TAG: "Neuroscience"

UC receives nearly a quarter of NIH brain research grants


14 projects are led by researchers from six UC campuses.

The National Institutes of Health awarded UC researchers nearly a quarter of the $46 million in grants announced today (Sept. 30) in support of President Barack Obama’s BRAIN Initiative.

UC scientists have long been at the frontline of efforts to understand the brain’s inner workings — a pre-eminence reflected by the grants: Of the 58 NIH awards, 14 are projects led by researchers from UC Berkeley, UC Davis, UC Irvine, UCLA, UC San Diego and UC San Francisco.

Collectively, UC researchers will receive more than $10 million of the $46 million that the NIH is awarding for 2014.

“The human brain is the most complicated biological structure in the known universe. We’ve only just scratched the surface in understanding how it works — or, unfortunately, doesn’t quite work when disorders and disease occur,” said NIH Director Dr. Francis S. Collins in a statement. “There’s a big gap between what we want to do in brain research and the technologies available to make exploration possible.”

The BRAIN Initiative was launched last year by Obama as a large-scale federal effort to help scientists develop new tools and technologies to gain a deeper understanding of how the brain functions and to accelerate the creation of new treatments for neurological disorders.

“These initial awards are part of a 12-year scientific plan focused on developing the tools and technologies needed to make the next leap in understanding the brain,” Collins said. “This is just the beginning of an ambitious journey and we’re excited about the possibilities.”

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‘Frenemy’ in Parkinson’s takes to crowdsourcing


Protein regulates neuronal communication by self-association.

The protein alpha-synuclein is a well-known player in Parkinson’s disease and other related neurological conditions, such as dementia with Lewy bodies. Its normal functions, however, have long remained unknown. An enticing mystery, say researchers, who contend that understanding the normal is critical in resolving the abnormal.

Alpha-synuclein typically resides at presynaptic terminals – the communication hubs of neurons where neurotransmitters are released to other neurons. In previous studies, Subhojit Roy, M.D., Ph.D., and colleagues at the UC San Diego School of Medicine had reported that alpha-synuclein diminishes neurotransmitter release, suppressing communication among neurons. The findings suggested that alpha-synuclein might be a kind of singular brake, helping to prevent unrestricted firing by neurons. Precisely how, though, was a mystery.

Then Harvard University researchers reported in a recent study that alpha-synuclein self-assembles multiple copies of itself inside neurons, upending an earlier notion that the protein worked alone. And in a new paper, published this month in Current Biology, Roy, a cell biologist and neuropathologist in the departments of pathology and neurosciences, and co-authors put two and two together, explaining how these aggregates of alpha-synuclein, known as multimers, might actually function normally inside neurons.

First, they confirmed that alpha-synuclein multimers do in fact congregate at synapses, where they help cluster synaptic vesicles and restrict their mobility. Synaptic vesicles are essentially tiny packages created by neurons and filled with neurotransmitters to be released. By clustering these vesicles at the synapse, alpha-synuclein fundamentally restricts neurotransmission. The effect is not unlike a traffic light – slowing traffic down by bunching cars at street corners to regulate the overall flow.

“In normal doses, alpha-synuclein is not a mechanism to impair communication, but rather to manage it. However it’s quite possible that in disease, abnormal elevations of alpha-synuclein levels lead to a heightened suppression of neurotransmission and synaptic toxicity,” said Roy.

“Though this is obviously not the only event contributing to overall disease neuropathology, it might be one of the very first triggers, nudging the synapse to a point of no return. As such, it may be a neuronal event of critical therapeutic relevance.”

Indeed, Roy noted that alpha-synuclein has become a major target for potential drug therapies attempting to reduce or modify its levels and activity.

Co-authors include Lina Wang, Utpal Das and Yong Tang, UC San Diego; David Scott, Massachusetts Institute of Technology; and Pamela J. McLean, Mayo Clinic-Jacksonville.

Funding support for this research came from National Institutes of Health (grant P50AG005131-project 2) and the UC San Diego Alzheimer’s Disease Research Center.

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Seeding innovations in brain research


UC Berkeley, UCSF, Berkeley Lab join forces on BRAINseed collaboration.

Michel Maharbiz of electrical engineering and computer science describes a project to probe more deeply into the cerebral cortex. (Photo by Roy Kaltschmidt, Berkeley Lab)

Two state-of-the-art research areas – nanotech and optogenetics – were the dominant theme last Thursday, Sept. 18, as six researchers from UC Berkeley, UC San Francisco and Lawrence Berkeley National Laboratory sketched out their teams’ bold plans to jump-start new brain research.

