TAG: "brain"

UCLA to develop ‘brain prothesis’


UCLA awarded $15M to create implantable device that could restore memory to millions.

Illustration of memory-restoring device to be developed by UCLA researchers.

UCLA has been tapped by the Defense Advanced Research Projects Agency to spearhead an innovative project aimed at developing a wireless, implantable brain device that could help restore lost memory function in individuals who have suffered debilitating brain injuries and other disorders.

The four-year effort, to be led by UCLA’s Program in Memory Restoration and funded by up to $15 million from DARPA, will involve a team of experts in neurosurgery, engineering, neurobiology, psychology and physics who will collaborate to create, surgically implant and test the new “neuroprosthesis” in patients.

Memory is the process by which neurons in certain brain regions encode information, store it and retrieve it. Various illnesses and injuries can disrupt this process, causing memory loss. Tramautic brain injury, which has affected more than 270,000 military members since 2000, as well as millions of civilians, is often associated with such memory deficits. Currently, no effective therapies exist to address the long-term affects of these injuries on memory.

“Losing our ability to remember past events and form new memories is one of the most dreaded afflictions of the human condition,” said UCLA’s lead investigator, Dr. Itzhak Fried, a professor of neurosurgery at the David Geffen School of Medicine at UCLA and a professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Developing models of the brain’s ‘memory works’

The ambitious, first-if-its-kind project at UCLA builds on Fried’s 2012 research — published in the New England Journal of Medicine with UCLA’s Nanthia Suthana and colleagues — demonstrating that human memory can be strengthened by stimulating the brain’s entorhinal cortex, a region involved in learning, memory and Alzheimer’s disease. Considered the entrance to the hippocampus, which helps form and store memories, the entorhinal cortex plays a crucial role in transforming daily experience into lasting memories.

“The entorhinal cortex is the ‘golden gate’ to the brain’s memory mainframe,” Fried said. “Every visual and sensory experience that we eventually commit to memory funnels through that doorway to the hippocampus. Our brain cells send signals through this hub in order to form memories that we can later consciously recall.”

In a key part of the project, the research team will stimulate and record the activity of single neurons and of small neuronal populations in patients who already have brain electrodes implanted as part of epilepsy treatment. UCLA’s Mayank Mehta, a professor of physics and neurobiology, and Harvard Medical School’s Gabriel Kreiman will then work with Fried’s group, using this information to develop computational models of the hippocampal–entorhinal system and determine how to intervene with electrical stimulation to help restore memory function.

Turning the models into a workable ‘neuroprosthesis’

The models will be transformed into therapeutics using technology developed by researchers from UCLA’s Henry Samueli School of Engineering and Applied Science. This group, led by associate professor of electrical engineering Dejan Markovic, will work with engineers from Lawrence Livermore National Laboratory and Stanford University to develop electronics for the implantable neuromodulation device. As part of the UCLA-led project, Lawrence Livermore will be awarded a separate $2.5 million grant from DARPA to build the device, which will have the ability to record and stimulate neurons to help restore memory.

Markovic said the goal is to create miniature wireless neural sensors that are far more sophisticated — much smaller and with much higher resolution — than those that exist today. The sensors will track and modulate neural activity with very precise spatial and temporal resolution, allowing the device to continuously update and modulate precise patterns of stimulation to optimize therapy and restore memory function.

“We are developing ultra–low-power electronics in order to measure activity of specific areas of the brain, perform neural signal analysis and wirelessly transmit that information to an outside device in close proximity to the implants,” Markovic said. “The implants and the outside device will talk to each other. The goals are to provide better therapy for people with neurological dysfunction and help those with epilepsy and brain injury to enhance and restore memory.”

“Currently, there is no effective treatment for memory loss caused by a condition such as traumatic brain injury,” said Lawrence Livermore project leader Satinderpall Pannu, director of the lab’s Center for Bioengineering, a facility dedicated to fabricating biocompatible neural interfaces. “This is a tremendous opportunity from DARPA to leverage Lawrence Livermore’s unique capabilities to develop cutting-edge medical devices that will change the health care landscape.”

Testing the new device in brain-injured patients

During the second phase of the program, Fried, using a minimally invasive procedure, will implant the neuromodulation device into the entorhinal area and hippocampus in patients with traumatic brain injury as part of a groundbreaking clinical trial.

