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Building New Thoughts From Scratch

Building New Thoughts From Scratch | Amazing Science | Scoop.it

Human brains flexibly combine the meanings of words to compose structured thoughts. For example, by combining the meanings of “bite,” “dog,” and “man,” we can think about a dog biting a man, or a man biting a dog. In two functional magnetic resonance imaging (fMRI) experiments using multivoxel pattern analysis (MVPA), a team of scientists now identified a region of left mid-superior temporal cortex (lmSTC) that flexibly encodes “who did what to whom” in visually presented sentences. They found that lmSTC represents the current values of abstract semantic variables (“Who did it?” and “To whom was it done?”) in distinct subregions. Experiment 1 first identified a broad region of lmSTC whose activity patterns (i) facilitate decoding of structure-dependent sentence meaning (“Who did what to whom?”) and (ii) predicted affect-related amygdala responses that depend on this information (e.g., “the baby kicked the grandfather” vs. “the grandfather kicked the baby”). Experiment 2 then identified distinct, but neighboring, subregions of lmSTC whose activity patterns carry information about the identity of the current “agent” (“Who did it?”) and the current “patient” (“To whom was it done?”). These neighboring subregions lie along the upper bank of the superior temporal sulcus and the lateral bank of the superior temporal gyrus, respectively. At a high level, these regions may function like topographically defined data registers, encoding the fluctuating values of abstract semantic variables. This functional architecture, which in key respects resembles that of a classical computer, may play a critical role in enabling humans to flexibly generate complex thoughts.


Via Donald J Bolger
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UPenn and German Researchers Help Identify Neural Basis of Multitasking

UPenn and German Researchers Help Identify Neural Basis of Multitasking | Amazing Science | Scoop.it

What makes someone better at switching between different tasks? Looking for the mechanisms behind cognitive flexibility, researchers at the University of Pennsylvania and Germany’s Central Institute of Mental Health in Mannheim and Charité University Medicine Berlin have used brain scans to shed new light on this question.


By studying networks of activity in the brain’s frontal cortex, a region associated with control over thoughts and actions, the researchers have shown that the degree to which these networks reconfigure themselves while switching from task to task predicts people’s cognitive flexibility.


Experiment participants who performed best while alternating between a memory test and a control test showed the most rearrangement of connections within their frontal cortices as well as the most new connections with other areas of their brains.


A more fundamental understanding of how the brain manages multitasking could lead to better interventions for medical conditions associated with reduced executive function, such as autism, schizophrenia or dementia.


Danielle Bassett, the Skirkanich Assistant Professor of Innovation in Penn’s School of Engineering and Applied Science, is senior author on the study. Manheim’s Urs Braun and Axel Schäfer were the lead authors. The research also featured work from Andreas Meyer-Lindenberg and Heike Tost of Mannheim, Henrik Walter of Charité, and others. It was published in the Proceedings of the National Academy of Sciences.


Rather than looking at the role a single region in the brain plays, Bassett and colleagues study the interconnections between the regions as indicated by synchronized activity. Using fMRI, they can measure which parts of the brain are “talking” to one another as study participants perform various tasks. Mapping the way this activity network reconfigures itself provides a more holistic view of how the brain operates.


“We try to understand how dynamic flexibility of brain networks can predict cognitive flexibility, or the ability to switch from task to task,” Bassett said. “Rather than being driven by the activity of single brain areas, we believe executive function is a network-level process.”

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Neuroscientists Find New Brain Network

Neuroscientists Find New Brain Network | Amazing Science | Scoop.it

Humans abound with remarkable skills: we write novels, build bridges, compose symphonies, and even navigate Boston traffic. But despite our mental prowess, we share a surprising deficit: our working memory can track only four items at one time.


“Would you buy a computer with a RAM capacity of 4?” asks David Somers, professor and chair of the Department of Psychological & Brain Sciences. “Not 4 MB or GB or 4K—just 4. So how the heck do humans do all this stuff?”


“There’s so much information out there, and our brains are very limited in what we’re able to process,” adds Samantha Michalka, a postdoctoral fellow at the Center for Computational Neuroscience & Neural Technology. “We desperately need attention to function in the world.”


Michalka is lead author and Somers is senior author of a new study that sheds light on this enduring mystery of neuroscience: how humans achieve so much with such limited attention. Funded by the National Science Foundation (NSF) and the National Institutes of Health (NIH), the work identifies a previously unknown attention network in the brain. It also reveals that our working memory for space and time can recruit our extraordinary visual and auditory processing networks when needed. The research appeared on August 19, 2015, in the journal Neuron.


Prior to this work, scientists believed that visual information from the eyes and auditory information from the ears merged before reaching the frontal lobes, where abstract thought occurs. The team of BU scientists, which also included Auditory Neuroscience Laboratory Director Barbara Shinn-Cunningham, performed functional MRI experiments to test the conventional wisdom. The experiments revealed that what was thought to be one large attention network in the frontal lobe is actually two interleaved attention networks, one supporting vision and one supporting hearing. “So instead of talking about a single attention network,” says Somers, “we now need to talk about a visual attention network and an auditory attention network that work together.”

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Nicole Wynne's comment, September 9, 2015 8:08 PM
I found this article rather interesting and reading how the vision and auditory systems work together. It also talks about how the auditory systems are dominate in some situations and vice versa. This article provides us with a picture of the brain and where these new found brain networks are. I would recommend this to someone who enjoys learning how the brain works and how it affects us.
Madison Carson's comment, September 16, 2015 11:59 PM
I found this article interesting because of the way humans can think about different things at one time but only have 4 functions. We don't really fully understand how our brains work but they are very complex. Maybe this study will help uplater on in the future
Scott Timmins's curator insight, September 8, 2016 7:29 AM

an auditory attention network along with a visual attention network!

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Why we’re smarter than chickens: Brain-specific exon skipping might be partly to blame

Why we’re smarter than chickens: Brain-specific exon skipping might be partly to blame | Amazing Science | Scoop.it

Toronto researchers have discovered that a single molecular event in our cells could hold the key to how we evolved to become the smartest animal on the planet. Benjamin Blencowe, a professor in the University of Toronto’s Donnelly Centre and Banbury Chair in Medical Research, and his team have uncovered how a small change in a protein called PTBP1 can spur the creation of neurons – cells that make the brain – that could have fuelled the evolution of mammalian brains to become the largest and most complex among vertebrates. The study is published in the August 20 issue of Science (http://www.sciencemag.org/lookup/doi/10.1126/science.aaa8381).

