsion reaction. Instead, it regulates the number of functioning receptors and indirectly the number of available ephrins on cells, where they serve as navigational aids. If the balance is disrupted, growing axons are misdirected.

This is an important finding, as EphA4 receptors perform essential functions during the development of neural networks in the brain and in the spinal cord. They are also involved in neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS). In the absence of EphA4 receptors, ALS manifests itself later and develops more slowly in a number of animal models. “It’s possible that the number of EphA4 receptors is kept low by the regulatory activity of proteases,” Rüdiger Klein reflects. “This could provide a way to exert a positive influence on the course of ALS.”

Scientific evidence does not support the brain game claims The...

Sat, 25 Oct 2014 18:00:45 -0400

Scientific evidence does not support the brain game claims

The Stanford Center for Longevity joined today with the Max Planck Institute for Human Development in issuing a statement skeptical about the effectiveness of so-called “brain game” products. Signing the document were 69 scholars, including six from Stanford and cognitive psychologists and neuroscientists from around the world.

Laura Carstensen, a Stanford psychology professor and the director of the Center for Longevity, said as baby boomers enter their golden years, commercial companies are all too often promising quick fixes for cognition problems through products that are unlikely to produce broad improvements in everyday functioning.

"It is customary for advertising to highlight the benefits and overstate potential advantages of their products," she said. "But in the case of brain games, companies also assert that the products are based on solid scientific evidence developed by cognitive scientists and neuroscientists. So we felt compelled to issue a statement directly to the public."

One problem is that while brain games may target very specific cognitive abilities, there is very little evidence that improvements transfer to more complex skills that really matter, like thinking, problem solving and planning, according to the scholars.

While it is true that the human mind is malleable throughout a lifetime, improvement on a single task – like playing computer-based brain games – does not imply a general, all-around and deeper improvement in cognition beyond performing better on just a particular game.

"Often, the cited research is only tangentially related to the scientific claims of the company, and to the games they sell," said Carstensen, the Fairleigh S. Dickinson, Jr. Professor in Public Policy.

Agreeing with this view were the experts who signed the Stanford-Planck consensus statement, which reads in part:

"We object to the claim that brain games offer consumers a scientifically grounded avenue to reduce or reverse cognitive decline when there is no compelling scientific evidence to date that they do. … The promise of a magic bullet detracts from the best evidence to date, which is that cognitive health in old age reflects the long-term effects of healthy, engaged lifestyles."

Activity and cognition

As the researchers point out, the time spent on computer games takes away from other activities like reading, socializing, gardening and exercising that may benefit cognitive functions.

"When researchers follow people across their lives, they find that those who live cognitively active, socially connected lives and maintain healthy lifestyles are less likely to suffer debilitating illness and early cognitive decline," as the statement describes it.

"In psychology," the scientists note, "it is good scientific practice to combine information provided by many tasks to generate an overall index representing a given ability."

The same standards should be applied to the brain game industry, the experts maintain. But this has not been the case, they add.

"To date, there is little evidence that playing brain games improves underlying broad cognitive abilities, or that it enables one to better navigate a complex realm of everyday life," the participants state.

One reason is the so-called “file drawer effect,” which refers to the practice of researchers filing away studies with negative outcomes. For example, brain game studies proclaiming even modest positive results are more likely to be published, cited and publicized than ones that do not produce those affirming results.

The road ahead

In the statement, Carstensen and her fellow scientists offer recommendations for how people should view older adult life and issues like brain games:

Legitimate research on brain games needs to be replicated and confirmed scientifically across multiple studies in different settings.
Physical exercise is beneficial to both general and cognitive health.
No studies have shown that brain games prevent diseases like Alzheimer’s or other forms of dementia.
Brain games are not like “one shot” vaccines – the gains won’t last long after the end of the activity.
People can cultivate their cognitive powers by leading physically active, intellectually challenging and socially engaged lives.

The Stanford Center on Longevity’s mission is to redesign long life. The center studies the nature and development of the human life span, looking for innovative ways to use science and technology to solve the problems of people over 50 by improving the wellbeing of people of all ages.

Scientists engineer toxin-secreting stem cells to treat brain...

Sat, 25 Oct 2014 15:01:13 -0400

Scientists engineer toxin-secreting stem cells to treat brain tumors

Harvard Stem Cell Institute scientists at Massachusetts General Hospital have devised a new way to use stem cells in the fight against brain cancer. A team led by neuroscientist Khalid Shah, MS, PhD, who recently demonstrated the value of stem cells loaded with cancer-killing herpes viruses, now has a way to genetically engineer stem cells so that they can produce and secrete tumor-killing toxins.