The rapid-fire talks kicked off a one-of-a-kind collaboration among the three institutions in which each put up $1.5 million over three years to seed innovative but risky research. Called BRAINseed, the partnership could yield discoveries that accelerate President Barack Obama’s national BRAIN (Brain Research through Advancing Innovative Neurotechnologies) Initiative and California’s own Cal-BRAIN Initiative.

“It’s clear to everybody that any attempt to understand how the brain works, or ultimately what we might mean by cognition, is so daunting and so large that no one institution could hope to be a stand-alone leader in such an effort,” said Graham Fleming, UC Berkeley vice chancellor for research. “The synergies between UCSF, Lawrence Berkeley National Lab and UC Berkeley are very strong, and we complement one another in very effective ways.”

“This tri-partnership is unprecedented in the history of our institutions,” noted Horst Simon, deputy director of Berkeley Lab. “We are putting money down to fund a real collaboration that makes people sit down together and address some of the most challenging questions today.”

“BRAINseed underscores the tremendous power embodied in the institutions in the Bay Area, and the potential for amazing things to happen if we can overcome the geographical separations,” said Keith Yamamoto, UCSF vice chancellor for research.

When Obama announced the federal BRAIN Initiative in April 2013, he allocated $110 million for fiscal year 2014. This funding is already supporting several projects at UC Berkeley. Obama has proposed even more funding in future years “to revolutionize our understanding of the human mind and uncover new ways to treat, prevent, and cure brain disorders like Alzheimer’s, schizophrenia, autism, epilepsy and traumatic brain injury.”

Similarly, Cal-BRAIN — short for California Blueprint for Research to Advance Innovations in Neuroscience — aims to “accelerate the development of brain mapping techniques, including the development of new technologies.” The initial appropriation in this year’s state budget was $2 million.

Both Cal-BRAIN and the national initiative are expected to spur new startups in the area of neurotechnology based on the tools and inventions created in research labs. The innovations developed through these initiatives could have broad applications in disease monitoring beyond the brain and even outside the health care field.

“What we want to do is build a climate of collaboration so that we are stronger competitors in the national brain program and Cal-BRAIN,” Fleming said. “We see BRAINseed as a model for future collaborations (among the three institutions).”

Probing deeper into the brain

The six winning projects of 17 proposals originally submitted focus on new methods of mapping the brain and studying neurons deeper in the brain than ever before.

Fiberless deep brain imaging: Using novel nanocrystals developed by Bruce Cohen at Lawrence Berkeley National Laboratory, and biosensing and bioactuating molecules synthesized by Chris Chang and Ehud Isacoff at UC Berkeley, researchers hope to probe cell-to-cell communication deeper in the brain than ever before. The technique takes advantage of the fact that near infrared (NIR) light with its shorter wavelengths penetrates deeper into the brain than does visible light. The nanocrystals from Cohen’s lab absorb the NIR light and convert it into visible light. The visible light can then trigger optogenetic photoswitches that turn neuron receptors on and off, as well as activate biosensors that record the release of neurotransmitters at the synapse. Coupled with techniques developed by Charly Craik and Robert Edwards at UCSF for targeting probes to specific cells, the researchers on this project hope to be able to study cell signaling in the many layers of the cortex.

Integrated nanosystems: Our senses of touch and hearing, as well as our ability to feel pain and detect the position of our body in space, are all made possible by a special class of proteins known as mechanoreceptors. Scientists studying this system in cell culture have traditionally used micropipettes to apply pressure to mechanoreceptors, while microelectrodes record the resulting neural activity. But small as they are, these devices are much too bulky to precisely stimulate single receptors or make accurate neural recordings. A team led by UCSF’s Young-wook Jun is devising a system to overcome these limitations. In the new setup, magnetic nanoparticles controlled by micromagnetic “tweezers” will have the capacity to stimulate individual mechanoreceptors, and high-resolution optical signals emitted by “quantum dots,” developed in the lab of Paul Alivisatos of UC Berkeley and Berkeley Lab, will offer a truer picture of neural activity in sensory neurons. They will collaborate with UCSF’s Yuh Nung Jan.

