Brain-to-brain interface allows transmission of tactile and motor information between rats

Researchers have electronically linked the brains of pairs of rats for the first time, enabling them to communicate directly to solve simple behavioral puzzles. A further test of this work successfully linked the brains of two animals thousands of miles apart—one in Durham, N.C., and one in Natal, Brazil.

The results of these projects suggest the future potential for linking multiple brains to form what the research team is calling an “organic computer,” which could allow sharing of motor and sensory information among groups of animals. The study was published Feb. 28, 2013, in the journal Scientific Reports.

"Our previous studies with brain-machine interfaces had convinced us that the rat brain was much more plastic than we had previously thought," said Miguel Nicolelis, M.D., PhD, lead author of the publication and professor of neurobiology at Duke University School of Medicine. "In those experiments, the rat brain was able to adapt easily to accept input from devices outside the body and even learn how to process invisible infrared light generated by an artificial sensor. So, the question we asked was, ‘if the brain could assimilate signals from artificial sensors, could it also assimilate information input from sensors from a different body?’"

To test this hypothesis, the researchers first trained pairs of rats to solve a simple problem: to press the correct lever when an indicator light above the lever switched on, which rewarded the rats with a sip of water. They next connected the two animals’ brains via arrays of microelectrodes inserted into the area of the cortex that processes motor information.

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Researchers Identify Possible Treatment Window for Memory Problems

Researchers have identified a possible treatment window for plaques in the brain that are thought to cause memory loss in diseases such as Alzheimer’s, according to a new study published in the February 27, 2013, online issue of Neurology®, the medical journal of the American Academy of Neurology.

“Our study suggests that plaques in the brain that are linked to a decline in memory and thinking abilities, called beta amyloid, take about 15 years to build up and then plateau,” said Clifford R. Jack, Jr., MD, with the Mayo Clinic in Rochester, Minn.

For the study, 260 people between the ages of 70 and 92 underwent two or more brain scans over an average of 1.3 years that measured plaque buildup in the brain. Of the participants, 78 percent did not have impaired thinking abilities or memory at the start of the study.

The study found that the rate of buildup accelerates initially, then slows down before plateauing at high levels. For example, lower rates of plaque buildup were found in both people who had low and high levels of the plaques at the start of the study while the rate of plaque accumulation was highest in participants with mid-range levels at the start of the study.

The study also found that the rate of buildup of plaques was more closely tied to the total amount of amyloid plaques in the brain than other risk factors, such as the level of cognitive impairment, age and the presence of the APOE gene, a gene linked to Alzheimer’s disease.

“Our results suggest that there is a long treatment window where medications may be able to help slow buildup of the amyloid plaques that are linked to cognitive decline,” said Jack. “On the other hand, trying to treat the plaque buildup after the amyloid plaque load has plateaued may not do much good.”

Infant brains imply adult ills: Researchers study traits in babies as young as two weeks

Brain images from newborns are giving scientists a glimpse of the future - not just into the lives of their tiny subjects but also paths to treatment for adult patients with schizophrenia and Alzheimer’s disease.

Researchers from the University of North Carolina-Chapel Hill found degeneration in the brains of 2-week-old infants, a result considered a “game changer” for the field of brain research, said Jay Giedd, a brain imaging specialist for the National Institute of Mental Health.

"Our original model was that the brain was fine until someone got the illness," Giedd said. "This work shows that these changes are there probably from conception. It also suggests that while these traits don’t cause brain damage, they set up the brain to be slightly different."

The researchers examined scans of 272 newborns. About 15 percent were found to have smaller medial temporal lobe sections. “The medial temporal lobe plays an important role in memory,” said Rebecca Knickmeyer, a UNC assistant professor of psychiatry and co-author of the research, published last month in Cerebral Cortex, an online journal.

"The idea is that this is an anatomical vulnerability. If you start out with less, you might hit active symptoms earlier in life."