In the AlphaMed Press journal STEM CELLS, Shah’s team shows how the toxin-secreting stem cells can be used to eradicate cancer cells remaining in mouse brains after their main tumor has been removed. The stem cells are placed at the site encapsulated in a biodegradable gel. This method solves the delivery issue that probably led to the failure of recent clinical trials aimed at delivering purified cancer-killing toxins into patients’ brains. Shah and his team are currently pursuing FDA approval to bring this and other stem cell approaches developed by them to clinical trials.

“Cancer-killing toxins have been used with great success in a variety of blood cancers, but they don’t work as well in solid tumors because the cancers aren’t as accessible and the toxins have a short half-life,” said Shah, who directs the Molecular Neurotherapy and Imaging Lab at Massachusetts General Hospital and Harvard Medical School.

“A few years ago we recognized that stem cells could be used to continuously deliver these therapeutic toxins to tumors in the brain, but first we needed to genetically engineer stem cells that could resist being killed themselves by the toxins,” he said. “Now, we have toxin-resistant stem cells that can make and release cancer-killing drugs.”

Cytotoxins are deadly to all cells, but since the late 1990s, researchers have been able to tag toxins in such a way that they only enter cancer cells with specific surface molecules; making it possible to get a toxin into a cancer cell without posing a risk to normal cells. Once inside of a cell, the toxin disrupts the cell’s ability to make proteins and, within days, the cell starts to die.

Shah’s stem cells escape this fate because they are made with a mutation that doesn’t allow the toxin to act inside the cell. The toxin-resistant stem cells also have an extra bit of genetic code that allows them to make and secrete the toxins. Any cancer cells that these toxins encounter do not have this natural defense and therefore die. Shah and his team induced toxin resistance in human neural stem cells and subsequently engineered them to produce targeted toxins.

“We tested these stem cells in a clinically relevant mouse model of brain cancer, where you resect the tumors and then implant the stem cells encapsulated in a gel into the resection cavity,” Shah said. “After doing all of the molecular analysis and imaging to track the inhibition of protein synthesis within brain tumors, we do see the toxins kill the cancer cells and eventually prolonging the survival in animal models of resected brain tumors.”

Shah next plans to rationally combine the toxin-secreting stem cells with a number of different therapeutic stem cells developed by his team to further enhance their positive results in mouse models of glioblastoma, the most common brain tumor in human adults. Shah predicts that he will bring these therapies into clinical trials within the next five years.

(Figure 1: A magnified image of a mouse brain showing memory...

Sat, 25 Oct 2014 12:01:26 -0400

(Figure 1: A magnified image of a mouse brain showing memory cells (red) that can be turned ‘on’ and ‘off’ using light delivered by a fiber optic cable (black). Credit: © Susumu Tonegawa)

Memories get the emotional switch

Memories of experiences are encoded in the brain along with contextual and emotional information such as where the experience took place and whether it was positive or negative. This allows for the formation of memory associations that might assist in survival. Just how this positive and negative encoding occurs, however, has remained unclear.

Susumu Tonegawa and colleagues from the RIKEN–MIT Center for Neural Circuit Genetics have now discovered that neurons in the hippocampus region of the brain can be artificially switched to encode memories as either positive or negative regardless of the original experience.

Tonegawa’s research team used genetic techniques to mark neurons in the dorsal dentate gyrus region of the hippocampus and the basolateral complex of the amygdala (BLA) in male mice. Memories are encoded in both these regions as specific groups of activated cells called ‘engrams’, but each region encodes the memory in slightly different ways: the BLA encodes positive and negative memory ‘valence’, while the dorsal dentate gyrus encodes contextual information such as emotion.

The genetic labeling, which involved using a light-sensitive ion channel called channelrhodopsin, was activated by the formation of either a positive memory, in this case exposure to females, or a negative memory associated with a foot shock. The cells that expressed this channel could be subsequently activated by exposure to light (Fig. 1); doing so induced aversive responses in mice that had experienced foot shocks, and appetitive responses in those that had experienced female interactions.