Brain size and complexity vary enormously across vertebrates, but it is not clear how these differences came about. Humans and frogs, for example, have been evolving separately for 350 million years and have very different brain abilities. Yet scientists have shown that they use a remarkably similar repertoire of genes to build organs in the body. So how is it that a similar number of genes, that are also switched on or off in similar ways in diverse vertebrate species, generate a vast range of organ size and complexity?

The key lays in the process that Blencowe’s group studies, known as alternative splicing (AS), whereby gene products are assembled into proteins, which are the building blocks of life. During AS, gene fragments – called exons – are shuffled to make different protein shapes. It’s like LEGO, where some fragments can be missing from the final protein shape.

AS enables cells to make more than one protein from a single gene, so that the total number of different proteins in a cell greatly surpasses the number of available genes. A cell’s ability to regulate protein diversity at any given time reflects its ability to take on different roles in the body. Blencowe’s previous work showed that AS prevalence increases with vertebrate complexity. So although the genes that make bodies of vertebrates might be similar, the proteins they give rise to are far more diverse in animals such as mammals, than in birds and frogs.

And nowhere is AS more widespread than in the brain. “We wanted to see if AS could drive morphological differences in the brains of different vertebrate species,” says Serge Gueroussov, a graduate student in Blencowe’s lab who is the lead author of the study. Gueroussov previously helped identify PTBP1 as a protein that takes on another form in mammals, in addition to the one common to all vertebrates. The second form of mammalian PTBP1 is shorter because a small fragment is omitted during AS and does not make it into the final protein shape. Could this newly acquired, mammalian version of PTBP1 give clues to how our brains evolved?

PTBP1 is both a target and major regulator of AS. PTBP1’s job in a cell is to stop it from becoming a neuron by holding off AS of hundreds of other gene products. Gueroussov showed that in mammalian cells, the presence of the second, shorter version of PTBP1 unleashes a cascade of AS events, tipping the scales of protein balance so that a cell becomes a neuron. What’s more, when Gueroussov engineered chicken cells to make the shorter, mammalian-like, PTBP1, this triggered AS events that are found in mammals.

“One interesting implication of our work is that this particular switch between the two versions of PTBP1 could have affected the timing of when neurons are made in the embryo in a way that creates differences in morphological complexity and brain size,” says Blencowe, who is also a professor in the Department of Molecular Genetics. As scientists continue to sift through countless molecular events occurring in our cells, they’ll keep finding clues as to how our bodies and minds came to be.


“This is the tip of an iceberg in terms of the full repertoire of AS changes that likely have contributed major roles in driving evolutionary differences,” says Blencowe.

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What Makes a Human Brain Unique? Experiment compares the way monkey and human brains process abstract information

What Makes a Human Brain Unique? Experiment compares the way monkey and human brains process abstract information | Amazing Science | Scoop.it

Neuroscientists have identified an area of the brain that might give the human mind its unique abilities, including language. The area lit up in human, but not monkey, brains when they were presented with different types of abstract information.


The idea that integrating abstract information drives many of the human brain's unique abilities has been around for decades. But a paper published in Current Biology, which directly compares activity in human and macaque monkey brains as they listen to simple auditory patterns, provides the first physical evidence that a specific area for such integration may exist in humans. Other studies that compare monkeys and humans have revealed differences in the brain’s anatomy, for example, but not differences that could explain where humans’ abstract abilities come from, say neuroscientists.


“This gives us a powerful clue about what is special about our minds,” says psychologist Gary Marcus at New York University. “Nothing is more important than understanding how we got to be how we are.”


A team of researchers headed by Stanislas Dehaene at the INSERM Cognitive Neuroimaging Unit at Gif-sur-Yvette near Paris, looked at changing patterns of activation in the brain as untrained monkeys and human adults listened to a simple sequence of tones, for example three identical tones followed by a different tone (like the famous four-note opening of Beethoven’s fifth symphony: da-da-da-DAH).


The researchers played several different sequences with this structure—known as AAAB—and other sequences to the subjects while they lay in a functional magnetic resonance imaging (fMRI) scanner. The fMRI technique picks up changes in blood flow in the brain that correlate with regional brain activity.


The team wanted to know whether the subjects of both species could recognize two different features of the sequences: the total number of tones, indicating an ability to count, and the way the tones repeat, indicating an ability to recognize this type of algebraic pattern.


In both monkeys and humans, an area of the brain, part of which has been associated with numbers, lit up in the fMRI scanner when the subjects identified a change in the number of tones. Both species also registered the repetition pattern in specific brain areas, which are known to be equivalent in humans and monkeys. But only the human brains showed a unique response to the combined changes in number and sequence, in the form of intense activation in an additional brain area called the inferior frontal gyrus.


“It is like the monkey recognizes a pattern but does not realize it is interesting and take it no further—only humans take it on to the next level of analysis,” says Marcus. The inferior frontal gyrus is a part of the cortex that is greatly expanded in humans compared with monkeys. Moreover, the inferior frontal gyrus in humans contains the Broca’s area, which processes language. And when Dehaene’s team read sentences to the humans, the language areas activated in each individual overlapped with those activated by the tone sequences.


But abstract information integration may be significant beyond language. “We had expected that humans have brain areas that put together information,” says cognitive biologist Tecumseh Fitch from the University of Vienna.“This type of computation may turn out to be also relevant to other characteristics that make humans unique, like music appreciation.”


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Memories Cemented by Flux of Prion-Like Proteins

Memories Cemented by Flux of Prion-Like Proteins | Amazing Science | Scoop.it

Persistent memories are doubly paradoxical. They are stable because they are built on physical connections that are dynamically maintained. Also, long-term memories are maintained through the work of prion-like proteins, even though prions are notorious for their contribution to neurodegenerative diseases—Alzheimer's, Parkinson's, and Huntington's—and the destruction of memory.


Prion-like proteins, assert researchers at Columbia University, can have a functional role within neurons instead of contributing to disease. These researchers first identified a functional prion within Aplysia, a giant sea slug. Then they found a similar prion within mice. And now, in a new study, the researchers have proposed a mechanism for how this prion maintains long-term memories.


The new study—“The Persistence of Hippocampal-Based Memory Requires Protein Synthesis Mediated by the Prion-like Protein CPEB3”—appeared June 17 in the journal Neuron. It explains how CPEB3, which stands for cytoplasmic polyadenylation element-binding protein, can account for the persistence of memory even though memories are built on molecular substrates that undergo rapid turnover.