The DARPA initiative aimed at developing these implantable brain devices, Restoring Active Memory (RAM), also involves the University of Pennsylvania. The program supports President Obama’s BRAIN initiative. Under the terms of a cooperative agreement with DARPA, UCLA is slated to receive up to $15 million for its work on the program, with full funding contingent on meeting a series of technical milestones.

The RAM program poses a formidable challenge reaching across multiple disciplines from basic brain research to medicine, computing and engineering,” Fried said. “But at the end of the day, it is the suffering individual, whether an injured member of the armed forces or a patient with Alzheimer’s disease, who is at the center of our thoughts and efforts.”

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$1M grant funds study into neurochemistry behind addiction


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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UCI researchers find epigenetic tie to neuropsychiatric disorders


“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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‘Support cells’ in brain play important role in Down syndrome


New research also suggests common antibiotic might help treat the genetic defect

Researchers from UC Davis School of Medicine and Shriners Hospitals for Children – Northern California have identified a group of cells in the brain that they say plays an important role in the abnormal neuron development in Down syndrome. After developing a new model for studying the syndrome using patient-derived stem cells, the scientists also found that applying an inexpensive antibiotic to the cells appears to correct many abnormalities in the interaction between the cells and developing neurons.

The findings, which focused on support cells in the brain called astroglial cells, appear online today in Nature Communications.

“We have developed a human cellular model for studying brain development in Down syndrome that allows us to carry out detailed physiological studies and screen possible new therapies,” said Wenbin Deng, associate professor of biochemistry and molecular medicine and principal investigator of the study. “This model is more realistic than traditional animal models because it is derived from a patient’s own cells.”

Down syndrome is the most common chromosomal cause of mild to moderate intellectual disabilities in the United States, where it occurs in one in every 691 live births. It develops when a person has three copies of the 21st chromosome instead of the normal two. While mouse models have traditionally been used in studying the genetic disorder, Deng said the animal model is inadequate because the human brain is more complicated, and much of that complexity arises from astroglia cells, the star-shaped cells that play an important role in the physical structure of the brain as well as in the transmission of nerve impulses.

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UCSF, Stanford team link shorter telomeres to smaller hippocampus


Cells’ protective DNA linked to size of brain region vital for memory.

A brain region that is vital for memory and shrinks in Alzheimer’s disease patients also is likely to be smaller in those whose white blood cells have shorter DNA-protecting end caps – called telomeres – according to a study by Stanford and UC San Francisco researchers published online July 14in the journal JAMA Neurology.

If the findings are confirmed in larger studies, the work is likely to fuel research on ways to manipulate cells to prevent aging of the brain and other organs, the researchers said.

UCSF telomere experts and Stanford researchers who specialize in studies of the hippocampus and aging found the link for the first time in humans. Previously, researchers studying mice found that lengthening telomeres can reverse brain aging.

In the new study the researchers studied 47 cognitively and physically healthy women ranging in age from 49 to 66. Nineteen of the 47 carry a gene called APO E4, which is associated with increased Alzheimer’s disease risk. The association between telomere length and the size of the hippocampus was greatest among women without the risky APO E4 gene — and for reasons that are unclear — was obscured in the women with APO E4.

According to Emily Jacobs, Ph.D., the lead author of the study, who analyzed the data as a UCSF postdoctoral fellow, “Our findings highlight how chromosomal aging is tied to broader aspects of physiological aging, in this case hippocampal volume. These data raise the possibility that leukocyte telomere length may provide an early marker of age-related neurodegeneration.”

Previous studies have found that short telomere length in white blood cells predicts cognitive decline, Jacobs said.

Jacobs, now an instructor of psychiatry at Harvard Medical School, led the analysis as a postdoctoral fellow in the laboratory of Elissa Epel, Ph.D., a professor in the Department of Psychiatry at UCSF who studies the role of psychological stress in telomere length and chronic disease.

Natalie Rasgon, M.D., Ph.D., professor of psychiatry and behavioral sciences at Stanford, the director of the Stanford Center for Neuroscience in Women’s Health and the principal investigator for the new study, leads ongoing research on brain aging, which incorporates non-invasive magnetic resonance imaging to measure hippocampal volume.