In vivo optogenetic mechanisms: We think of the action of neurotransmitters as rapid and localized, but the effects of acetylcholine (ACh) in the brain are actually quite diffuse and unfold slowly. The hormone-like characteristics of ACh make it difficult to understand through conventional neurophysiology experiments. As a result, ACh transmission, which plays a role in Alzheimer’s and Parkinson’s diseases and in addiction, is poorly understood despite decades of study. UC Berkeley’s Richard Kramer has devised a system that enables researchers to use light to switch ACh receptors on and off in animals. Using this system, Kramer and UCSF’s Michael P. Stryker will be able to study how ACh modulates behavior in a wholly new way.

Acousto-optic virtual waveguides: Optogenetics approaches to probe the brain’s grey matter, or cortex, work only as deep as the light can penetrate, typically only a fraction of a millimeter below the surface. UC Berkeley engineers have developed a novel way to channel light deeper – more than a millimeter deep – to probe cell-to-cell signaling. Engineer Michel Maharbiz proposes to use ultrasound to create ‘waveguides’ that can steer light below the surface of the cortex, stimulating photoswitches that enable the study of neurotransmitters. With light-sensitive probes developed at Berkeley Lab and cell-imaging techniques from UCSF, the technology would open new avenues for non-invasive in-vivo imaging and stimulation of local brain areas. Maharbiz’s collaborators are Jim Schuck of Berkeley Lab, Reza Alam of UC Berkeley and Vikaas Singh Sohal of UCSF.

Optical integrators of neuronal activity: One of the greatest challenges in understanding the brain is connecting what happens over large volumes and hundreds of thousands of neurons to the signals transmitted at the individual synapse, the connection between nerve cells where communication takes place. Because calcium is key to neuronal signaling, a team led by Evan Miller, UC Berkeley assistant professor of molecular and cell biology and of chemistry, plans to use probes developed in his lab that ‘remember’ calcium concentration. Along with co-collaborators Pam den Besten and Terumi Kohwi-Shigematsu at UCSF and Berkeley Lab, respectively, Miller plans to investigate neuronal activity in models of disease. They can then correlate this with what happens over a larger volume of the brain. The technique combines “click chemistry” pioneered at UC Berkeley with probes generated in the Department of Chemistry to integrate images over different scales. This technique is a vital first step in developing tools that remember neuronal activity and enable 3D reconstruction of activity across entire brain regions with cellular resolution.

Development of instrumentation and computational methods: Though great progress has been made in mapping the function of the human brain, researchers have been stymied by limitations in both recording devices and the ability to analyze and understand brain signals. UCSF’s Edward F. Chang, M.D., is leading a team that aims to achieve up to a thousandfold increase in the density and electronic sophistication of recording arrays. The vast amount of data collected by these arrays will be stored and analyzed by some of the world’s most powerful computers at the National Energy Research Scientific Computing Center (NERSC), enabling a new level of understanding of the brain in both health and disease. Chang’s collaborators are Peter Denes and Kristofer Bouchard of Berkeley Lab and Fritz Sommer of UC Berkeley.

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‘Dimmer switch’ discovered for mood disorders


UC San Diego study’s findings have implications for how to treat depression.

Basal ganglia neurons (green) feed into the brain and release glutamate (red) and GABA (blue) and sometimes a mix of both neurotransmitters (white).

Researchers at the UC San Diego School of Medicine have identified a control mechanism for an area of the brain that processes sensory and emotive information that humans experience as “disappointment.”

The discovery of what may effectively be a neurochemical antidote for feeling let-down is reported today (Sept. 18) in the online edition of Science.

“The idea that some people see the world as a glass half empty has a chemical basis in the brain,” said senior author Roberto Malinow, M.D., Ph.D., professor in the Department of Neurosciences and neurobiology section of the Division of Biological Sciences. “What we have found is a process that may dampen the brain’s sensitivity to negative life events.”

Because people struggling with depression are believed to register negative experiences more strongly than others, the study’s findings have implications for understanding not just why some people have a brain chemistry that predisposes them to depression but also how to treat it.

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Neural compensation found in people with Alzheimer’s-related protein


Study provides evidence of plasticity in aging brain that appears to be beneficial.

Shown are scans that represent all subjects with beta-amyloid deposits in their brain. The yellow and orange colors show areas where greater brain activation was associated with the formation of more detailed memories. (Image courtesy of Jagust Lab)

The human brain is capable of a neural workaround that compensates for the buildup of beta-amyloid, a destructive protein associated with Alzheimer’s disease, according to a new study led by UC Berkeley researchers.

The findings, published today (Sept. 14) in the journal Nature Neuroscience, could help explain how some older adults with beta-amyloid deposits in their brain retain normal cognitive function while others develop dementia.