A similar protein exists in humans, suggesting that human memories, too, rely on functional prions. This protein, said Eric Kandel, M.D., the leader of the Columbia team, may have the same role in memory. “Until this has been examined,” he prudently added, “we won't know.”


When disease-causing prions form within a neuron, they cause damage by grouping together in sticky aggregates that disrupt cellular processes. Prion aggregates are highly stable and accumulate in infected tissue, causing tissue damage and cell death. The dying cell releases the prion proteins, which are then taken up by other cells—and are thus considered infectious.


Surprisingly, the very features that make prions so dangerous—the ability to self-propagate and the ability to induce other proteins to take on their alternative shape—can serve useful ends. To show how, the Columbia team challenged mice to repeatedly navigate a maze, allowing the animals to create a long-term memory. But when the researchers knocked out the animal's CPEB3 gene two weeks after the memory was made, the memory disappeared.


“Both memory storage and its underlying synaptic plasticity are mediated by the increase in level and in the aggregation of the prion-like translational regulator CPEB3,” the authors of the Neuron study wrote. “Genetic ablation of CPEB3 impairs the maintenance of both hippocampal long-term potentiation and hippocampus-dependent spatial memory.”

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The highest form of intelligence: Sarcasm increases creativity for both expressers and recipients

The highest form of intelligence: Sarcasm increases creativity for both expressers and recipients | Amazing Science | Scoop.it
Despite sarcasm’s nasty reputation, new research finds that it can boost creativity and problem-solving in the workplace.


Despite being the lingua franca of the Internet, sarcasm isn’t known as a sophisticated form of wit or a conversational style that wins friends. From the Greek and Latin for “to tear flesh,” sarcasm has been called “hostility disguised as humor,” the contempt-laden speech favored by smart alecks and mean girls that’s best to avoid.


But new research by Francesca Gino of Harvard Business SchoolAdam Galinsky, the Vikram S. Pandit Professor of Business at Columbia Business School, and Li Huang of INSEAD, the European business school, finds that sarcasm is far more nuanced, and actually offers some important, overlooked psychological and organizational benefits.


“To create or decode sarcasm, both the expressers and recipients of sarcasm need to overcome the contradiction (i.e., psychological distance) between the literal and actual meanings of the sarcastic expressions. This is a process that activates and is facilitated by abstraction, which in turn promotes creative thinking,” said Gino via email.


While practitioners of sarcasm have long believed intuitively that the “mental gymnastics” it requires indicate “superior cognitive processes” at work, the authors say, it hasn’t been clear until now in which direction the causal link flowed, or that sarcasm boosted creativity in those receiving it, not just those dishing it out.


“Not only did we demonstrate the causal effect of expressing sarcasm on creativity and explore the relational cost sarcasm expressers and recipients have to endure, we also demonstrated, for the first time, the cognitive benefit sarcasm recipients could reap. Additionally, for the first time, our research proposed and has shown that to minimize the relational cost while still benefiting creatively, sarcasm is better used between people who have a trusting relationship,” said Gino.


In a series of studies, participants were randomly assigned to conditions labeled sarcastic, sincere, or neutral. As part of a simulated conversation task, they then expressed something sarcastic or sincere, received a sarcastic or sincere reply, or had a neutral exchange.


“Those in the sarcasm conditions subsequently performed better on creativity tasks than those in the sincere conditions or the control condition. This suggests that sarcasm has the potential to catalyze creativity in everyone,” said Galinsky via email. “That being said, although not the focus of our research, it is possible that naturally creative people are also more likely to use sarcasm, making it an outcome instead of [a] cause in this relationship.”


Of course, using sarcasm at work or in social situations is not without risk. It’s a communication style that can easily lead to misunderstanding and confusion or, if it’s especially harsh, bruised egos or acrimony. But if those engaged in sarcasm have developed mutual trust, there’s less chance for hurt feelings, the researchers found, and even if conflict arises, it won’t derail the creative gains for either party.

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Researchers find the organization of the human brain to be nearly ideal

Researchers find the organization of the human brain to be nearly ideal | Amazing Science | Scoop.it

Have you ever won­dered why the human brain evolved the way it did? A new study by North­eastern physi­cist Dmitri Kri­oukov and his col­leagues sug­gests an answer: to expe­dite the transfer of infor­ma­tion from one brain region to another, enabling us to operate at peak capacity.


The paper, pub­lished in the July 3 issue of Nature Com­mu­ni­ca­tions, reveals that the struc­ture of the human brain has an almost ideal net­work of connections—the links that permit infor­ma­tion to travel from, say, the audi­tory cortex (respon­sible for hearing) to the motor cortex (respon­sible for move­ment) so we can do every­thing from raise our hand in class in response to a ques­tion to rock out to the beat of The 1975.


The find­ings rep­re­sent more than a con­fir­ma­tion of our evo­lu­tionary progress. They could have impor­tant impli­ca­tions for pin­pointing the cause of neu­ro­log­ical dis­or­ders and even­tu­ally devel­oping ther­a­pies to treat them.


An optimal net­work in the brain would have the smallest number of con­nec­tions pos­sible, to min­i­mize cost, and at the same time it would have max­imum navigability—that is, the most direct path­ways for routing sig­nals from any pos­sible source to any pos­sible des­ti­na­tion,” says Kri­oukov. It’s a bal­ance, he explains, raising and low­ering his hands to indi­cate a scale. The study presents a new strategy to find the con­nec­tions that achieve that bal­ance or, as he puts it, “the sweet spot.”

Kri­oukov, an asso­ciate pro­fessor in the Depart­ment of Physics, studies net­works, from those related to mas­sive Internet datasets to those defining our brains. In the new research, he and his co-authors used sophis­ti­cated sta­tis­tical analyses based on Nobel lau­reate John Nash’s con­tri­bu­tions to game theory to con­struct a map of an ide­al­ized brain network—one that opti­mized the transfer of infor­ma­tion. They then com­pared the ide­al­ized map of the brain to a map of the brain’s real net­work and asked the ques­tion “How close are the two?”

Remark­ably so. They were sur­prised to learn that 89 per­cent of the con­nec­tions in the ide­al­ized brain net­work showed up in the real brain net­work as well. “That means the brain was evo­lu­tion­arily designed to be very, very close to what our algo­rithm shows,” says Krioukov
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Brain circuit in fruit fly that reacts to taste pheromones uncovered

Brain circuit in fruit fly that reacts to taste pheromones uncovered | Amazing Science | Scoop.it

The neural pathway that control the perception of a taste pheromone has been genetically labelled with a fluorescent gene tag.