While cautioning that this is a small study requiring replication, Rasgon said, “The results are very exciting and thought-provoking. It raises the possibility that we might be able to modulate telomere length to reduce vulnerability to dementia.”

Elizabeth Blackburn, Ph.D., professor of biochemistry and biophysics at UCSF, who shared a Nobel Prize for her discoveries of how telomeres allow chromosomes to be copied in a complete way during cell divisions, and of how they protect chromosomes against degradation, is a study co-author. Jue Lin, Ph.D., an associate researcher who works in Blackburn’s lab, also is a co-author.

Rasgon, Epel, Blackburn, Lin and colleagues intend to expand the current cross-sectional findings by monitoring telomere and hippocampus status over time.

“The main importance of all of these efforts is for the early detection of vulnerable populations who may go on to develop cognitive decline and dementia,” Rasgon said.

According to Epel, “Blood telomere length is a reliable predictor of diseases of aging, and it appears to relate to aspects of brain aging as well. Studies of stress reduction and lifestyle interventions suggest telomere length may be malleable.  But it is still a big question as to whether increasing telomere length over time will actually prevent cognitive decline or other aging-related conditions.”

The study co-authors, noting that chronic exposure of cells to inflammatory and oxidizing molecules and to glucocorticoid hormones can accelerate telomere shortening and lead to hippocampal atrophy, said it will be important to study cellular mechanisms in more detail to better understand how changes in telomere length — as well as changes in the activity of a telomere-lengthening enzyme called telomerase – either reflect or drive age-related cognitive decline.

Funding for work described in the JAMA Neurology study was provided by the National Institutes of Health and by the Robert Wood Johnson Foundation Health and Society Scholars program. Epel, Lin and Blackburn were co-founders of Telomere Diagnostics Inc., a telomere-length measurement company.

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How to prevent concussion among young football players


Former Bruin, NFL players talk about their head injuries at UCLA-hosted event.

Patrick Larimore, former team captain for the UCLA Bruins, suffered six concussions during his career before he made the agonizing decision to leave football. (Photo by Reed Hutchinson, UCLA)

“Welcome to the future of high school football,” Terry O’Neil said as he greeted nearly 90 coaches, physicians, sports advocates and parents who came to Carnesale Commons July 8 to learn about what they can do to help players reduce the risk of concussion.

The diverse group gathered to learn about football techniques that would be legal under a bill authored by Assemblyman Ken Cooley aimed at preventing concussions in high school football players by reducing high-impact contact during field practice.

The event was cosponsored by the UCLA Steve Tisch BrainSPORT Program, Cooley and O’Neil’s organization, Practice Like Pros, a nonprofit that’s educating college and high school coaches about the benefits of adopting professional teams’ approaches to reserving full-contact for game day.

“Two-thirds to three-quarters of all concussions happen during practice with a player’s own team mates, not during games,” explained speaker Dr. Christopher Giza, director of the BrainSPORT program and a professor of neurosurgery and pediatric neurology at the David Geffen School of Medicine at UCLA and Mattel Children’s Hospital. “We need to teach new techniques that don’t use the head as a weapon and customize helmets for smaller athletes to help kids safely play the sports they enjoy.”

Patrick Larimore understands the issue intimately.  UCLA’s former football team captain and defensive MVP in 2011, he suffered six concussions during his career, along with depression, disrupted sleep and painful headaches, before making the agonizing decision to shelve his National Football League dreams and leave football in 2012.

“Playing linebacker, I got hit every day,” recalled Larimore. “Every time you suffer a concussion, it increases the risk of suffering another. I’m an example of that. I owe it to the young kids playing now to spread the word about the dangers of traumatic brain injury.”

Former NFL Hall of Fame quarterback Warren Moon agrees. During his 33-year career, he also suffered six concussions, starting at age 11 during Pop Warner football in Baldwin Hills before going on to play for Hamilton High, the NFL’s Houston Oilers, Minnesota Vikings, Seattle Seahawks and Kansas City Chiefs.

According to Moon, athletes’ glory days shouldn’t end in high school. “We want kids to move onto the next level of football, be it college or pro. We want them to live healthy lives with productive futures.”