The researchers also found specific gene traits associated with Alzheimer’s in babies with the smaller media temporal lobes.

"We were interested because it was generally known that people’s genes contribute to psychiatric conditions later in life, but pretty much all the existing studies were in adults," Knickmeyer said. "Our question was ‘When were these genes exerting their effect?’ Now we know it’s much earlier than previously thought, perhaps before birth."

Research such as this would benefit from the Brain Activity Map under development through the National Institutes of Health. The project’s 10-year goal is to create a map of the brain’s nearly 30,000 genes as well as the circuitry system that transmits information via brain waves.

President Obama mentioned the project in his State of the Union address and is expected to include funding for the project in the upcoming federal budget. Foundations and some private companies have also expressed interest in assisting in the project, which is expected to push brain research to a higher level.

"As brain scientists, we were giddy to hear this," Giedd said. "Motivation is sky high. If they fund this, we believe our work will really take off." Giedd, who is familiar with but did not participate in the infant brain study, said the search for treatments or cures for diseases such as Alzheimer’s, autism, schizophrenia and Parkinson’s disease have been stymied by the many mysteries that remain regarding how the brain functions.

"If we understood more about the mechanisms that cause these diseases, we could step in and do something about it," Giedd said. "The brain is so complicated. Most diseases don’t just involve one or two or even three genes. It might be 60 or 100 genes, along with upbringing, diet and environment. There are so many parameters to the equation."

Knickmeyer said her research team plans to follow up with the newborns as they grow into adulthood to see whether the traits displayed by infants change over time or remain stable throughout their lives.

Daniel Kaufer, cognitive neurology and memory disorders chief for UNC’s Department of Neurology, said he thinks the time is right for great advances in brain research.

"We are at the crossroads of two important events: the realization that brain disorders may occur long before symptoms begin, and the development of brain imaging technology to record brain processes," Kaufer said.

Learning more about the brain’s functions through gene mapping may be the third piece of the puzzle. “Right now, there is no map of the human brain,” said Murali Doraiswamy, professor of psychiatry and behavioral sciences at Duke University School of Medicine.

Doraiswamy said the brain carries thousands of genes that influence thought, perception, emotion, memory and other mental activities. “We want to find out how much is nature and how much is nurture,” he added. “I think we are at the forefront of something very insightful, but also a little frightening.”

MAPPING A NEW WORLD

The Brain Activity Map is being planned as a decade-long research effort to create a comprehensive outline of the structure of the human brain and its neurons.

Funding is expected to come from a variety of sources, including the federal government, private industry and research foundations.

Details of the project have not yet been made public. But it is being compared to the DNA sequencing effort known as the Human Genome Project, which ran from 1990 to 2003 and cost $3.8 billion.

Research reveals Huntington’s hope

Researchers in Scotland and Germany have discovered a molecular mechanism that shows promise for developing a cure for Huntington’s Disease (HD).

Scientists from the University of Dundee, the German Center for Neurodegenerative Diseases (DZNE) in Bonn, the Max-Planck Institute for Molecular Genetics in Berlin and the Johannes Gutenberg-Universität Mainz have found a mechanism that specifically stirs and induces the synthesis of disease-making protein in HD patients.

Their data lead to the conclusion that a selective overproduction of aberrant Huntington protein in patients is a key step in the establishment of the disease, which affects 1 in 10,000 people in Western countries and is so far incurable.

"This is a very promising strategy to develop a small molecule drug therapy that is able to inhibit the production of disease-making protein," said Professor Susann Schweiger of the University of Dundee and Johannes Gutenberg-Universität Mainz.

"Theoretically, if you don’t have the disease-making protein then you don’t have the disease. Obviously we still have work to do to develop a drug to target these mechanisms and inhibit the production of this protein but we think this research is attractive to drug discovery and ongoing work in this area is being carried out."