“This study provides evidence that there is plasticity or compensation ability in the aging brain that appears to be beneficial, even in the face of beta-amyloid accumulation,” said study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the School of Public Health and Lawrence Berkeley National Laboratory.

Previous studies have shown a link between increased brain activity and beta-amyloid deposits, but it was unclear whether the activity was tied to better mental performance.

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Brain inflammation disrupts memory retrieval networks


UC Irvine research sheds light on cognitive losses seen with chemotherapy.

In their study, UCI neurobiologists Jennifer Czerniawski and John Guzowski show for the first time a link among immune system activation, altered neural circuit function and impaired discrimination memory.

Brain inflammation can rapidly disrupt our ability to retrieve complex memories of similar but distinct experiences, according to UC Irvine neuroscientists Jennifer Czerniawski and John Guzowski.

Their study – which appears today in The Journal of Neuroscience – specifically identifies how immune system signaling molecules, called cytokines, impair communication among neurons in the hippocampus, an area of the brain critical for discrimination memory. The findings offer insight into why cognitive deficits occurs in people undergoing chemotherapy and those with autoimmune or neurodegenerative diseases.

Moreover, since cytokines are elevated in the brain in each of these conditions, the work suggests potential therapeutic targets to alleviate memory problems in these patients.

“Our research provides the first link among immune system activation, altered neural circuit function and impaired discrimination memory,” said Guzowski, the James L. McGaugh Chair in the Neurobiology of Learning & Memory. “The implications may be beneficial for those who have chronic diseases, such as multiple sclerosis, in which memory loss occurs and even for cancer patients.”

What he found interesting is that increased cytokine levels in the hippocampus only affected complex discrimination memory, the type that lets us differentiate among generally similar experiences – what we did at work or ate at dinner, for example. A simpler form of memory processed by the hippocampus – which would be akin to remembering where you work – was not altered by brain inflammation.

In the study, Czerniawski, a UCI postdoctoral scholar, exposed rats to two similar but discernable environments over several days. They received a mild foot shock daily in one, making them apprehensive about entering that specific site. Once the rodents showed that they had learned the difference between the two environments, some were given a low dose of a bacterial agent to induce a neuroinflammatory response, leading to cytokine release in the brain. Those animals were then no longer able to distinguish between the two environments.

Afterward, the researchers explored the activity patterns of neurons – the primary cell type for information processing – in the rats’ hippocampi using a gene-based cellular imaging method developed in the Guzowski lab. In the rodents that received the bacterial agent (and exhibited memory deterioration), the networks of neurons activated in the two environments were very similar, unlike those in the animals not given the agent (whose memories remained strong). This finding suggests that cytokines impaired recall by disrupting the function of these specific neuron circuits in the hippocampus.

“The cytokines caused the neural network to react as if no learning had taken place,” said Guzowski, associate professor of neurobiology & behavior. “The neural circuit activity was back to the pattern seen before learning.”

The work may also shed light on a chemotherapy-related mental phenomenon known as “chemo brain,” in which cancer patients find it difficult to efficiently process information. UCI neuro-oncologists have found that chemotherapeutic agents destroy stem cells in the brain that would have become neurons for creating and storing memories.

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Study ties honesty to prefrontal region of brain


Results indicate that willpower is necessary for honesty when it is advantageous to lie.

Are humans programmed to tell the truth? Not when lying is advantageous, says a new study led by assistant professor Ming Hsu at UC Berkeley’s Haas School of Business. The report ties honesty to a region of the brain that exerts control over automatic impulses.

Hsu, who heads the Neuroeconomics Laboratory at the Haas School of Business and holds a joint appointment with the Helen Wills Neuroscience Institute, said the results, just published in the journal Nature Neuroscience, indicate that willpower is necessary for honesty when it is personally advantageous to lie.

It is well-established that the brain’s dorsolateral prefrontal cortex is important for exerting control over impulses, but the role of this region in honesty and deception has been a matter of debate.

“So far, studies investigating the role of the dorsolateral prefrontal cortex in honesty have primarily used correlational methods, like neuroimaging,” said study co-author Adrianna Jenkins of the Neuroeconomics Laboratory. “So it hasn’t been clear whether this region is involved in curbing honesty or enabling it.”

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How sleep impacts PTSD


Fragmented REM sleep may hinder effective treatment of post-traumatic stress disorder.