The researchers then used light to activate the hippocampal or BLA neurons that had been labeled during the formation of a positive memory while exposing the mice to foot shocks. The next time the animals were tested, light activation of those hippocampal neurons that had initially induced appetitive responses instead led the mice to exhibit aversive responses. However, BLA neurons could not be switched in this way, indicating that only neurons in the hippocampus have plasticity in their encoding of positive or negative memories.

The valence of hippocampal neurons, the researchers found, could be switched from both good to bad and bad to good using this technique, with the switch attributed to a change in the strength of connections between the hippocampal and BLA neurons of each engram.

The findings provide new insight into how memories can be altered after they are formed. The possibility of inducing similar changes to memory valence in humans could also offer hope of a treatment for those suffering from conditions such as post-traumatic stress disorder.

A New Window of Opportunity to Prevent Cardiovascular and Cerebrovascular Diseases

Fri, 24 Oct 2014 18:00:56 -0400

Future prevention and treatment strategies for vascular diseases may lie in the evaluation of early...

Reminiscing can help boost mental performance To solve a mental...

Fri, 24 Oct 2014 15:01:05 -0400

Reminiscing can help boost mental performance

To solve a mental puzzle, the brain’s executive control network for externally focused, goal-oriented thinking must activate, while the network for internally directed thinking like daydreaming must be turned down to avoid interference – or so we thought.

New research led by Cornell University neuroscientist Nathan Spreng shows for the first time that engaging brain areas linked to so-called “off-task” mental activities (such as mind-wandering and reminiscing) can actually boost performance on some challenging mental tasks. The results advance our understanding of how externally and internally focused neural networks interact to facilitate complex thought, the authors say.

“The prevailing view is that activating brain regions referred to as the default network impairs performance on attention-demanding tasks because this network is associated with behaviors such as mind-wandering,” said Spreng. “Our study is the first to demonstrate the opposite – that engaging the default network can also improve performance.”

There are plenty of neuroimaging studies showing that default network activation interferes with complex mental tasks – but in most, Spreng explained, the mental processes associated with default network conflict with task goals. If you start thinking about what you did last weekend while taking notes during a lecture, for example, your note-taking and ability to keep up will suffer.

Spreng and his team developed a new approach in which off-task processes such as reminiscing can support rather than conflict with the aims of the experimental task. Their novel task, “famous faces n-back,” tests whether accessing long-term memory about famous people, which typically engages default network brain regions, can support short-term memory performance, which typically engages executive control regions.

While undergoing brain scanning, 36 young adults viewed sets of famous and anonymous faces in sequence and were asked to identify whether the current face matched the one presented two faces back. The team found participants were faster and more accurate when matching famous faces than when matching anonymous faces and that this better short-term memory performance was associated with greater activity in the default network. The results show that activity in the default brain regions can support performance on goal-directed tasks when task demands align with processes supported by the default network, the authors say.

“Outside the laboratory, pursuing goals involves processing information filled with personal meaning – knowledge about past experiences, motivations, future plans and social context,” Spreng said. “Our study suggests that the default network and executive control networks dynamically interact to facilitate an ongoing dialogue between the pursuit of external goals and internal meaning.”

(Image caption: Neurons with the Unc5-receptor send their axons...

Fri, 24 Oct 2014 12:01:37 -0400

(Image caption: Neurons with the Unc5-receptor send their axons in a cell culture in all directions. The processes avoid the parallel orientated stripes containing the FLRT3-protein (red). Credit: ©Seiradake et al, Neuron 2014)

Navigation for nerve cells

During brain development, the precursors of nerve cells sometimes have to migrate long distances from their place of origin to their destination. In this process, proteins, such as FLRTs (pronounced “flirts”), act as guide molecules. Researchers at the Max Planck Institute of Neurobiology in Martinsried, together with colleagues at the Universities of Oxford and Frankfurt have now discovered that FLRT proteins on the surface of progenitor cells can induce repellent and attractant signals depending on its binding partner. The scientists used X-ray crystallography to reveal the structural bases for both FLRT-mediated adhesion and repulsion. They applied this knowledge to elucidate how these opposed signals control cellular migration. Which signal predominates depends on the particular type of cell migration. The results further show that FLRTs also exert attractant and repellent effects in the walls of blood vessels and therefore control the development of other tissue types as well.

Pyramidal cells are the central nerve cells in the cerebral cortex. During embryonic development, the precursors of pyramidal cells follow the paths of glial cell axons to migrate from their original location to the surface of the cerebral cortex. As soon as they reach their intended layer, they develop into mature pyramidal cells and interlink to form a functional network. Pyramidal cells also spread to a limited extent within these layers, though the importance of such tangential migration is still poorly understood.