New research, published today in eLife, identified the neural circuit in the brain of the fruitfly (Drosophila melanogaster) that is responsible for detecting a taste pheromone, which controls the decision of male flies to mate with females.


In the natural world, sense of taste controls many behavioral decisions. For many animals, pheromones, which are chemical signals used for communication, influence the choice to mate. However, very little is known about how taste pheromones are processed in the brain.


The recent work by Joanne Yew, assistant researcher at the Pacific Biosciences Research Center (PBRC), a newly integrated research unit of the School of Ocean and Earth Science and Technology (SOEST) at the University of Hawai'i - Mānoa, and colleagues explicitly tracked this process - identifying the taste cells on the fruitfly's legs which detect the pheromone, locating the neurons in the brain which respond to the pheromone, and mapping the connection between the two populations of cells.


The pheromone, named CH503, is produced by males, passed to females during mating, and stops other males from mating with the female - it is an anti-aphrodisiac for other males.


Many taste cells are found on the forelegs of flies, so Yew and colleagues used genetic manipulation to turn off activity in individual classes of these taste cells. They then tested whether males could still respond to the pheromone. Using this strategy, they were able to identify one class of taste receptors, called Gr68a, that is responsible for detecting the pheromone.


"Normally, males are repulsed by females that have been perfumed with the pheromone. However, when activity in Gr68a neurons is turned off, males will actively try to mate with females perfumed with the pheromone," said Yew.


Next, the researchers turned off activity in different groups of cells in the central brain to determine whether males could still respond to the pheromone. One group of cells which produces the chemical Tachykinin appeared to be essential for detecting the pheromone.


Finally, the scientists established that the Gr68a neurons in the leg connect with the Tachykinin neurons in the brain. To do this, they introduced 2 sensors into the Gr68a and Tachykinin neuron populations. The sensors light up when neurons in the region are close enough to form connections. The researchers were able to detect connectivity between the two populations of neurons.


"This work identifies a molecular signal, Tachykinin, that controls the perception of taste pheromones and provides an anatomical map of where this information is processed in the brain," said Yew. "By understanding the cellular basis of how taste information is encoded, we will be able to study how sensory signals shape programmed behaviors and influence complex social decisions such as the choice to mate. Potentially, we could devise a way to manipulate Tachykinin in pest populations to control reproduction."

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It Feels Instantaneous, but How Long Does it Really Take to Think a Thought?

It Feels Instantaneous, but How Long Does it Really Take to Think a Thought? | Amazing Science | Scoop.it

As inquisitive beings, we are constantly questioning and quantifying the speed of various things. With a fair degree of accuracy, scientists have quantified the speed of light, the speed of sound, the speed at which the earth revolves around the sun, the speed at which hummingbirds beat their wings, the average speed of continental drift….


These values are all well-characterized. But what about the speed of thought? It’s a challenging question that’s not easily answerable – but we can give it a shot. To quantify the speed of anything, one needs to identify its beginning and end. For our purposes, a “thought” will be defined as the mental activities engaged from the moment sensory information is received to the moment an action is initiated. This definition necessarily excludes many experiences and processes one might consider to be “thoughts.”


Here, a “thought” includes processes related to perception (determining what is in the environment and where), decision-making (determining what to do) and action-planning (determining how to do it). The distinction between, and independence of, each of these processes is blurry. Further, each of these processes, and perhaps even their sub-components, could be considered “thoughts” on their own. But we have to set our start- and endpoints somewhere to have any hope of tackling the question.


Finally, trying to identify one value for the “speed of thought” is a little like trying to identify one maximum speed for all forms of transportation, from bicycles to rockets. There are many different kinds of thoughts that can vary greatly in timescale. Consider the differences between simple, speedy reactions like the sprinter deciding to run after the crack of the starting pistol (on the order of 150 milliseconds [ms]), and more complex decisions like deciding when to change lanes while driving on a highway or figuring out the appropriate strategy to solve a math problem (on the order of seconds to minutes).


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When we learn something new, our brain cells break their DNA, creating damage that neurons must immediately repair

When we learn something new, our brain cells break their DNA, creating damage that neurons must immediately repair | Amazing Science | Scoop.it

The process that allows our brains to learn and generate new memories also leads to degeneration as we age, according to a new study by researchers at MIT. The finding, reported in a paper published today in the journal Cell, could ultimately help researchers develop new approaches to preventing cognitive decline in disorders such as Alzheimer’s disease.


Each time we learn something new, our brain cells break their DNA, creating damage that the neurons must immediately repair, according to Li-Huei Tsai, the Picower Professor of Neuroscience and director of the Picower Institute for Learning and Memory at MIT. This process is essential to learning and memory. “Cells physiologically break their DNA to allow certain important genes to be expressed,” Tsai says. “In the case of neurons, they need to break their DNA to enable the expression of early response genes, which ultimately pave the way for the transcriptional program that supports learning and memory, and many other behaviors.”


However, as we age, our cells’ ability to repair this DNA damage weakens, leading to degeneration, Tsai says. “When we are young, our brains create DNA breaks as we learn new things, but our cells are absolutely on top of this and can quickly repair the damage to maintain the functionality of the system,” Tsai says. “But during aging, and particularly with some genetic conditions, the efficiency of the DNA repair system is compromised, leading to the accumulation of damage, and in our view this could be very detrimental.”


In previous research into Alzheimer’s disease in mice, the researchers found that even in the presymptomatic phase of the disorder, neurons in the hippocampal region of the brain contain a large number of DNA lesions, known as double strand breaks.


To determine how and why these double strand breaks are generated, and what genes are affected by them, the researchers began to investigate what would happen if they created such damage in neurons. They applied a toxic agent to the neurons known to induce double strand breaks, and then harvested the RNA from the cells for sequencing.


They discovered that of the 700 genes that showed changes as a result of this damage, the vast majority had reduced expression levels, as expected. Surprisingly though, 12 genes — known to be those that respond rapidly to neuronal stimulation, such as a new sensory experience — showed increased expression levels following the double strand breaks.


To determine whether these breaks occur naturally during neuronal stimulation, the researchers then treated the neurons with a substance that causes synapses to strengthen in a similar way to exposure to a new experience. “Sure enough, we found that the treatment very rapidly increased the expression of those early response genes, but it also caused DNA double strand breaks,” Tsai says.


