TAG: "Neuroscience"

Kids with autism, SPD show brain wiring differences


UCSF study builds on its research showing kids with SPD have measurable brain differences.

Pratik Mukherjee, UC San Francisco

Researchers at UC San Francisco have found that children with sensory processing disorders have decreased structural brain connections in specific sensory regions different than those in autism, further establishing SPD as a clinically important neurodevelopmental disorder.

The research, published in the journal PLOS ONE, is the first study to compare structural connectivity in the brains of children with an autism diagnosis versus those with an SPD diagnosis, and with a group of typically developing boys. This new research follows UCSF’s groundbreaking study published in 2013 that was the first to find that boys affected with SPD have quantifiable regional differences in brain structure when compared to typically developing boys. This work showed a biological basis for the disease but prompted the question of how these differences compared with other neurodevelopmental disorders.

“With more than 1 percent of children in the U.S. diagnosed with an autism spectrum disorder, and reports of 5 to 16 percent of children having sensory processing difficulties, it’s essential we define the neural underpinnings of these conditions, and identify the areas they overlap and where they are very distinct,” said senior author Pratik Mukherjee, M.D., Ph.D., a professor of radiology and biomedical imaging and bioengineering at UCSF.

SPD can be hard to pinpoint, as more than 90 percent of children with autism also are reported to have atypical sensory behaviors, and SPD has not been listed in the Diagnostic and Statistical Manual used by psychiatrists and psychologists.

Elysa Marco, UC San Francisco

“One of the most striking new findings is that the children with SPD show even greater brain disconnection than the kids with a full autism diagnosis in some sensory-based tracts,” said Elysa Marco, M.D., cognitive and behavioral child neurologist at UCSF Benioff Children’s Hospital San Francisco and the study’s corresponding author. “However, the children with autism, but not those with SPD, showed impairment in brain connections essential to the processing of facial emotion and memory.”

Children with SPD struggle with how to process stimulation, which can cause a wide range of symptoms including hypersensitivity to sound, sight and touch, poor fine motor skills and easy distractibility. Some SPD children cannot tolerate the sound of a vacuum, while others can’t hold a pencil or struggle with emotional regulation. Furthermore, a sound that is an irritant one day can be tolerated the next. The disease can be baffling for parents and has been a source of much controversy for clinicians who debate whether it constitutes its own disorder, according to the researchers.

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Aging brain influenced by experiences throughout life


Study from UC Davis and University of Victoria examines demographics and cognitive aging.

Early life experiences, such as childhood socioeconomic status and literacy, may have greater influence on the risk of cognitive impairment late in life than such demographic characteristics as race and ethnicity, a large study by researchers with the UC Davis Alzheimer’s Disease Center and the University of Victoria, Canada, has found.

“Declining cognitive function in older adults is a major personal and public health concern,” said Bruce Reed, professor of neurology and associate director of the UC Davis Alzheimer’s Disease Center.

“But not all people lose cognitive function, and understanding the remarkable variability in cognitive trajectories as people age is of critical importance for prevention, treatment and planning to promote successful cognitive aging and minimize problems associated with cognitive decline.”

The study, “Life Experiences and Demographic Influences on Cognitive Function in Older Adults,” is published online in Neuropsychology, a journal of the American Psychological Association. It is one of the first comprehensive examinations of the multiple influences of varied demographic factors early in life and their relationship to cognitive aging.

The research was conducted in a group of over 300 diverse men and women who spoke either English or Spanish. They were recruited from senior citizen social, recreational and residential centers, as well as churches and health-care settings. At the time of recruitment, all study participants were 60 or older, and had no major psychiatric illnesses or life threatening medical illnesses. Participants were Caucasian, African-American or Hispanic.

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Study links autistic behaviors to enzyme


Deleting the enzyme favorably impacts behaviors associated with fragile X syndrome.

Iryna Ethell, UC Riverside (Photo by L. Duka)

Fragile X syndrome (FXS) is a genetic disorder that causes obsessive-compulsive and repetitive behaviors, and other behaviors on the autistic spectrum, as well as cognitive deficits. It is the most common inherited cause of mental impairment and the most common cause of autism.