The gene responsible for causing Huntington’s Disease was first identified in 1993, leading to hopes that a specific therapy for HD would soon be on the market. However, cell biology and brain pathology of HD showed it to be more complicated than originally anticipated and only symptomatic treatments to slightly relieve the distress of single components of the disease are currently available.

The new discovery once again raises hopes that a curative therapy can be established. The scientists found that it was mainly three proteins - the mammalian target of rapamycin (mTOR), protein phosphatase 2A (PP2A) and Midline 1 (MID1) - that specifically drive the production of disease-making protein in HD patients.

As a result, more and more aberrant protein is produced with time, which leads to a protein overload in the cell. By interfering with the function of the three proteins it is possible to disrupt this circle and prevent the synthesis of aberrant protein in HD patients.

The Dundee-Germany research is published in the latest edition of the Nature Communications journal.

Microglia controls neuron production as brain develops

In a surprise breakthrough, researchers at the UC Davis MIND Institute and their colleagues have found that microglia remove healthy neural progenitor cells (NPCs) through phagocytosis to control neuron production during brain development. This newly discovered mechanism keeps neuron numbers in check, preventing brain overgrowth.

The discovery could open up new avenues for brain research and lead to therapies for a variety of neurological conditions.

The study was published online in the The Journal of Neuroscience.

Microglia are the immune component cell of the central nervous system. Similar to macrophages, microglia provide the brain’s primary defense against pathogens and foreign bodies, clear away dying cells and help repair neural damage. When inactive, they act as sentinels. When a problem is located, they activate and eliminate it. However, until recently, no one had realized the important roles they play in brain development.

"We have known for some time that neurons can undergo apoptosis, a form of cell death, and ultimately be removed by microglia," said Stephen Noctor, assistant professor in the Department of Psychiatry and Behavioral Sciences and the study’s lead author. "But this is new. Microglia are actually eating healthy progenitor cells, thereby regulating the number of neurons produced in the developing brain."

During development, NPCs produce neurons in the brain’s proliferative zones. However, creating too many or too few neurons can have dire consequences.

"If you have too many cells, there’s only so much trophic support (brain infrastructure for cell growth and survival) to keep neurons alive," Noctor said. "All these cells competing for resources could easily throw off connectional properties, altering the way surviving neurons interact. Likewise, having too few cortical cells would have profoundly negative consequences."

(Image: Antoine Triller, Alain Bessis & Serge Marty - Département de Biologie, ENS)

'Network' analysis of the brain may explain features of autism

A look at how the brain processes information finds a distinct pattern in children with autism spectrum disorders. Using EEGs to track the brain’s electrical cross-talk, researchers from Boston Children’s Hospital have found a structural difference in brain connections. Compared with neurotypical children, those with autism have multiple redundant connections between neighboring brain areas at the expense of long-distance links.

The study, using a “network analysis” like that used to study airlines or electrical grids, may help in understanding some classic behaviors in autism. It was published February 27 in BioMed Central’s open access journal BMC Medicine, accompanied by a commentary.

"We examined brain networks as a whole in terms of their capacity to transfer and process information," says Jurriaan Peters, MD, of the Department of Neurology at Boston Children’s Hospital, who is co-first author of the paper with Maxime Taquet, a PhD student in Boston Children’s Computational Radiology Laboratory. "What we found may well change the way we look at the brains of autistic children."

Peters, Taquet and senior authors Simon Warfield, PhD, of the Computational Radiology Laboratory and Mustafa Sahin, MD, PhD, of Neurology, analyzed EEG recordings from two groups of autistic children: 16 children with classic autism, and 14 children whose autism is part of a genetic syndrome known as tuberous sclerosis complex (TSC). They compared these readings with EEGs from two control groups—46 healthy neurotypical children and 29 children with TSC but not autism.

In both groups with autism, there were more short-range connections within different brain region, but fewer connections linking far-flung areas.

A brain network that favors short-range over long-range connections seems to be consistent with autism’s classic cognitive profile—a child who excels at specific, focused tasks like memorizing streets, but who cannot integrate information across different brain areas into higher-order concepts.