This migration of precursor pyramidal cells is controlled by FLRTs (fibronectin-leucine-rich transmembrane proteins) located on the cell surface. According to the researchers at the Max Planck Institute in Martinsried, FLRTs and the Unc5 receptor form a group of guidance proteins with opposing effects on cell migration. On one hand, they act as a repellent. This is the case when a FLRT molecule binds to an Unc5 receptor on the surface of a progenitor cell. “In this way, as the precursor cell migrates radially, it receives a signal to continue migrating at an adjusted speed to not move prematurely into outer layers,” explains Rüdiger Klein from the Max Planck Institute of Neurobiology.

However, if two identical FLRT molecules bind to each other, this triggers an adhesive signal. The scientists’ results show that pyramidal cells are guided in this manner as they spread tangentially, without affecting their ability to find their target layer. Thus, there are proteins with attractant and repellent effects located on the surface of precursor pyramidal cells. “By integrating these opposing signals, cells can navigate through brain tissue. During radial migration FLRTs induce repulsion; during tangential dispersion FLRT attraction dominates,” says Klein.

In their study the scientists also investigated whether the mechanisms of FLRT adhesion and repulsion are present in other cell types. Their findings show that cells in the walls of blood vessels in the retina and the umbilical cord are also controlled by a combination of attractant and repellent signals modulated by FLRT and Unc5 proteins.

New insight on why people with Down syndrome invariably develop...

Fri, 24 Oct 2014 09:00:35 -0400

New insight on why people with Down syndrome invariably develop Alzheimer’s disease

A new study by researchers at Sanford-Burnham Medical Research Institute reveals the process that leads to changes in the brains of individuals with Down syndrome—the same changes that cause dementia in Alzheimer’s patients. The findings, published in Cell Reports, have important implications for the development of treatments that can prevent damage in neuronal connectivity and brain function in Down syndrome and other neurodevelopmental and neurodegenerative conditions, including Alzheimer’s disease.

Down syndrome is characterized by an extra copy of chromosome 21 and is the most common chromosome abnormality in humans. It occurs in about one per 700 babies in the United States, and is associated with a mild to moderate intellectual disability. Down syndrome is also associated with an increased risk of developing Alzheimer’s disease. By the age of 40, nearly 100 percent of all individuals with Down syndrome develop the changes in the brain associated with Alzheimer’s disease, and approximately 25 percent of people with Down syndrome show signs of Alzheimer’s-type dementia by the age of 35, and 75 percent by age 65. As the life expectancy for people with Down syndrome has increased dramatically in recent years—from 25 in 1983 to 60 today—research aimed to understand the cause of conditions that affect their quality of life are essential.

"Our goal is to understand how the extra copy of chromosome 21 and its genes cause individuals with Down syndrome to have a greatly increased risk of developing dementia," said Huaxi Hu, Ph.D., professor in the Degenerative Diseases Program at Sanford-Burnham and senior author of the paper. "Our new study reveals how a protein called sorting nexin 27 (SNX27) regulates the generation of beta-amyloid—the main component of the detrimental amyloid plaques found in the brains of people with Down syndrome and Alzheimer’s. The findings are important because they explain how beta-amyloid levels are managed in these individuals."

Beta-Amyloid, Plaques and Dementia

Xu’s team found that SNX27 regulates beta-amyloid generation. Beta-amyloid is a sticky protein that’s toxic to neurons. The combination of beta-amyloid and dead neurons form clumps in the brain called plaques. Brain plaques are a pathological hallmark of Alzheimer’s disease and are implicated in the cause of the symptoms of dementia.

"We found that SNX27 reduces beta-amyloid generation through interactions with gamma-secretase—an enzyme that cleaves the beta-amyloid precursor protein to produce beta-amyloid," said Xin Wang, Ph.D., a postdoctoral fellow in Xu’s lab and first author of the publication. "When SNX27 interacts with gamma-secretase, the enzyme becomes disabled and cannot produce beta-amyloid. Lower levels of SNX27 lead to increased levels of functional gamma-secretase that in turn lead to increased levels of beta-amyloid."