Now biomedical scientists at UC Riverside have published a study that sheds light on the cause of autistic behaviors in FXS. Appearing online today (July 23) in the Journal of Neuroscience, and highlighted also on the cover in this week’s print issue of the journal, the study describes how MMP-9, an enzyme, plays a critical role in the development of autistic behaviors and synapse irregularities, with potential implications for other autistic spectrum disorders.

MMP-9 is produced by brain cells. Inactive, it is secreted into the spaces between cells of the brain, where it awaits activation. Normal brains have quite a bit of inactive MMP-9, and the activation of small amounts has significant effects on the connections between neurons, called synapses. Too much MMP-9 activity causes synapses in the brain to become unstable, leading to functional deficits.

“Our study targets MMP-9 as a potential therapeutic target in fragile X and shows that genetic deletion of MMP-9 favorably impacts key aspects of FXS-associated anatomical alterations and behaviors in a mouse model of fragile X,” said Iryna Ethell, a professor of biomedical sciences in the UC Riverside School of Medicine, who co-led the study. “We found that too much MMP-9 activity causes synapses to become unstable, which leads to functional deficits that depend on where in the brain that occurs.”

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$1M grant funds study into neurochemistry behind addiction


Research could lead to improved therapies for those inclined toward addictive behaviors.

We’ve all heard the term “addictive personality,” and many of us know individuals who are consistently more likely to take the extra drink or pill that puts them over the edge. But the specific balance of neurochemicals in the brain that spurs him or her to overdo it is still something of a mystery.

“There’s not really a lot we know about specific molecules that are linked to vulnerability to addiction,” said Tod Kippin, a neuroscientist at UC Santa Barbara who studies cocaine addiction. In a general sense, it is understood that animals — humans included — take substances to derive that pleasurable rush of dopamine, the neurochemical linked with the reward center of the brain. But, according to Kippin, that dopamine rush underlies virtually any type of reward animals seek, including the kinds of urges we need to have in order to survive or propagate, such as food, sex or water. Therefore, therapies that deal with that reward system have not been particularly successful in treating addiction.

However, thanks to a collaboration between UCSB researchers Kippin; Tom Soh, professor of mechanical engineering and of materials; and Kevin Plaxco, professor of chemistry and biochemistry — and funding from a $1 million grant from the W. M. Keck Foundation — the neurochemistry of addiction could become a lot less mysterious and a lot more specific. Their study, “Continuous, Real-Time Measurement of Psychoactive Molecules in the Brain,” could, in time, lead to more effective therapies for those who are particularly inclined toward addictive behaviors.

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Researchers find epigenetic tie to neuropsychiatric disorders


Flawed dopamine signaling linked to mass alteration of gene activity in prefrontal cortex.

“Our work presents new leads to understanding neuropsychiatric disorders,” UC Irvine's Emiliana Borrelli said.

Dysfunction in dopamine signaling profoundly changes the activity level of about 2,000 genes in the brain’s prefrontal cortex and may be an underlying cause of certain complex neuropsychiatric disorders, such as schizophrenia, according to UC Irvine scientists.

This epigenetic alteration of gene activity in brain cells that receive this neurotransmitter showed for the first time that dopamine deficiencies can affect a variety of behavioral and physiological functions regulated in the prefrontal cortex.

The study, led by Emiliana Borrelli, a UCI professor of microbiology & molecular genetics, appears online in the journal Molecular Psychiatry.

“Our work presents new leads to understanding neuropsychiatric disorders,” Borrelli said. “Genes previously linked to schizophrenia seem to be dependent on the controlled release of dopamine at specific locations in the brain. Interestingly, this study shows that altered dopamine levels can modify gene activity through epigenetic mechanisms despite the absence of genetic mutations of the DNA.”

Dopamine is a neurotransmitter that acts within certain brain circuitries to help manage functions ranging from movement to emotion. Changes in the dopaminergic system are correlated with cognitive, motor, hormonal and emotional impairment. Excesses in dopamine signaling, for example, have been identified as a trigger for neuropsychiatric disorder symptoms.