“I’ve seen colleagues suffer from Alzheimer’s, Parkinson’s, dementia and short-term memory loss,” Moon added. “I never know when these symptoms might creep into my life. I’m watching myself for those signs all the time.”

Cooley summed up the mission behind the legislation.

“The real purpose of AB 2127 is to deal with the impact of adverse concussion news in the brains of parents who love their kids,” said Cooley, “so they are looking at their baby boy and worrying about, ‘What will happen if my son wants to play football?’”

Assembly Bill 2127 has passed the State Assembly and Senate and now awaits Gov. Jerry Brown’s signature. If it is approved, California would become the 16th state in the past 16 months to limit full-contact practice in high school.

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Minor head injury not reason enough for CT scan in children


Study helps emergency physicians avoid CT scans that carry cancer risks for young patients.

Nathan Kuppermann, UC Davis

A nationwide study of more than 40,000 children evaluated in hospital emergency departments for head trauma found that if children had only loss of consciousness, and no other signs or symptoms related to the head trauma, they are very unlikely to have sustained serious brain injuries. Children who have only isolated loss of consciousness after head trauma do not routinely require computed tomography (CT) scans of the head, reported researchers from UC Davis Health System and Boston Children’s Hospital.

Although CT scans are the standard way to determine if a child has life-threatening bleeding in the brain that may necessitate surgical intervention, the radiation involved carries a small but quantifiable long-term risk of cancer. As such, the data indicates CT evaluation for children with head trauma should not be routinely used if they are at low risk for clinically significant traumatic brain injuries.

The findings were published today in the journal JAMA Pediatrics in an article titled “Isolated loss of consciousness in children with minor blunt head trauma.”

“Fear of missing a clinically significant head injury, and the wide availability of CT scanners, have been the main factors driving an increase in the use of CT imaging over the past two decades,” said Nathan Kuppermann, professor and chair of the UC Davis Department of Emergency Medicine, and principal investigator of the original study from which the data and current analysis of head injuries were derived. “Our findings can help doctors confidently make a decision to forego CT testing when their patients are unlikely to benefit from it, enabling physicians to first observe their patients for a period of time before deciding on CT use.”

Whether the presence of a single factor suggestive of brain injury is reason enough to justify obtaining a CT scan has been a question Kuppermann and colleagues with the Pediatric Emergency Care Applied Research Network (PECARN) have been actively exploring through a series of studies over the past few years. The current study found that children who lost consciousness after head trauma, but then were awake and alert in the emergency department, and had none of the other five factors determined important by PECARN guidelines for identifying children at low risk for clinically significant brain injuries after head trauma (called the PECARN traumatic brain injury prediction rules), had a very low rate of clinically important brain injuries – only 0.5 percent, or 1 in 200 children.

If a child had isolated loss of consciousness without any other signs or symptoms of head trauma (i.e., including factors outside of the PECARN traumatic brain injury prediction rules), the incidence of an important brain injury dropped to only 0.2 percent, or 1 in 500 children. Furthermore, the duration of the loss of consciousness did not significantly affect risk.

“Children with clinically important brain injuries rarely have loss of consciousness alone, and almost always present other symptoms, such as vomiting or showing signs of neurological problems,” said Lois K. Lee, lead author of the current study and director of trauma research at Boston Children’s Hospital. “Being able to make treatment decisions backed by strong data helps doctors and parents feel better about deciding whether further testing is really needed.”

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Biomarker predicts effectiveness of brain cancer treatment


UC San Diego researchers study microRNAs.

Clark Chen, UC San Diego

Researchers at the UC San Diego School of Medicine have identified a new biomarker that predicts whether glioblastoma – the most common form of primary brain cancer – will respond to chemotherapy. The findings are published in the July print issue of Oncotarget.

“Every patient diagnosed with glioblastoma is treated with a chemotherapy called temozolomide. About 15 percent of these patients derive long-lasting benefit,” said Clark C. Chen, M.D., Ph.D., vice chairman of academic affairs, Division of Neurosurgery, UC San Diego School of Medicine, and the study’s principal investigator. “We need to identify which patients benefit from temozolomide and which another type of treatment. All therapies involve risk and the possibility of side effects. Patients should not undergo therapies if there’s no likelihood of benefit.”

