TAG: "Neuroscience"

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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Tackling tomorrow’s health challenges


Stanley Prusiner among UC participants at New York Times health conference.

New York Times correspondent Elisabeth Rosenthal and Nobel laureate Stanley Prusiner discuss developments in Alzheimer's research at the Health for Tomorrow conference at UCSF Mission Bay. (Photos by Susan Merrell, UC San Francisco)

By Alec Rosenberg

Nobel Prize winner Stanley Prusiner is not resting on his laurels.

Instead, the 72-year-old UC San Francisco neurologist has set his sights on solving one of the biggest challenges facing health care today: Alzheimer’s disease.

Prusiner made a passionate plea for tackling Alzheimer’s and other neurodegenerative diseases Thursday (May 29) at the New York Times Health for Tomorrow conference at UCSF Mission Bay Conference Center. The conference, which featured experts from the University of California and across the country, addressed the changing landscape of health care.

Alzheimer’s already has a large impact on health care: It’s the sixth-leading cause of death in the U.S. — more than breast cancer and prostate cancer combined — and nearly half of people age 85 and older have the disease, Prusiner said. Without action, it will get worse — the prevalence of the disease is projected to triple by 2050 to as many as 16 million Americans.

“This is a huge, huge problem, and we’re not doing nearly enough,” said Prusiner, a UC San Francisco professor of neurology and director of the Institute for Neurodegenerative Diseases. “This is such an important area. There is no substitute for research. That’s going to really make a difference.”

Stanley Prusiner, UC San Francisco

Filling the pipeline

The National Institutes of Health provides only $500 million in research funding for Alzheimer’s, compared with more than $5 billion for cancer research, even though each costs society about $200 billion a year, Prusiner noted.

While many drugs treat cancer and hundreds more are in the pipeline, no single drug today halts or slows neurodegenerative diseases, he said. Prusiner, who just wrote a memoir, “Madness and Memory,” about his Nobel Prize-winning discovery of prions — infectious proteins that could be at the root of neurodegenerative diseases such as Alzheimer’s and Parkinson’s — aims to change that.

In April, UCSF formed a new collaboration with Japan-based pharmaceutical company Daiichi Sankyo Co. Ltd. This joint venture, capitalizing on Prusiner’s research, is focusing on developing drugs and molecular diagnostics for multiple neurodegenerative diseases, including Alzheimer’s and Parkinson’s.

“I’m very optimistic now that we are going to get there,” Prusiner said. “This is a huge step forward. We need 10 more of these around the world.”

UC President Janet Napolitano

Making progress

UC is conducting research on health’s most pressing problems, teaching the next generation of health professionals and working to improve health care quality, access and affordability, said UC President Janet Napolitano, who delivered welcoming remarks at the conference.

“There are no quick fixes, but I think working together we can make steady progress,” Napolitano said.

Indeed, research is being conducted throughout UC on Alzheimer’s and many other health issues. Napolitano noted that UC San Francisco leads a team that was just awarded a $26 million federal grant — part of President Obama’s Brain Initiative — to create an implantable device that will retrain the brain to recover from mental illness. She also pointed to research by conference speakers David Kilgore of UC Irvine and Michael Fischbach of UC San Francisco.

David Kilgore, UC Irvine

Countering ‘diabesity’

Kilgore, a clinical professor of family medicine, talked about the problem of “diabesity”: Diabetes rates have tripled in the last 20 years, while more than two-thirds of adults are considered to be overweight or obese. Among Kilgore’s patients at a UC Irvine clinic, 70 percent have diabetes, often in combination with other chronic diseases.

“The challenge of chronic disease has completely changed what it’s like to be a primary care physician,” Kilgore said.

More prevention is needed, Kilgore said. He started group medical visits for patients with diabetes. They receive extra information about nutrition, exercise and receive a healthy cooking lesson.

“They love it,” Kilgore said.

UC San Francisco's Michael Fischbach and Stanford's Justin Sonnenburg discuss research into gut bacteria.