Borrelli and her team wanted to understand what would happen if dopamine signaling was hindered. To do this, they used mice that lacked dopamine receptors in midbrain neurons, which radically affected regulated dopamine synthesis and release.

The researchers discovered that this receptor mutation profoundly altered gene expression in neurons receiving dopamine at distal sites in the brain, specifically in the prefrontal cortex. Borrelli said they observed a remarkable decrease in expression levels of some 2,000 genes in this area, coupled with a widespread increase in modifications of basic DNA proteins called histones – particularly those associated with reduced gene activity.

Borrelli further noted that the dopamine receptor-induced reprogramming led to psychotic-like behaviors in the mutant mice and that prolonged treatment with a dopamine activator restored regular signaling, pointing to one possible therapeutic approach.

The researchers are continuing their work to gain more insights into the genes altered by this dysfunctional dopamine signaling.

Borrelli is affiliated with UCI’s Center for Epigenetics & Metabolism and manages the INSERM/UCI U904 laboratory there. Karen Brami-Cherrier, Andrea Anzalone, Maria Ramos and Fabio Macciardi of UCI, as well as Ignasi Forne and Axel Imhof of Ludwig Maximilian University of Munich, contributed to the study, which received support from the National Institutes of Health (grant DA024689) and INSERM (grant 44790).

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New direction suggested for treating mental health disorders


Experts urge new discipline combining benefits of neuroscience, psychology treatments.

Michelle Craske, UCLA

When a patient talks with a psychological therapist, what changes occur in the patient’s brain that relieve mental disorders? UCLA psychology professor Michelle Craske says the honest answer is that we don’t know. But, according to Craske and two colleagues, we need to find out.

Mental health disorders — such as depression, schizophrenia, post-traumatic stress disorder, obsessive–compulsive disorder and eating disorders — affect 1 in 4 people worldwide. Psychological treatments “hold the strongest evidence base for addressing many such conditions,” but they need improvement, according to a study by Craske, Cambridge University professor Emily Holmes and MIT professor Ann Graybiel.

Their article was published online July 16 in the journal Nature.

For some conditions, such as bipolar disorder, psychological treatments are not effective or are in their infancy, the life scientists report, and a “culture gap” between neuroscientists and clinical scientists has hindered the progress of mental health treatments. The authors call on scientists from both disciplines to work together to advance the understanding and treatment of psychological disorders.

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Personalized approach enhances communications skills in children with autism


Computer tablets play key role in the blended therapy, UCLA-led study finds.

Connie Kasari, UCLA

A UCLA-led study has found that the communication skills of minimally verbal children with autism can be greatly improved through personalized interventions that are combined with the use of computer tablets.

The three-year study examined different approaches to improving communication abilities among children with autism spectrum disorder and minimal verbal skills. Approximately 30 percent of children with ASD overall remain minimally verbal even after years of intervention.

UCLA professor Connie Kasari, the paper’s senior author, worked with researchers at Vanderbilt University and the Kennedy Krieger Institute. They found that children’s language skills greatly improved when spoken- and social-communication therapy was tailored based on their individual progress and delivered using computer tablets.

The trial involved 61 children with ASD, ages 5 to 8. For six months, each child received communication therapy focusing on social communication gestures, such as pointing, as well as play skills and spoken language.

Half of the children were randomly selected to also use speech-generating applications on computer tablets for at least half of the time during their sessions. The tablets were programmed with audio clips of words the children were learning about during their therapy sessions and images of the corresponding objects. Working with a therapist, the child could tap a picture of a block, for example, and the tablet would play audio of the word “block.”

The researchers found that children who had access to the tablets during therapy were more likely to use language spontaneously and socially than the children who received the communication intervention alone — and that incorporating the tablets at the beginning of the treatment was more effective than introducing it later in the therapy.

“It was remarkable how well the tablet worked in providing access to communication for these children,” said Kasari, professor of human development and psychology in the UCLA Graduate School of Education and professor of psychiatry at UCLA’s Semel Institute for Neuroscience and Human Behavior. “Children who received the behavioral intervention along with the tablet to support their communication attempts made much faster progress in learning to communicate, and especially in using spoken language.”

Researchers also conducted follow-up visits with the children three months after the initial study period and found that their improvement had been maintained during that time.