"For example, a child with autism may not understand why a face looks really angry, because his visual brain centers and emotional brain centers have less cross-talk," Peters says. "The brain cannot integrate these areas. It’s doing a lot with the information locally, but it’s not sending it out to the rest of the brain."

Discovery on animal memory opens doors to research on memory impairment diseases

If you ask a rat whether it knows how it came to acquire a certain coveted piece of chocolate, Indiana University neuroscientists conclude, the answer is a resounding, “Yes.” A study newly published in the journal Current Biology offers the first evidence of source memory in a nonhuman animal.

The findings have “fascinating implications,” said principal investigator Jonathon Crystal, both in evolutionary terms and for future research into the biological underpinnings of memory, as well as the treatment of diseases marked by memory failure such as Alzheimer’s, Parkinson’s and Huntington’s, or disorders such as schizophrenia, PTSD and depression.

The study further opens up the possibility of creating animal models of memory disorders.

"Researchers can now study in animals what was once thought an exclusively human domain," said Crystal, professor in the Department of Psychological and Brain Sciences in the College of Arts and Sciences. "If you can export types of behaviors such as source memory failures to transgenic animal models, you have the ability to produce preclinical models for the treatment of diseases such as Alzheimer’s."

Of the various forms of memory identified by scientists, some have long been considered distinctively human. Among these is source memory. When someone retells a joke to the person who told it to him, it is an everyday example of source memory failure. The person telling the joke forgot the source of the information — how he acquired it — though not the information he was told. People combine source information to construct memories of discrete events and to distinguish one event or episode from another.

Nonhuman animals, by contrast, have been thought to have limited forms of memory, acquired through conditioning and repetition, habits rather than conscious memories. The kind of memory failures most devastating to those directly affected by Alzheimer’s have typically been considered beyond the scope of nonhuman minds.

The study owes much to another quality these rodents share with humans: They love chocolate. “There’s no amount of chocolate you can give to a rat which will stop it from eating more chocolate,” Crystal said.

Research shows why not everyone learns from their mistakes

Some people do not learn from their mistakes because of the way their brain works, according to research led by an academic at Goldsmiths, University of London.

The research, led by Professor Joydeep Bhattacharya in the Department of Psychology at Goldsmiths, examined what it is about the brain that defines someone as a ‘good learner’ from those who do not learn from their mistakes.

Professor Bhattacharya said: “We are always told how important it is to learn from our errors, our experiences, but is this true? If so, then why do we all not learn from our experiences in the same way? It seems some people rarely do, even when they were informed of their errors in repeated attempts.

"This study presents a first tantalising insight into how our brain processes the performance feedback and what it does with this information, whether to learn from it or to brush it aside."

The study, published in a recent issue of the Journal of Neuroscience, investigated brainwave patterns of 36 healthy human volunteers performing a simple time estimation task. Researchers asked the participants to estimate a time interval of 1.7 seconds and provided feedback on their errors. The participants were then measured to see whether they incorporated the feedback to improve their future performances.

'Good learners', who were successful in incorporating the feedback information in adjusting their future performance, presented increased brain responses as fast as 200 milliseconds after the feedback on their performance was presented on a computer screen.

This brain response was weaker in the poor learners who did not learn the task well and who showed decreased responses to their performance errors. The researchers further found that the good learners showed increased communication between brain areas involved with performance monitoring and sensorimotor processes.

Caroline Di Bernardi Luft, one of the research paper’s co-authors from the Federal University of Santa Catarina, commented: “Good learners used the feedback not only to check their past performance, but also to adjust their next performance accordingly.”

The brain responses correlated highly with how well the volunteers learned this simple task over the course of the experiment, and how good they were at maintaining the learned skill without any guiding feedback.

"Though these results are very encouraging in establishing a correlation between brains responses and learning performance, future studies are needed to identify a causal role of these effects," Professor Bhattacharya added.