Going with the gut

Fischbach, a UC San Francisco assistant professor of bioengineering and therapeutic sciences, discussed his research on the gut with collaborator Justin Sonnenburg, a Stanford University microbiologist who has a bachelor’s degree from UC Davis and a doctorate from UC San Diego. They are studying gut bacteria and how it could help reveal the causes and new treatments for Crohn’s disease and obesity.

“The beauty of being in basic research is you don’t know where you’re going to end up,” Fischbach said after their panel presentation. “It’s nice to be on a journey where you don’t know where the ship lands. I hope it’s going to improve human health.”

Seeking solutions

The Health for Tomorrow conference addressed issues ranging from the impacts of the Affordable Care Act to rethinking how to deliver care in the 21st century to issues of access, affordability and applying technology. Speakers included Marilyn Tavenner, administrator of the Centers for Medicare & Medicaid Services; Diana Dooley, secretary of the California Health and Human Services Agency; New York Times correspondent Elisabeth Rosenthal; CEOs Toby Cosgrove of the Cleveland Clinic and Bernard Tyson of Kaiser Permanente; and several with UC ties.

As part of the conference, five entrepreneurs were invited to give short talks about their health-related startup companies. Three of them studied at UC:

  • Erik Douglas, CEO of CellScope, has a doctorate degree from UC Berkeley and UC San Francisco. The company’s first product, CellScope Oto, turns a smartphone into a digitally connected otoscope, enabling remote care for ear infections, the leading reason for pediatric visits.
  • Anupam Pathak, Lift Labs founder and CEO, has B.S. and M.S. degrees from UC Berkeley. Lift Labs makes active stabilization tools for people living with tremor. Its pocket-sized Liftware, which has a spoon and other attachments, is a “Swiss Army knife for people with tremors.”
  • Joanna Strober, founder and CEO of Kurbo Health, has a J.D. from UCLA. She founded Kurbo after becoming concerned about the consequences of her middle son being overweight. Kurbo has developed a mobile app designed for children and their families to help them lose weight and live healthier lives.

The Health for Tomorrow conference can be viewed on demand, broken down by panel, at www.nythealthfortomorrow.com.

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Untangling brain circuits in mental illness


UCSF-UC Berkeley team leads $26M project, part of President Obama’s Brain Initiative.

Depression. Anxiety Disorders. Addiction.

They’re some of the most common conditions affecting people’s health, and for millions with the most severe cases, conventional treatments such as psychotherapy and medication don’t work adequately – or simply don’t work at all.

What if there were a treatment that could target the specific brain circuits that caused these conditions and offer patients a long-lasting solution?

A team of scientists and physicians led by UC San Francisco, in collaboration with UC Berkeley, is launching a $26 million project, funded by the Defense Advanced Research Projects Agency (DARPA), to map the human brain circuits that go awry in neuropsychiatric disorders and employ advanced technology to correct these patterns.

It’s one of the first projects launched in support of the $100 million Brain Initiative (Brain Research through Advancing Innovative Neurotechnologies), announced by President Barack Obama last year to support research on treating, preventing and perhaps curing brain disorders such as Alzheimer’s, schizophrenia, autism, epilepsy and traumatic brain injury. Because psychiatric conditions disproportionately affect soldiers and veterans, DARPA – a major partner in the Brain Initiative – is seeking the most original approaches to treatment-resistant mental illnesses.

“Human brain recording can now reveal aspects of mental illness that have been inaccessible to scientists and doctors,” said UCSF neurosurgeon Edward F. Chang, M.D., who is leading the project. “By analyzing patterns of interaction among brain regions known to be involved in mental illness we can get a more detailed look than ever before at what might be malfunctioning, and we can then develop technology to correct it.”

The technology itself already exists to help people with their motor skills.

For years, doctors have been doing deep brain stimulation to correct circuitry in movement disorders such as Parkinson’s disease.  And for patients who are paralyzed or are missing limbs, scientists at the Center for Neural Engineering and Prostheses (CNEP) – where Chang is co-director – have been working in the field of brain-machine interfaces to develop a tiny implantable device for the brain that can convert their thoughts into control commands for a robotic arm or exoskeleton.