The study was the first ASD research to use a sequential multiple assignment randomized trial, or SMART, design. The approach, which enables researchers to tailor interventions according to how each child in the study responds, was designed by Daniel Almirall and Susan Murphy, biostatisticians at the University of Michigan who were members of the research team. It also was the first randomized, controlled trial on this underserved population of children to use a computer tablet combined with an effective behavioral intervention.

Other study authors were Rebecca Landa of Kennedy Krieger and Johns Hopkins University, and Ann Kaiser of Vanderbilt. The study was funded by a High Risk High Impact grant from the Autism Speaks Foundation.

The findings were published in the June issue of the Journal of the American Academy of Child and Adolescent Psychiatry.

Based on this study, Kasari, who also is a member of UCLA’s Center for Autism Research and Treatment, received a $13 million grant from the National Institutes of Health’s Autism Centers of Excellence to fund continued research involving minimally verbal children.

The ACE Network–funded research, which is now under way, compares two types of intensive, daily instruction for children who attend schools in underserved communities and have an autism spectrum disorder and minimal communication abilities. The study also uses a SMART design and computer tablets. Researchers on the five-year network study are enrolling nearly 200 children at UCLA, Weill Cornell Medical Center in New York City, the University of Rochester and Vanderbilt University in Nashville.

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Novel biomarker predicts febrile seizure-related epilepsy


Noninvasive diagnostic technique could greatly enhance use of preventive therapies.

Tallie Baram, UC Irvine

A newly discovered biomarker – visible in brain scans for hours after febrile seizures – predicts which individuals will subsequently develop epilepsy, according to UC Irvine researchers. This diagnostic ability could lead to improved use of preventive therapies for the disorder.

A team led by Dr. Tallie Z. Baram found that rats exhibiting this novel signal in magnetic resonance imaging scans of their brains manifested symptoms of epilepsy months after experiencing very long febrile seizures. Those that did not possess this biomarker remained free of the disorder. The study appears in today’s (June 25) issue of The Journal of Neuroscience.

Up to 40 percent of children who have fever-related seizures lasting more than 30 minutes (known as febrile status epilepticus) will eventually develop epilepsy. However, it has not been possible to predict early on who will get the disorder, which can arise 10 or more years later.

ManKin Choy, a postdoctoral scholar in Baram’s group, induced long febrile seizures in young rats. The rodents had brain scans after two, four and 18 hours, then were allowed to grow and evaluated for the emergence of epilepsy. Choy identified a new type of signal in certain parts of the brain in some post-seizure rats, and these same ones developed epilepsy after several months.

“We were stunned to find that specific regions of the brain in rats ‘destined’ to become epileptic were ‘lighting up’ so early,’’ said Baram, the Danette Shepard Chair in Neurological Studies. “The signal indicating which rats would go on to have spontaneous epileptic seizures months later was in brain regions known to be involved in temporal lobe epilepsy, which is the type of the disease associated with long febrile seizures in children.”

“This remarkable discovery led us to ask two key questions,” she added. “First, can we figure out what is going on in the brain that causes this new signal? And second, can we detect a similar predictive signal in children?”

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Cal-BRAIN kickstarts California efforts to map the brain


UC-led statewide initiative signed into law.

UC San Diego's Ralph Greenspan (center) is helping lead the Cal-BRAIN initiative.

The California budget signed by Gov. Jerry Brown today (June 20) creates a statewide research grants program called Cal-BRAIN, an initiative led by UC San Diego. With an initial allocation of $2 million, Cal-BRAIN – short for California Blueprint for Research to Advance Innovations in Neuroscience – is a state complement to the federal BRAIN Initiative announced by President Barack Obama in April 2013. It aims to “accelerate the development of brain mapping techniques, including the development of new technologies.”

UC San Diego played a significant role in the national initiative and will now lead the state effort to revolutionize our understanding of the brain and the diagnosis and treatment of brain disorders of all kinds. By improving our ability to see what goes on in the brain in much greater detail and at a much faster timescale, we aim to make discoveries around autism, Alzheimer’s, PTSD and other behavioral health issues and injuries that affect everyone from our children to our homeless veterans.