To pinpoint which patients were most likely respond to temozolomide, the researchers studied microRNAs that control the expression of a protein called methyl-guanine-methyl-transferase or MGMT. This protein dampens the cancer-killing effect of temozolomide. Tumors with high levels of MGMT are associated with a poor response to temozolomide therapy.

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Running, combined with visual experience, restores brain function


Experiments reveal unexpected potential in the adult brain’s capacity for self-repair.

Michael STryker, UC San Francisco

In a new study by UC San Francisco scientists, running, when accompanied by visual stimuli, restored brain function to normal levels in mice that had been deprived of visual experience in early life.

In addition to suggesting a novel therapeutic strategy for humans with blindness in one eye caused by a congenital cataract, droopy eyelid, or misaligned eye, the new research — the latest in a series of UCSF studies exploring effects of locomotion on brain function — suggests that the adult brain may be far more capable of rewiring and repairing itself than previously thought.

In 2010, Michael P. Stryker, Ph.D., the W.F. Ganong Professor of Physiology, and postdoctoral fellow Cris Niell, Ph.D., now at the University of Oregon, made the surprising discovery that neurons in the visual area of the mouse brain fired much more robustly whenever the mice walked or ran.

Earlier this year, postdoctoral fellow Yu Fu, Ph.D., Stryker and a number of colleagues built on these findings, identifying and describing the neural circuit responsible for this locomotion-induced “high-gain state” in the visual cortex of the mouse brain.

Neither of these studies made clear, however, whether this circuit might have broader functional or clinical significance.

It has been known since the 1960s that visual areas of the brain do not develop normally if deprived of visual input during a “critical period” of brain development early in life. For example, in humans, if amblyopia (“lazy eye”) or other major eye problems are not surgically corrected in infancy, vision will never be normal in the affected eye — if such individuals lose sight in their “good” eye in later life, they are blind.

In the new research, published June 26, 2014 in the online journal eLife, Stryker and UCSF postdoctoral fellow Megumi Kaneko, M.D., Ph.D., closed one eyelid of mouse pups at about 20 days after birth, and that eye was kept closed until the mice reached about five months of age.

As expected, the mice in which one eye had been closed during the critical developmental period showed sharply reduced neural activity in the part of the brain responsible for vision in that eye.

As in the previous UCSF experiments in this area, some mice were allowed to run freely on Styrofoam balls suspended on a cushion of air while recordings were made from their brains.

Little improvement was seen in the mice that had been deprived of visual input either when they were simply allowed to run or when they received visual training with the deprived eye not accompanied by walking or running.

But when the mice were exposed to the visual stimuli while they were running or walking, the results were dramatic: within a week the brain responses to those stimuli from the deprived eye were nearly identical to those from the normal eye, indicating that the circuits in the visual area of the brain representing the deprived eye had undergone a rapid reorganization, known in neuroscience as “plasticity.”

Interestingly, this recovery was stimulus-specific: if the brain activity of the mice was tested using a stimulus other than that they had seen while running, little or no recovery of function was apparent.

“We have no idea yet whether running puts the human cortex into a high-gain state that enhances plasticity, as it does the visual cortex of the mouse,” Stryker said, “but we are designing experiments to find out.”

The research was supported by grants from the National Institutes of Health.

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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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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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How our brains store recent memories, cell by single cell


Findings may shed light on how to treat neurological conditions like Alzheimer’s, epilepsy.

Human neuron showing actin formation in response to stimulation. (Image by Michael A. Colicos, UC San Diego)

Confirming what neurocomputational theorists have long suspected, researchers at the Dignity Health Barrow Neurological Institute in Phoenix and UC San Diego report that the human brain locks down episodic memories in the hippocampus, committing each recollection to a distinct, distributed fraction of individual cells.

The findings, published in today’s (June 16) early edition of PNAS, further illuminate the neural basis of human memory and may, ultimately, shed light on new treatments for diseases and conditions that adversely affect it, such as Alzheimer’s disease and epilepsy.

“To really understand how the brain represents memory, we must understand how memory is represented by the fundamental computational units of the brain – single neurons – and their networks,” said Peter N. Steinmetz, M.D., Ph.D., program director of neuroengineering at Barrow and senior author of the study. “Knowing the mechanism of memory storage and retrieval is a critical step in understanding how to better treat the dementing illnesses affecting our growing elderly population.”

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