This new project plans to leverage brain-machine interfaces to do the same for psychiatric patients – but instead of driving a robotic arm or exoskeleton, the device would be able to detect abnormal brain activity and deliver electrical stimulation within the brain to alleviate the symptoms.

And because of its natural plasticity, the brain eventually could “unlearn” these abnormal signaling patterns and the patient could potentially be cured.

The ambitious project will involve more than a dozen scientists, engineers and physicians at UC Berkeley, Lawrence Livermore National Laboratory, Cornell University and New York University, as well as industry partners Posit Science and Cortera Neurotechnologies.

Team members include Vikaas Sohal, M.D., Ph.D., assistant professor of psychiatry at UCSF; UCSF neurosurgeon Philip A. Starr, M.D., Ph.D.; José M. Carmena, Ph.D., CNEP co-director and UC Berkeley associate professor of electrical engineering and computer sciences and of neuroscience; and UC Berkeley colleagues Jonathan Wallis, Ph.D.,  and Robert Knight, M.D., professors of psychology and of neuroscience; Jan Rabaey, Ph.D., Elad Alon, Ph.D., and Michel Maharbiz, Ph.D., professor and associate professors, respectively, of electrical engineering and computer sciences; and Friedrich (Fritz) Sommer, Ph.D., adjunct associate professor at the Redwood Center for Theoretical Neuroscience.

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UCSF 2.0: Creating new partnerships


Collaborations on brain diseases point to promising possibilities.

UC San Francisco's Adam Gazzaley and colleagues are reporting in the journal Nature that they have found a way to reverse some of the negative effects of aging on the brain, using a video game designed to improve cognitive control.

No single institution can address the next decade’s health, research and education challenges on its own. As players from a wide range of industries continue to venture into health and health care, it will be imperative for UC San Francisco to form new partnerships to address familiar health challenges in creative, novel ways.

UCSF has actively increased its portfolio of partnerships in the past few years, announcing several major projects this year alone.

Most recently, UCSF formed a new collaboration between the Institute for Neurodegenerative Diseases and the Japan-based global pharmaceutical company Daiichi Sankyo Co. Ltd. This joint venture, capitalizing on the Nobel Prize-winning research of Stanely Prusiner, M.D., is focusing on developing therapeutics and molecular diagnostics for multiple neurodegenerative diseases.

The collective feedback from faculty and staff who participated in the planning initiative known as UCSF 2.0 calls on the University to “amplify its network of collaborators.” One big idea is for UCSF to lead the creation of a Bio Silicon Valley, taking advantage of its close proximity to the Bay Area’s innovation milieu by bridging biological, social, and technological sciences to revolutionize biomedical research.

Making the right connections

Neuroscientist Adam Gazzaley, M.D., Ph.D., director of the UCSF Neuroscience Imaging Center and a faculty member since 2004, is among a group of innovators who are doing just that. He partnered with Swartz Center at UC San Diego and Nvidia, which makes high-end computational computer chips, to create a new imaging technology called GlassBrain. The technology allows him to view the brain without using a big imaging machine or wiring the patient to a computer with the ultimate aim to find treatments for a variety of brain diseases, including Alzheimer’s and multiple sclerosis.

Gazzaley, an associate professor of neurology, physiology and psychiatry, says UCSF can help faculty make the right connections with partners across sectors.

“We need to know what companies are looking for and how to align our goals,” he said. “We just have to point in same direction and appeal to their public interests. What I found in my experience doing this is that we have to demonstrate our value as a real partner and not just be a charity case.”

UCSF also can help by embracing the entrepreneurial spirit by providing opportunities for faculty and students to share ideas and tools.

“I want us to have a platform that enables us to be more creative and aggressive in thinking how software and hardware can be a new medicine to improve brain health,” Gazzaley said. “Often, high-tech innovations take a decade to move beyond the entertainment industry and reach science and medicine. That needs to change.”

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Brain’s response to sexual images linked to number of sexual partners


UCLA researchers say finding could lead to strategies to reduce risky sex.