In this leadership role, UC San Diego will guide the collaboration among the UC campuses and is currently discussing a significant financial investment of non-state, university resources in Cal-BRAIN.

Ralph Greenspan, director of UC San Diego’s Center for Brain Activity Mapping, established at the university in May 2013, is co-author with Paul Alivisatos, director of the Lawrence Berkeley National Laboratory, of a proposal to the University of California Office of the President and to the state Legislature that served as a blueprint for the bill just signed into law.

The proposal calls for organizational hubs in Southern and Northern California, at UC San Diego and Berkeley Lab, to coordinate research activities, facilitate communication and seek additional funds from private and industry partners.

Both Cal-BRAIN and the national initiative are expected to spur not only a new academic discipline but also a new industry cluster of “neurotechnology.” And the tools and inventions needed for mapping the brain will also likely have broad applications to a range of disease monitoring beyond the brain and even to fields beyond health.

“UC San Diego’s leadership role in Cal-BRAIN is of vital importance — not only to the university and the San Diego region but for the state as a whole,” said UC San Diego Chancellor Pradeep K. Khosla. “We will be developing the next technology cluster in ‘neurotech’ just as we did in high-tech, clean-tech and more, creating high paying jobs and world renowned results. I am confident that, with our strengths in neuroscience and biotechnology in San Diego, we will be producing ground-breaking research with significant social impacts.”

Since helping state Senate Majority Leader Ellen Corbett to convene the first hearing on California’s possible role in the BRAIN Initiative at UC San Diego in October 2013, Greenspan and other representatives from the university have traveled numerous times to Sacramento, presenting the case for Cal-BRAIN before members of the state Senate and state Assembly.

Senate President Pro Tem Darrell Steinberg (D-Sacramento) and state Sen. Marty Block (D-San Diego) were early champions. Assembly Speaker Toni Atkins (D-San Diego) also supported the bill.

“UC San Diego is a world leader in the biosciences, and it is a perfect fit to have UC San Diego serve as the Southern California hub of Cal-BRAIN,” Atkins said. “Cal-BRAIN will help develop brain mapping technologies and has the potential to make significant advances in treating conditions such as Alzheimer’s and Parkinson’s. I am proud San Diego will be at the forefront of this important effort.”

Greenspan – who is also associate director of the Kavli Institute for Brain and Mind at UC San Diego and professor in residence of neurobiology and cognitive science – is one of the original writers, as was Alivisatos of LBNL, of the white paper that sparked the national BRAIN Initiative.

“Our vision was for Cal-BRAIN to serve as a driver for trying out different possible technologies and converging on a unified approach for doing effective brain mapping, in which UC San Diego will play a key role,” Greenspan said. “Cal-BRAIN is a great start to realizing the ultimate goal: mapping the brain’s trillions of connections in real time.”

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A cure for Alzheimer’s requires a parallel team effort


UC expert simulates benefits of a hypothetical megafund devoted to Alzheimer’s therapeutics.

Kenneth Kosik, UC Santa Barbara

For the more than 5 million Americans and 35 million people worldwide suffering from Alzheimer’s disease, the rate of progress in developing effective therapeutics has been unacceptably slow.

To address this urgent need, UC Santa Barbara’s Kenneth S. Kosik and colleagues are calling for a parallel drug development effort in which multiple mechanisms for treating Alzheimer’s are investigated simultaneously rather than the current one-at-a-time approach. In an article published today (June 18) in Science Translational Medicine, the research team — Kosik; Andrew W. Lo and Jayna Cummings of the MIT Sloan School of Management’s Laboratory for Financial Engineering and Carole Ho of Genentech Inc. — presents a simulation of a hypothetical megafund devoted to bringing Alzheimer’s disease therapeutics to fruition.

According to Kosik, the Harriman Professor of Neuroscience Research and co-director of the Neuroscience Research Institute at UCSB, a “multiple-shots-on-goal” approach not only accelerates the search for a cure but also increases the probability of at least one or two successes within the next decade, thereby reducing the financial risk to investors. “But more basic research is needed to increase the probability of success, decrease the correlation among projects and make available more potential targets,” he added.