In further studies the researchers were able to confirm that an enzyme known as topoisomerase IIβ is responsible for the DNA breaks in response to stimulation, according to the paper’s lead author Ram Madabhushi, a postdoc in Tsai’s laboratory. “When we knocked down this enzyme, we found that both double strand break formation and the expression of early response genes was reduced,” Madabhushi says.


Finally, the researchers attempted to determine why the genes need such a drastic mechanism to allow them to be expressed. Using computational analysis, they studied the DNA sequences near these genes and discovered that they were enriched with a motif, or sequence pattern, for binding to a protein called CTCF. This “architectural” protein is known to create loops or bends in DNA.


In the early-response genes, the bends created by this protein act as a barrier that prevents different elements of DNA from interacting with each other — a crucial step in the genes’ expression. The double strand breaks created by the cells allow them to collapse this barrier, and enable the early response genes to be expressed, Tsai says.

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Injectable brain implant spies on individual neurons

Injectable brain implant spies on individual neurons | Amazing Science | Scoop.it
Electronic mesh has potential to unravel workings of mammalian brain.


A simple injection is now all it takes to wire up a brain. A diverse team of physicists, neuroscientists and chemists has implanted mouse brains with a rolled-up, silky mesh studded with tiny electronic devices, and shown that it unfurls to spy on and stimulate individual neurons.

The implant has the potential to unravel the workings of the mammalian brain in unprecedented detail. “I think it’s great, a very creative new approach to the problem of recording from large number of neurons in the brain,” says Rafael Yuste, director of the Neuro­technology Center at Columbia University in New York, who was not involved in the work.


If eventually shown to be safe, the soft mesh might even be used in humans to treat conditions such as Parkinson’s disease, says Charles Lieber, a chemist at Harvard University on Cambridge, Massachusetts, who led the team. The work was published inNature Nanotechnology on 8 June1.


Neuroscientists still do not understand how the activities of individual brain cells translate to higher cognitive powers such as perception and emotion. The problem has spurred a hunt for technologies that will allow scientists to study thousands, or ideally millions, of neurons at once, but the use of brain implants is currently limited by several disadvantages. So far, even the best technologies have been composed of relatively rigid electronics that act like sandpaper on delicate neurons. They also struggle to track the same neuron over a long period, because individual cells move when an animal breathes or its heart beats.


The Harvard team solved these problems by using a mesh of conductive polymer threads with either nanoscale electrodes or transistors attached at their intersections. Each strand is as soft as silk and as flexible as brain tissue itself. Free space makes up 95% of the mesh, allowing cells to arrange themselves around it.

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Harpal S.sandhu's curator insight, June 9, 2015 7:14 PM

new diagnostic methodology

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Memories that have been "lost" as a result of amnesia can be recalled by activating brain cells with light

Memories that have been "lost" as a result of amnesia can be recalled by activating brain cells with light | Amazing Science | Scoop.it

In a paper published today in the journal Science, researchers at MIT reveal that they were able to reactivate memories that could not otherwise be retrieved, using a technology known as optogenetics.

The finding answers a fiercely debated question in neuroscience as to the nature of amnesia, according to Susumu Tonegawa, the Picower Professor in MIT's Department of Biology and director of the RIKEN-MIT Center at the Picower Institute for Learning and Memory, who directed the research by lead authors Tomas Ryan, Dheeraj Roy, and Michelle Pignatelli.


Neuroscience researchers have for many years debated whether retrograde amnesia -- which follows traumatic injury, stress, or diseases such as Alzheimer's -- is caused by damage to specific brain cells, meaning a memory cannot be stored, or if access to that memory is somehow blocked, preventing its recall. "The majority of researchers have favored the storage theory, but we have shown in this paper that this majority theory is probably wrong," Tonegawa says. "Amnesia is a problem of retrieval impairment."


Memory researchers have previously speculated that somewhere in the brain network is a population of neurons that are activated during the process of acquiring a memory, causing enduring physical or chemical changes. If these groups of neurons are subsequently reactivated by a trigger such as a particular sight or smell, for example, the entire memory is recalled. These neurons are known as "memory engram cells."


In 2012 Tonegawa's group used optogenetics -- in which proteins are added to neurons to allow them to be activated with light -- to demonstrate for the first time that such a population of neurons does indeed exist in an area of the brain called the hippocampus. However, until now no one has been able to show that these groups of neurons do undergo enduring chemical changes, in a process known as memory consolidation. One such change, known as "long-term potentiation" (LTP), involves the strengthening of synapses, the structures that allow groups of neurons to send signals to each other, as a result of learning and experience.


To find out if these chemical changes do indeed take place, the researchers first identified a group of engram cells in the hippocampus that, when activated using optogenetic tools, were able to express a memory. When they then recorded the activity of this particular group of cells, they found that the synapses connecting them had been strengthened. "We were able to demonstrate for the first time that these specific cells -- a small group of cells in the hippocampus -- had undergone this augmentation of synaptic strength," Tonegawa says.


The researchers then attempted to discover what happens to memories without this consolidation process. By administering a compound called anisomycin, which blocks protein synthesis within neurons, immediately after mice had formed a new memory, the researchers were able to prevent the synapses from strengthening. When they returned one day later and attempted to reactivate the memory using an emotional trigger, they could find no trace of it. "So even though the engram cells are there, without protein synthesis those cell synapses are not strengthened, and the memory is lost," Tonegawa says.


But startlingly, when the researchers then reactivated the protein synthesis-blocked engram cells using optogenetic tools, they found that the mice exhibited all the signs of recalling the memory in full.

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Researchers erase memories in mice with a beam of light

Researchers erase memories in mice with a beam of light | Amazing Science | Scoop.it

A team of researchers with member affiliations to several institutions in the U.S. and Japan has developed a new device that allowed them to alter the spines on a neural dendrite in a mouse brain that was first modified naturally by an event that caused a memory to form. As they explain in their paper published in the journal Nature, altering the spine caused a learned memory to be forgotten. Ju Lu and Yi Zuo both with the University of California, offer a News & Views piece on where such work is leading.