Songbirds’ brains coordinate singing with intricate timing

As a bird sings, some neurons in its brain prepare to make the next sounds while others are synchronized with the current notes—a coordination of physical actions and brain activity that is needed to produce complex movements, new research at the University of Chicago shows.

In an article in the current issue of Nature, neuroscientist Daniel Margoliash and colleagues show, for the first time, how the brain is organized to govern skilled performance—a finding that may lead to new ways of understanding human speech production.

The new study shows that birds’ physical movements actually are made up of a multitude of smaller actions. “It is amazing that such small units of movements are encoded, and so precisely, at the level of the forebrain,” said Margoliash, a professor of organismal biology and anatomy and psychology at UChicago.

“This work provides new insight into how the physics of controlling vocal signals are represented in the brain to control vocalizations,” said Howard Nusbaum, a professor of psychology at UChicago and an expert on speech.

By decoding the neural representation of communication, Nusbaum explained, the research may shed light on speech problems such as stuttering or aphasia (a disorder following a stroke). And it offers an unusual window into how the brain and body carry out other kinds of complex movement, from throwing a ball to doing a backflip.

“A big question in muscle control is how the motor system organizes the dynamics of movement,” said Margoliash. Movements like reaching or grasping are difficult to study because they entail many variables, such as the angles of the shoulder, elbow, wrist and fingers; the forces of many muscles; and how these change over time,” he said.

"With all this complexity, it has been difficult to determine which of the many variables that describe movements are represented in the brain, and which of those are used to control movements," he said.

"It’s difficult to find a natural framework with which to analyze the activity of single neurons. The bird study provided us a perfect opportunity,” Margoliash said. Margoliash is a pioneer in the study of brain function in birds, with studies that include how learning occurs when a bird sleeps and recalls singing a song.

The great orchestral work of speech

What goes on inside our heads is similar to an orchestra. For Peter Hagoort, Director at the Max Planck Institute for Psycholinguistics, this image is a very apt one for explaining how speech arises in the human brain. “There are different orchestra members and different instruments, all playing in time with each other, and sounding perfect together.”

When we speak, we transform our thoughts into a linear sequence of sounds. When we understand language, exactly the opposite occurs: we deduce an interpretation from the speech sounds we hear. Closely connected regions of the brain – like the Broca’s area and Wernicke’s area – are involved in both processes, and these form the neurobiological basis of our capacity for language.

The 58-year-old scientist, who has had a strong interest in language and literature since his youth, has been searching for the neurobiological foundations of our communication since the 1990s. Using imaging processes, he observes the brain “in action” and tries to find out how this complex organ controls the way we speak and understand speech.

Making language visible

Hagoort is one of the first researchers to combine psychological theories with neuroscientific methods in his efforts to understand this complex interaction. Because this is not possible without the very latest technology, in 1999, Hagoort established the Nijmegen-based Donders Centre for Cognitive Neuroimaging where an interdisciplinary team of researchers uses state-of-the-art technology, for example MRI and PET scanners, to find out how the brain succeeds in combining functions like memory, speech, observation, attention, feelings and consciousness.

The Dutch scientist is particularly fascinated by the temporal sequence of speech. He discovered, for example, that the brain begins by collecting grammatical information about a word before it compiles information about its sound. This first reliable real-time measurement of speech production in the brain provided researchers with a basis for observing speakers in the act of speaking. They were then able to obtain new insights about why the complex orchestral work of language is impaired, for example, after strokes and in the case of disorders like dyslexia and autism.

“Language is an essential component of human culture, which distinguishes us from other species,” says Hagoort. “Young children understand language before they even start to speak. They master complex grammatical structures before they can add 3 and 13. Our brain is tuned for language at a very early stage,” stresses Hagoort, referring to research findings. The exact composition of the orchestra in our heads and the nature of the score on which the process of speech is based are topics which Hagoort continues to research.