Unlike cancer and heart disease, which have many therapeutic targets — proteins and nucleic acids to which drugs are directed — the basic science of Alzheimer’s disease biology is still in its early days. What’s more, not enough Alzheimer’s disease targets exist to mitigate risk and thereby attract private-sector investment. But given how much the U.S. government is already paying each year for Alzheimer’s disease-related treatments through Medicare and Medicaid — more than $150 billion in 2013 — a government-supported public-private partnership may yield an excellent return on investment from the taxpayer’s perspective.

Using generic information on the drug development process and qualitative judgments by two of the co-authors (Kosik and Ho) who are experts in neurodegenerative diseases and translational medicine, the simulation shows that a hypothetical portfolio of 64 distinct Alzheimer’s disease drug development programs costing $38.4 billion would yield an expected financial return of -14.3 percent and a 13 percent probability that no project will reach approval. This level of risk implies that large-scale private-sector funding is unlikely to be directed to such an effort.

The analysis may help to explain why no new drugs for treating Alzheimer’s disease have been approved by the U.S. Food and Drug Administration since 2003. Currently only four drugs are on the market, and all four treat only the symptoms of Alzheimer’s disease without altering its course. However, when measured against the potential cost savings to the U.S. taxpayer over a 20-year horizon, therapeutics that delay the onset of Alzheimer’s disease or limit the progression of the disease can generate the equivalent of double-digit investment returns from the taxpayer’s perspective.

To quantify these potential cost savings, the authors used projections developed by the Alzheimer’s Association and found that savings could range from $813 billion to $1.5 trillion over a 30-year period, more than offsetting the cost of a $38 billion megafund. Domestically, the cost of treating Alzheimer’s disease is approximately $200 billion per year, of which an estimated 70 percent is covered by Medicare and Medicaid. Total related costs worldwide are already estimated to be about 1 percent of global gross domestic product.

Given that Alzheimer’s disease has the potential to bankrupt medical systems — the Alzheimer’s Association projects that the costs of care could soar to $1 trillion in the U.S. by 2050 — governments around the world have a strong incentive to invest more heavily in the development of Alzheimer’s disease therapeutics and catalyze greater private-sector participation.

“Unless government funding for basic research in the molecular biology of neurodegenerative diseases increases dramatically in the near future,” Kosik said, “it seems unlikely that the private sector will be able to produce effective Alzheimer’s disease therapies over the next few decades.”

Although the implications of the simulation seem clear, the authors acknowledge the need for much more research to calibrate the parameters of their analysis as well as to develop a more comprehensive set of potential Alzheimer’s disease targets with which to compute investment returns.

“My colleagues and I hope that this simulation will be the starting point for a more active collaboration among all stakeholders to explore the potential of a public-private partnership focused on Alzheimer’s disease therapeutics,” Kosik concluded.

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Your genes affect your betting behavior


Decisions influenced by variants of dopamine-regulating genes in a person’s brain.

Investors and gamblers take note: your betting decisions and strategy are determined, in part, by your genes.

University of California, Berkeley, and University of Illinois at Urbana-Champaign (UIUC) researchers have shown that betting decisions in a simple competitive game are influenced by the specific variants of dopamine-regulating genes in a person’s brain.

Dopamine is a neurotransmitter – a chemical released by brain cells to signal other brain cells – that is a key part of the brain’s reward and pleasure-seeking system. Dopamine deficiency leads to Parkinson’s disease, while disruption of the dopamine network is linked to numerous psychiatric and neurodegenerative disorders, including schizophrenia, depression and dementia.

While previous studies have shown the important role of the neurotransmitter dopamine in social interactions, this is the first study tying these interactions to specific genes that govern dopamine functioning.

“This study shows that genes influence complex social behavior, in this case strategic behavior,” said study leader Ming Hsu, an assistant professor of marketing in UC Berkeley’s Haas School of Business and a member of the Helen Wills Neuroscience Institute. “We now have some clues about the neural mechanisms through which our genes affect behavior.”