As part of trying to understand how the human (and other animal) brain works, scientists focus on subsets of its functionality, one of which is memory. How are memories created, stored, changed and manipulated? A lot of it is still a mystery, but as the work done by this latest team demonstrates, biomedical researchers are getting closer. In this new effort, the team taught a mouse to stay atop a rolling pipe, then shined a light on the part of its brain that had changed as it learned, causing the change to revert back to its pre-learned state and in so doing, causing the mouse to forget what it had learned. In order to make this bit of magic happen, the team had to first design and build a device that allowed for such manipulation—they call it AS-PaRac—it is an optoprobe that is capable of causing changes to spines that grow on the edges of dentrites, the listening or input part used by neurons to communicate with one another. Prior work has suggested that their tips grow bigger as part of storing a new memory.


With their new device in hand, the researchers first trained a mouse to stay on a pipe as it rolled, they then identified which dentrite was involved in storing that memory and which particular spine—they were actually able to see that its tip had grown in size. Then, they used the AS-PaRac to force the spine tip back to the size it was before the mouse learned to balance on the pipe. Doing so caused the mouse to forget what it had learned. To make sure the change was isolated, the team repeated the experiment, but the second time around, they taught the mouse another trick—reducing the same spine caused the mouse to once again forget how to do the first trick, but not the second.


Lu and Zuo note that this is just the beginning, they believe it will not be long before the researchers can go in and make the same spine bigger with the AS-PaRac, causing a mouse to learn how to stay atop a pipe without ever having been taught.

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Newly Discovered Prion May Cause A Neurodegenerative Disease That Is Transmissible

Newly Discovered Prion May Cause A  Neurodegenerative Disease That Is Transmissible | Amazing Science | Scoop.it

Animal experiments show how a just-discovered prion triggers a rare Parkinson’s-like disease.


Scientists claim to have discovered the first new human prion in almost 50 years. Prions are misfolded proteins that make copies of themselves by inducing others to misfold. By so doing, they multiply and cause disease. The resulting illness in this case is multiple system atrophy (MSA), a neurodegenerative disease similar to Parkinson's. The study, published August 31 in Proceedings of the National Academy of Sciences, adds weight to the idea that many neurodegenerative diseases are caused by prions.


In the 1960s researchers led by Carleton Gajdusek at the National Institutes of Health transmitted kuru, a rare neurodegenerative disease found in Papua New Guinea, and Creutzfeldt–Jakob disease (CJD), a rare human dementia, to chimpanzees by injecting samples from victims' brains directly into those of chimps. It wasn't until 1982, however, that Stanley Prusiner coined the term prion (for “proteinaceous infectious particle”) to describe the self-propagating protein responsible.


Prusiner and colleagues at the University of California, San Francisco, showed this process caused a whole class of diseases, called spongiform encephalopathies (for the spongelike appearance of affected brains), including the bovine form known as “mad cow” disease. The same protein, PrP, is also responsible for kuru, which was spread by cannibalism; variant-CJD, which over 200 people developed after eating beef infected with the bovine variety; and others. The idea that a protein could transmit disease was radical at the time but the work eventually earned Prusiner the 1997 Nobel Prize in Physiology or Medicine. He has long argued prions may underlie other neurodegenerative diseases but the idea has been slow to gain acceptance.


In 2013 a team in Prusiner's lab, including neuroscientist Kurt Giles, were trying to transmit Parkinson's disease to mice genetically engineered to produce a human protein involved in Parkinson’s, alpha-synuclein, by injecting them with brain samples from deceased patients. They failed, but for comparison they also used two MSA samples—those mice got sick. “The controls were the ones that worked,” Giles says. “So we got lots more samples.” For the new study, the team obtained 12 more MSA samples from three brain banks in London, Boston and Sydney.


The result was the same: the mice injected with these samples all developed disease within 3.5 to five months. The gene inserted in the mice has a mutation associated with a hereditary form of Parkinson's, which researchers think makes the alpha-synuclein more likely to misfold. Mice with two copies develop disease spontaneously, after about 10 months, but mice with one copy remain healthy. Injecting either type with MSA samples resulted in neurodegeneration and death for both in the same short time span.


Presumably what happens is that alpha-synuclein prions in the MSA brain samples propagate by inducing the human alpha-synuclein proteins in the mice, which are prone to misfold, to take their particular aberrant shape Afterward, these mice's brains also showed buildups of alpha-synuclein in cells, and samples from these brains also caused disease in other mice. Neither a sample from a disease-free brain nor samples from Parkinson's patients, had these effects.


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Brain scans better forecast math learning in kids than do skill tests, study finds

Brain scans better forecast math learning in kids than do skill tests, study finds | Amazing Science | Scoop.it

Brain scans from 8-year-old children can predict gains in their mathematical ability over the next six years, according to a new study from the Stanford University School of MedicineThe research tracked 43 children longitudinally for six years, starting at age 8, and showed that while brain characteristics strongly indicated which children would be the best math learners over the following six years, the children’s performance on math, reading, IQ and memory tests at age 8 did not.


The study, published online Aug. 18 in The Journal of Neuroscience, moves scientists closer to their goal of helping children who struggle to acquire math skills. “We can identify brain systems that support children’s math skill development over six years in childhood and early adolescence,” said the study’s lead author, Tanya Evans, PhD, postdoctoral scholar in psychiatry and behavioral sciences.


“A long-term goal of this research is to identify children who might benefit most from targeted math intervention at an early age,” said senior author Vinod Menon, PhD, professor of psychiatry and behavioral sciences. “Mathematical skills are crucial in our increasingly technological society, and our new data show which brain features forecast future growth in math abilities.”


At the start of the study, the children received structural and functional magnetic resonance imaging brain scans. None of the kids had neurological or psychiatric disorders, and their intelligence fell in a range considered normal for their age. The scans were conducted while the children lay quietly in the scanner; the scans measured brain structure and intrinsic functional connections between brain regions, and were not tied to performance on any particular math task.


The 8-year-olds also took standardized tests (given outside the scanner) to measure IQ, as well as reading, math and working-memory skills. All of the children returned for at least one follow-up assessment of these skills before age 14, and many children had other additional follow-ups.

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Russian Scientists Create Artificial Brain that can Educate Itself

Russian Scientists Create Artificial Brain that can Educate Itself | Amazing Science | Scoop.it

Russian scientists are one step closer to crafting full artificial intelligence. A physical model of a brain has been designed, with the ability to educate itself. Tomsk State University in western Siberia housed an international team of scientists who “built mathematical and computer models of the human brain,” said the head of the laboratory, Professor FIT Vladimir Syryamkin.


“After that it was designed radio-electronic device comprising perceptrons. It is capable of handling various information (video, audio, etc.) Now we are working to establish the basic system robotic system, which is an intelligent control center.” Though, full brain replication isn’t an easy task, as scientists need to copy 100 million neurons in the brain and one trillion compounds.