Nicole Prause, UCLA

Like most things, sex requires motivation. An attractive face, a pleasant fragrance, perhaps a sexy image. Yet people differ in their response to sex cues, some react strongly; some don’t. A greater responsiveness to sexual cues might provide greater motivation for a person to act sexually, and risky sexual behaviors typically occur when a person is motivated by particularly potent, sexual reward cues.

Now researchers at UCLA have, for the first time, directly linked brain responses  and real-world sexual behaviors. Specifically, the researchers found that how strongly the brain responded to viewing such images was related to the number of sex partners a person had in the previous year.

Led by Nicole Prause, a research scientist in the department of psychiatry in the UCLA Semel Institute for Neuroscience and Human Behavior, the study was published in the current online edition of the journal Social Cognitive and Affective Neuroscience. Prause and her colleagues used electroencephalogram (EEG) to measure a particular type of electrical activity in the brains of people as they were viewing a variety of images — some romantic, some pornographic, and some having nothing at all to do with sex.

Understanding how the brain responds to sexual images could help scientists create a brain stimulation intervention to reduce sensitivity to sexual reward and thus reduce some people’s proclivity to engage in risky sexual activities.

“These are the first data we know of that link brain responses to actual sexual risk behaviors,” said Prause, who directs the Sexual Psychophysiology and Affective Neuroscience Laboratory at UCLA. “If your brain responds very strongly even to very tame pictures of sex, then you seem to be easily sexually excited in the real world, too. If we show very explicit sex pictures, eventually everyone’s brain responds strongly. It is those weaker images, just hinting at sex, that show the difference.”

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Better cognition seen with gene variant carried by 1 in 5 people


Finding could have implications for treating age-related diseases like Alzheimer’s.

A scientific team led by the Gladstone Institutes and UC San Francisco has discovered that a common form of a gene already associated with long life also improves learning and memory, a finding that could have implications for treating age-related diseases like Alzheimer’s.

The researchers found that people who carry a single copy of the KL-VS variant of the KLOTHO gene perform better on a wide variety of cognitive tests. When the researchers modeled the effects in mice, they found it strengthened the connections between neurons that make learning possible – what is known as synaptic plasticity – by increasing the action of a cell receptor critical to forming memories.

The discovery is a major step toward understanding how genes improve cognitive ability and could open a new route to treating diseases like Alzheimer’s. Researchers have long suspected that some people may be protected from the disease because of their greater cognitive capacity, or reserve. Since elevated levels of the klotho protein appear to improve cognition throughout the lifespan, raising klotho levels could build cognitive reserve as a bulwark against the disease.

“As the world’s population ages, cognitive frailty is our biggest biomedical challenge,” said Dena Dubal, M.D., Ph.D., assistant professor of neurology, the David A. Coulter Endowed Chair in Aging and Neurodegeneration at UCSF and lead author of the study, published today in Cell Reports. “If we can understand how to enhance brain function, it would have a huge impact on people’s lives.”

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Blood-pressure drug prevents epilepsy after brain injury


Drug may forestall further brain damage caused by seizures in those with epilepsy.

Daniela Kaufer, UC Berkeley

Between 10 and 20 percent of all cases of epilepsy result from severe head injury, but a new drug promises to prevent post-traumatic seizures and may forestall further brain damage caused by seizures in those who already have epilepsy.

A team of researchers from UC Berkeley, Ben-Gurion University in Israel and Charité-University Medicine in Germany reports in the current issue of the journal Annals of Neurology that a commonly used hypertension drug prevents a majority of cases of post-traumatic epilepsy in a rodent model of the disease. If independent experiments now under way in rats confirm this finding, human clinical trials could start within a few years.

“This is the first-ever approach in which epilepsy development is stopped, as opposed to common drugs that try to prevent seizures once epilepsy develops,” said co-author Daniela Kaufer, UC Berkeley associate professor of integrative biology and a member of the Helen Wills Neuroscience Institute. “Those drugs have a very limited success and many side effects, so we are excited about the new approach.”