The implications for business are potentially vast but unclear, Hsu said, though one possibility is training workforces to be more strategic. But the findings could significantly affect our understanding of diseases involving dopamine, such as schizophrenia, as well as disorders of social interaction, such as autism.

“When people talk about dopamine dysfunction, schizophrenia is one of the first diseases that come to mind,” Hsu said, noting that the disease involves a very complex pattern of social and decision making deficits. “To the degree that we can better understand ubiquitous social interactions in strategic settings, it may help us understand how to characterize and eventually treat the social deficits that are symptoms of diseases like schizophrenia.”

Hsu, UIUC graduate student Eric Set and their colleagues, including Richard P. Ebstein and Soo Hong Chew from the National University of Singapore, will publish their findings the week of June 16 in the online early edition of the Proceedings of the National Academy of Sciences.

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Livermore Lab to develop next-generation neural devices with $5.6M grant


Technology will help doctors better understand, treat PTSD, traumatic brain injury.

Lawrence Livermore National Laboratory engineer Kedar Shah works on a neural device at the Lab's Center for Micro- and Nanotechnology.

Lawrence Livermore National Laboratory recently received $5.6 million from the Department of Defense’s Defense Advanced Research Projects Agency (DARPA) to develop an implantable neural interface with the ability to record and stimulate neurons within the brain for treating neuropsychiatric disorders.

The technology will help doctors to better understand and treat post-traumatic stress disorder (PTSD), traumatic brain injury (TBI), chronic pain and other conditions.

Several years ago, researchers at Lawrence Livermore in conjunction with Second Sight Medical Products developed the world’s first neural interface (an artificial retina) that was successfully implanted into blind patients to help partially restore their vision. The new neural device is based on similar technology used to create the artificial retina.

“DARPA is an organization that advances technology by leaps and bounds,” said LLNL’s project leader Satinderpall Pannu, director of the Lab’s Center for Micro- and Nanotechnology and Center for Bioengineering, a facility dedicated to fabricating biocompatible neural interfaces. “This DARPA program will allow us to develop a revolutionary device to help patients suffering from neuropsychiatric disorders and other neural conditions.”

The project is part of DARPA’s SUBNETS (Systems-Based Neurotechnology for Emerging Therapies) program. The agency is launching new programs to support President Obama’s BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative, a new research effort aimed to revolutionize our understanding of the human mind and uncover ways to treat, prevent and cure brain disorders.

LLNL and Medtronic are collaborating with UC San Francisco, UC Berkeley, Cornell University, New York University, PositScience Inc. and Cortera Neurotechnologies on the DARPA SUBNETS project. Some collaborators will be developing the electronic components of the device, while others will be validating and characterizing it.

As part of its collaboration with LLNL, Medtronic will consult on the development of new technologies and provide its investigational Activa PC+S deep brain stimulation (DBS) system, which is the first to enable the sensing and recording of brain signals while simultaneously providing targeted DBS. This system has recently been made available to leading researchers for early-stage research and could lead to a better understanding of how various devastating neurological conditions develop and progress. The knowledge gained as part of this collaboration could lead to the next generation of advanced systems for treating neural disease.

The LLNL Neural Technology group will develop an implantable neural device with hundreds of electrodes by leveraging their thin-film neural interface technology, a more than tenfold increase over current Deep Brain Stimulation (DBS) devices. The electrodes will be integrated with electronics using advanced LLNL integration and 3D packaging technologies. The goal is to seal the electronic components in miniaturized, self-contained, wireless neural hardware. The microelectrodes that are the heart of this device are embedded in a biocompatible, flexible polymer.

Surgically implanted into the brain, the neural device is designed to help researchers understand the underlying dynamics of neuropsychiatric disorders and re-train neural networks to unlearn these disorders and restore proper function. This will enable the device to be eventually removed from the patient instead of being dependent on it.

Using the Center for Micro- and Nanotechnology’s unique capabilities, Pannu and his team of engineers have achieved 25 patents and many publications during the last decade. The team’s goal with the DARPA SUBNETS program is to build a prototype neural device in four years for clinical trials at UCSF.

“We are very excited about this project,” Pannu said. “This is a great opportunity to develop therapies that have the potential to advance health care for our service members, veterans and the general public.”

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