“This physical model is capable of self-learning and life experience. This mechanism is both simple and complex. The artificial medium of natural intelligence takes external stimuli such as light, sound, etc. Through trial and error, he tries to find a solution that helps to avoid the impact of the stimulus. For example, when exposed to a bright light source will first try to look away, if it does not help, move away from him. As long as the brain will not find the right solution, its neurons (perceptrons) will be in an excited state. When the artificial intelligence that decision will, he will remember it and will be used in similar situations,” reads the press release.


The main developer Vladimir Shumilov believes, “In the end, an artificial brain should be analogous to the biological model. We have a tremendous amount of work, but a very important step has been taken – we were able to reveal the secret of brain neural network. In our physical model, as in the human brain, the formation of new neural connections and damping existing. In humans, it is the process of forgetting.”


The team hopes its artificial intelligent brain will have medical applications, like helping drug correction for patients with various dementias. Additionally, the scientists hope to integrate their AI brain into robotic systems and neurocomputers.

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Lucile Debethune's curator insight, August 20, 2015 10:16 AM

Dans le même mouvement que d'autre recherche, à la fois sur la modélisation du cerveau, sur l'autoapprentissage des IA... et lutter contre les démences 

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Newly discovered brain network recognizes what’s new, what’s familiar

Newly discovered brain network recognizes what’s new, what’s familiar | Amazing Science | Scoop.it

New research from Washington University in St. Louis has identified a novel learning and memory brain network, dubbed the Parietal Memory Network (PMN), that processes incoming information based on whether it’s something we’ve experienced previously or appears to be new and unknown — helping us recognize, for instance, whether a face is that of a familiar friend or a complete stranger.


The study pulls together evidence from multiple neuroimaging studies and methods to demonstrate the existence of this previously unknown and distinct functional brain network, one that appears to have broad involvement in human memory processing.


“When an individual sees a novel stimulus, this network shows a marked decrease in activity,” said Adrian Gilmore, first author of the study and a fifth-year psychology doctoral student at Washington University. When an individual sees a familiar stimulus, this network shows a marked increase in activity.”


The new memory and learning network shows consistent patterns of activation and deactivation in three distinct regions of the parietal cortex in the brain’s left hemisphere — the precuneus, the mid-cingulate cortex, and the dorsal angular gyrus. Activity within the PMN during the processing of incoming information (encoding) can be used to predict how well that information will be stored in memory and later made available for successful retrieval.


Researchers identified interesting characteristics of the PMN by analyzing data from a range of previously published neuroimaging studies. Using converging bits of evidence from dozens of fMRI brain experiments, their study shows how activity in the PMN changes during the completion of specific mental tasks and how the regions interact during resting states when the brain is involved in no particular activity or mental challenge.


This study builds on research by Marcus Raichle, MD, the Alan A. and Edith L. Wolff Distinguished Professor of Medicine, and other neuroscience researchers at Washington University, which established the existence of another functional brain network that remains surprisingly active when the brain is not involved in a specific activity, a system known as the Default Mode Network.


Like the Default Mode Network, key regions of the PMN were shown to hum in a similar unison while the brain is in relative periods of rest. And while key regions of the PMN are located close to the Default Mode Network, the PMN appears to be its own distinct and separate functional network, preliminary findings suggest.

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Sex does matter: Key molecular process in brain is different in males and females

Sex does matter: Key molecular process in brain is different in males and females | Amazing Science | Scoop.it

Male and female brains operate differently at a molecular level, a Northwestern University research team reports in a new study of a brain region involved in learning and memory, responses to stress and epilepsy.


Many brain disorders vary between the sexes, but how biology and culture contribute to these differences has been unclear. Now Northwestern neuroscientists have found an intrinsic biological difference between males and females in the molecular regulation of synapses in the hippocampus. This provides a scientific reason to believe that female and male brains may respond differently to drugs targeting certain synaptic pathways.


“The importance of studying sex differences in the brain is about making biology and medicine relevant to everyone, to both men and women,” said Catherine S. Woolley, senior author of the study. “It is not about things such as who is better at reading a map or why more men than women choose to enter certain professions.” Among their findings, the scientists found that a drug called URB-597, which regulates a molecule important in neurotransmitter release, had an effect in females that it did not have in males. While the study was done in rats, it has broad implications for humans because this drug and others like it are currently being tested in clinical trials in humans.


“Our study starts to put some specifics on what types of molecular differences there are in male and female brains,” Woolley said. Woolley is the William Deering Chair in Biological Sciences, professor of neurobiology in the Weinberg College of Arts and Sciences and a member of the Women’s Health Research Institute at Northwestern University Feinberg School of Medicine. The study of inhibitory synapses and endocannabinoids, which regulate neurotransmitters, was published today in The Journal of Neuroscience. It is the first study to detail where males and females differ in a key molecular pathway in the brain.

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Researchers pinpoint where the brain unites our eyes’ double vision

Researchers pinpoint where the brain unites our eyes’ double vision | Amazing Science | Scoop.it

Using prisms and an advanced brain scanner, researchers have found the point in the human brain at which the vision of two eyes becomes one image.


If you have two working eyes, you are live streaming two images of the world into your brain. Your brain combines the two to produce a view of the world that appears as though you had a single eye — like the Cyclops from Greek mythology. And that's a good thing, as the combination of the two images makes for a much more useful impression of the world. With one eye shut, catching a ball or parking a car become far more difficult.


"If you're reaching out with your hand, you want to aim not at where things appear to be, but where they are," says Bas Rokers, psychology professor at the University of Wisconsin-Madison. "Two eyes are giving you two images that don't by themselves tell you where things are relative to your hand. It's the integrated information that tells you where things are."


Using prisms and an advanced brain scanner, Rokers and collaborators at Utrecht University in the Netherlands have found the point in the human brain — very early in image processing in the visual cortex — in which the transformation to a cyclopean view of the world takes place.


Their work, published recently in the journal Current Biology, may aid in the treatment of vision problems like amblyopia, or lazy eye.


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Knowledge does not equal understanding – or how to unlearn 'how to ride a bike'

Knowledge does not equal understanding – or how to unlearn 'how to ride a bike' | Amazing Science | Scoop.it
Riding a bicycle is a life skill we learn as kids that sticks with us for a lifetime. Once you learn it, you never forget it. But what if there was a special kind of bike that will make everything you learned useless?