The team, led by Kaufer; neurosurgeon Alon Friedman, associate professor of physiology and neurobiology at the Ben-Gurion University of the Negev; and Uwe Heinemann of the Charite, provides the first explanation for how brain injury caused by a blow to the head, stroke or infection leads to epilepsy. Based on 10 years of collaborative research, their findings point a finger at the blood-brain barrier – the tight wall of cells lining the veins and arteries in the brain that is breached after trauma.

“This study for the first time offers a new mechanism and an existing, FDA-approved drug to potentially prevent epilepsy in patients after brain injuries or after they develop an abnormal blood-brain barrier,” Friedman said.

The drug, losartan (Cozaar), prevented seizures in 60 percent of the rats tested, when normally 100 percent of the rats develop seizures after injury. In the 40 percent of rats that did develop seizures, they averaged about one quarter the number of seizures typical for untreated rats. Another experiment showed that administration of losartan for three weeks at the time of injury was enough to prevent most cases of epilepsy in normal lab rats in the following months.

“This is a very exciting result, telling us that the drug worked to prevent the development of epilepsy and not by suppressing the symptoms,” Kaufer said.

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Private partnerships for public benefit


Nobel laureate’s research into neurodegenerative diseases gets boost from Japanese firm.

Nobel laureate Stanley Prusiner (left), director of the UCSF Institute of Neurodegenerative Diseases, recently launched a partnership with pharmaceutical company Daiichi Sankyo that will accelerate his research into prion diseases. He credits the partnership largely to groundwork laid by IND’s associate director, David Ramsay (right).

Stanley Prusiner, M.D., is used to overcoming challenges in his career.

In 1982, as a UC San Francisco junior faculty member in the Department of Neurology, Prusiner published an article describing his discovery of an unprecedented class of pathogens that he named “prions.” These infectious proteins are now understood to be involved in numerous neurodegenerative diseases in humans and animals, including Alzheimer’s, Parkinson’s, frontotemporal dementia and Creutzfeldt-Jakob disease (CJD).

The article sparked a firestorm at the time.

Prusiner’s contention that a protein alone could be infectious flew in the face of the commonly held scientific belief that infections could only be transmitted by viruses, bacteria, fungi and parasites – all of which have genomes composed of either DNA or RNA. Proteins, however, are composed of amino acids.

Despite what he described as a “torrent of criticism” from the scientific community, the media and even funders of his research, Prusiner remained undeterred. He took comfort in the unwavering support of close colleagues, and mounting scientific evidence – much of it stemming his UCSF lab – that backed his claims.

The groundbreaking work led to Prusiner’s 1997 Nobel Prize in Physiology or Medicine.

“People often ask me why I persisted in doing research on a subject that was so controversial,” Prusiner said in his Nobel acceptance speech. “I frequently respond by telling them that only a few scientists are granted the great fortune to pursue topics that are so new and different that only a small number of people can grasp [their] meaning initially.”

In the decades since his discovery, Prusiner – now director of the Institute for Neurodegenerative Diseases (IND) at UCSF – has been committed to getting answers about prion diseases, and ultimately treatments and cures.

Even with a Nobel Prize under his belt, the road continues to pose challenges.

Federal funding from the National Institutes of Health (NIH) has been crucial to his research, but the recent recession – and resulting sequestration – highlighted the need to strengthen relationships with private industry. In 2013, the NIH awarded a total of $22.5 billion in funding to U.S. institutions, the lowest amount since 2003.

But this month, Prusiner’s work got a huge boost from an exciting new collaboration between the IND and the Japan-based global pharmaceutical company Daiichi Sankyo Co. Ltd. It will focus on developing therapeutics and molecular diagnostics for multiple neurodegenerative diseases.

“Alzheimer’s alone kills as many people every year as cancer does, but it only receives one-tenth of the funding that we dedicate to cancer research. This collaboration won’t fill that funding gap, but it will offer the tremendous value of Daiichi Sankyo’s scientific expertise to make progress on these diseases,” he said.

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