SNX27’s Role in Brain Function

Previously, Xu and colleagues found that SNX27 deficient mice shared some characteristics with Down syndrome, and that humans with Down syndrome have significantly lower levels of SNX27. In the brain, SNX27 maintains certain receptors on the cell surface—receptors that are necessary for neurons to fire properly. When levels of SNX27 are reduced, neuron activity is impaired, causing problems with learning and memory. Importantly, the research team found that by adding new copies of the SNX27 gene to the brains of Down syndrome mice, they could repair the memory deficit in the mice.

The researchers went on to reveal how lower levels of SNX27 in Down syndrome are the result of an extra copy of an RNA molecule encoded by chromosome 21 called miRNA-155. miRNA-155 is a small piece of genetic material that doesn’t code for protein, but instead influences the production of SNX27.

With the current study, researchers can piece the entire process together—the extra copy of chromosome 21 causes elevated levels of miRNA-155 that in turn lead to reduced levels of SNX27. Reduced levels of SNX27 lead to an increase in the amount of active gamma-secretase causing an increase in the production of beta-amyloid and the plaques observed in affected individuals.

"We have defined a rather complex mechanism that explains how SNX27 levels indirectly lead to beta-amyloid," said Xu. "While there may be many factors that contribute to Alzheimer’s characteristics in Down syndrome, our study supports an approach of inhibiting gamma-secretase as a means to prevent the amyloid plaques in the brain found in Down syndrome and Alzheimer’s."

"Our next step is to develop and implement a screening test to identify molecules that can reduce the levels of miRNA-155 and hence restore the level of SNX27, and find molecules that can enhance the interaction between SNX27 and gamma-secretase. We are working with the Conrad Prebys Center for Chemical Genomics at Sanford-Burnham to achieve this," added Xu.

Human skin cells reprogrammed directly into brain cells

Thu, 23 Oct 2014 18:01:09 -0400

Scientists have described a way to convert human skin cells directly into a specific type of brain...

Brain simulation raises questions What does it mean to simulate...

Thu, 23 Oct 2014 15:01:08 -0400

Brain simulation raises questions

What does it mean to simulate the human brain? Why is it important to do so? And is it even possible to simulate the brain separately from the body it exists in? These questions are discussed in a new paper published in the scientific journal Neuron today.

Simulating the brain means modeling it on a computer. But in real life, brains don’t exist in isolation. The brain is a complex and adaptive system that is seated within our bodies and entangled with all the other adaptive systems inside us that together make up a whole person. And the fact that the brain is a brain inside our bodies is something we can’t ignore when we attempt to simulate it realistically. Today, two Human Brain Project (HBP) researchers, Kathinka Evers, philosopher at the Centre for Research Ethics and Bioethics at Uppsala University and Yadin Dudal, neuroscientist at the Weizmann Institute of Science, publish a paper in Neuron that discusses the questions raised by brain simulations within and beyond the EU flagship project HBP.

For many scientists, understanding means being able to create a mental model that allows them to predict how a system would behave under different conditions. For the brain sciences, this type of understanding is currently only possible for a limited number of basic functions. In the article, Kathinka Evers and Yadin Dudal discuss the goal of simulation. In broad terms it has to do with understanding. But what does understanding mean in neuroscience?

As it dwells inside our bodies, the brain is always a result of what the individual has experienced up to that point. That is why, when we simulate the brain, we have to take this ‘experienced brain’ into account and try and reflect that.

According to Kathinka Evers, leader of the Ethics and Society part of the Human Brain Project, neglecting this experience would severely limit the outcome of any brain simulation. But if we are to include experience we have to simulate real-life situations.

“That is a daunting task: a large part of that experience is the brain’s interaction with the rest of the human body existing and interacting in a still larger social context”, says Kathinka Evers.

What outcome would be realistic to hope for in the Human Brain Project’s simulation? In neuroscience, computer simulations of specific systems are already in use. These simulations are a complement to other tools scientists use.

But there are some warnings to issue here. According to Kathinka Evers and Yadin Dudal, our knowledge to date is still very limited. There are many neuroscientists who think that it is too early for large scale brain simulations. Collecting the data we need for this is not an easy task. Another problem is whether we truly can understand what we are about to build. There are also technical limitations: there simply isn’t enough computing power available today.

But if we do manage to simulate the brain, would that mean we have created artificial consciousness? And can a computer be conscious at all? According to Kathinka Evers and Yadin Dudal, that depends on what consciousness is: If it is the result of certain types of organization or functions of biological matter, like the cells in the human body, then a computer can never gain consciousness. But if it is a matter of organization alone, without the need for biological matter, then the answer could be yes. But it is still a very hypothetical stance.