You may think that I am saying nonsense, but there is actually a bike that nobody can ride unless they unlearn riding a bike. Watch the video and you’ll understand.
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Babies Can Form Abstract Relations Before They Even Learn Words

Babies Can Form Abstract Relations Before They Even Learn Words | Amazing Science | Scoop.it

According to a new study published in the journal Child Development, infants are capable of understanding abstract relations like ‘same’ and ‘different.’


“This suggests that a skill key to human intelligence is present very early in human development, and that language skills are not necessary for learning abstract relations,” said Dr Alissa Ferry of the Scuola Internazionale Superiore di Studi Avanzati in Italy, lead author of the study.


To trace the origins of relational thinking in infants, Dr Ferry and her colleagues from Northwestern University tested whether 7-month-old infants could understand the simplest and most basic abstract relation – the same-different relation.


Infants were shown pairs of items that were either the same (two Elmo dolls) or different (Elmo doll and a toy camel) until their looking time declined.


In the test phase, the infants looked longer at pairs showing the novel relation, even when the test pairs were composed of new objects. That is, infants who had learned the same relation looked longer at test pairs showing the different relation during test, and vice versa.


This suggests that the infants had encoded the abstract relation and detected when the relation changed. “We found that infants are capable of learning these relations. Additionally, infants exhibit the same patterns of learning as older children and adults – relational learning benefits from seeing multiple examples of the relation and is impeded when attention is drawn to the individual objects composing the relation,” Dr Ferry said.

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Scientists have managed to build a fully functional neuron by using organic bioelectronics

Scientists have managed to build a fully functional neuron by using organic bioelectronics | Amazing Science | Scoop.it

Scientists at Karolinska Institutet have managed to build a fully functional neuron by using organic bioelectronics. This artificial neuron contain no ‘living’ parts, but is capable of mimicking the function of a human nerve cell and communicate in the same way as our own neurons do.


Neurons are isolated from each other and communicate with the help of chemical signals, commonly called neurotransmitters or signal substances. Inside a neuron, these chemical signals are converted to an electrical action potential, which travels along the axon of  the neuron until it reaches the end. Here at the synapse, the electrical signal is converted to the release of chemical signals, which via diffusion can relay the signal to the next nerve cell.


To date, the primary technique for neuronal stimulation in human cells is based on electrical stimulation. However, scientists at the Swedish Medical Nanoscience Centre (SMNC) at Karolinska Institutet's Department of Neuroscience in collaboration with collegues at Linköping University, have now created an organic bioelectronic device that is capable of receiving chemical signals, which it can then relay to human cells.


“Our artificial neuron is made of conductive polymers and it functions like a human neuron”, says lead investigator Agneta Richter-Dahlfors, professor of cellular microbiology. “The sensing component of the artificial neuron senses a change in chemical signals in one dish, and translates this into an electrical signal. This electrical signal is next translated into the release of the neurotransmitter acetylcholine in a second dish, whose effect on living human cells can be monitored.“

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Mind reading: Neuroscientists capture the moment a brain records an idea

Mind reading: Neuroscientists capture the moment a brain records an idea | Amazing Science | Scoop.it

Cutting-edge brain imaging technology has offered the first glimpse into how new concepts develop in the human brain. 


The research, carried out at Carnegie Mellon University and published in Human Brain Mappinginvolved teaching people a new concept and observing how it was coded in the same areas of the brain through neural representations.


The "olinguito" -- a largely fruit-eating carnivore species that lives in rainforest treetops, newly discovered in 2013 -- was initially used as a concept. Marcel Just, a professor of cognitive neuroscience in the Dietrich College of Humanities and Social Sciences, commented: "When people learned that the olinguito eats mainly fruit instead of meat, a region of their left inferior frontal gyrus -- as well as several other areas -- stored the new information according to its own code."


The findings revealed that this new knowledge of the olinguito was encoded in exactly the same parts of the brain by everyone who learned it, indicating that the brain may operate its own kind of universal filing system.


In the latest research, 16 study participants were taught information about the diet and dwelling habits of eight extinct animals, in order to study the growth of the neural representations of these concepts in their brains. Drawing on the previous findings, the team predicted where this new knowledge would be stored.


Just and Andrew Bauer, lead author of the study, then used functional magnetic resonance imaging (fMRI) to monitor these concepts emerging in the brain, and found that each new concept developed its own "unique activation signature". This allowed a computer program to effectively work out which of the eight animals a participant was thinking about at any given time -- essentially allowing the scientists to read their minds.

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A patient’s budding brain in a dish? Networking neurons thrive in 3-D human "organoid"

A patient’s budding brain in a dish? Networking neurons thrive in 3-D human "organoid" | Amazing Science | Scoop.it

A patient tormented by suicidal thoughts gives his psychiatrist a few strands of his hair. She derives stem cells from them to grow budding brain tissue harboring the secrets of his unique illness in a petri dish. She uses the information to genetically engineer a personalized treatment to correct his brain circuit functioning. Just Sci-fi? Yes, but...


An evolving “disease-in-a-dish” technology, funded by the National Institutes of Health (NIH), is bringing closer the day when such a seemingly futuristic personalized medicine scenario might not seem so far-fetched. Scientists have perfected mini cultured 3-D structures that grow and function much like the outer mantle – the key working tissue, or cortex — of the brain of the person from whom they were derived. Strikingly, these “organoids” buzz with neuronal network activity. Cells talk with each other in circuits, much as they do in our brains.


Sergiu Pasca, M.D. , of Stanford University, Palo Alto, CA, and colleagues, debut what they call “human cortical spheroids,” May 25, 2015 online in the journal Nature Methods.


“There’s been amazing progress in this field over the past few years,” said Thomas R. Insel, M.D., Director of the NIH’s National Institute of Mental Health, which provided most of the funding for the study. “The cortex spheroids grow to a state in which they express functional connectivity, allowing for modeling and understanding of mental illnesses. They do not even begin to approach the complexity of a whole human brain. But that is not exactly what we need to study disorders of brain circuitry. As we seek advances that promise enormous potential benefits to patients, we are ever mindful of the ethical issues they present.”


Prior to the new study, scientists had developed a way to study neurons differentiated from stem cells derived from patients’ skin cells — using a technology called induced pluripotent stem cells (iPSCs). They had even produced primitive organoids by coaxing neurons and support cells to organize themselves, mimicking the brain’s own architecture. But these lacked the complex circuitry required to even begin to mimic the workings of our brains.

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