The effectiveness of post-traumatic stress disorder (PTSD) treatment may hinge significantly upon sleep quality, report researchers at the UC San Diego School of Medicine and Veterans Affairs San Diego Healthcare System in a paper published today (Aug. 26) in the Journal of Neuroscience.

“I think these findings help us understand why sleep disturbances and nightmares are such important symptoms in PTSD,” said Sean P.A. Drummond, Ph.D., professor of psychiatry and director of the Behavioral Sleep Medicine Program at the VA San Diego Healthcare System. “Our study suggests the physiological mechanism whereby sleep difficulties can help maintain PTSD. It also strongly implies a mechanism by which poor sleep may impair the ability of an individual to fully benefit from exposure-based PTSD treatments, which are the gold standard of interventions.

“The implication is that we should try treating sleep before treating the daytime symptoms of PTSD and see if those who are sleeping better when they start exposure therapy derive more benefit.”

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UC scientists awarded 8 grants in support of BRAIN Initiative


Projects seek to gain understanding of the brain.

Eight University of California scientists are among 36 recipients nationwide who have been awarded early concept grants for brain research from the National Science Foundation, the agency announced today (Aug. 18).

The awards were made to fund research projects that the federal science agency determined could produce “potentially transformative insights into understanding the brain.” The funding comes from the agency’s allocation for President Obama’s BRAIN Initiative, a multi-agency research effort that seeks to accelerate the development of new neurotechnologies that promise to help researchers answer fundamental questions about how the brain works.

The NSF’s 36 early concept grant awards, which total $10.8 million, are intended to “enable new technologies to better understand how complex behaviors emerge from the activity of brain circuits,” the agency said.

Each of these Early Concept Grants for Exploratory Research, or EAGER, awards will receive $300,000 over a two-year period to “develop a range of conceptual and physical tools, from real-time whole brain imaging, to new theories of neural networks, to next-generation optogenetics,” the NSF said.

UC scientists played a major role in the creation of Obama’s BRAIN initiative in April 2013 and also led a similar state initiative that, two months ago, was awarded $2 million in the budget signed into law by Gov. Jerry Brown. The state’s research grant effort, known as Cal-BRAIN – short for California Blueprint for Research to Advance Innovations in Neuroscience – aims to “accelerate the development of brain mapping techniques, including the development of new technologies.”

“These awards are yet another manifestation of the excellence of our neuroscience faculty and our long tradition in neuroscience research, which were key factors in building the number one ranked neuroscience graduate program in the nation and establishing our Kavli Institute for Brain and Mind,” said UC San Diego Chancellor Pradeep K. Khosla.

UC early concept grant awardees include:

UC Berkeley
Ehud Isacoff

UC Davis
Martin Usrey
Karen Zito

UC San Diego
Brenda Bloodgood
Andrea Chiba
David Kleinfeld
Charles Stevens

UC San Francisco
Steven Finkbeiner

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Mapping the infant brain


Findings may be key in identifying, treating earliest signs of neurodevelopmental disorders.

A recent study conducted by researchers at the UC San Diego School of Medicine and the University of Hawaii demonstrates a new approach to measuring early brain development of infants, resulting in more accurate whole brain growth charts and providing the first estimates for growth trajectories of subcortical areas during the first three months after birth. Assessing the size, asymmetry and rate of growth of different brain regions could be key in detecting and treating the earliest signs of neurodevelopmental disorders, such as autism or perinatal brain injury.

The study will be published in JAMA Neurology today (Aug. 11).

For the first time, researchers used magnetic resonance imaging (MRI) of the newborn brain to calculate the volume of multiple brain regions and to map out regional growth trajectories during the infant’s first 90 days of life. The study followed the brain growth of full term and premature babies with no neurological or major health issues.

“A better understanding of when and how neurodevelopmental disorders arise in the postnatal period may help assist in therapeutic development, while being able to quantify related changes in structure size would likely facilitate monitoring response to therapeutic intervention. Early intervention during a period of high neuroplasticity could mitigate the severity of the disorders in later years,” said Dominic Holland, Ph.D., first author of the study and researcher in the Department of Neurosciences at UC San Diego School of Medicine.

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Target ID’d for rare inherited neurological disease in men


Finding provides insight for Kennedy’s disease, other neurodegenerative diseases.

Researchers at the UC San Diego School of Medicine have identified the mechanism by which a rare, inherited neurodegenerative disease causes often crippling muscle weakness in men, in addition to reduced fertility.

The study, published today (Aug. 10) in the journal Nature Neuroscience, shows that a gene mutation long recognized as a key to the development of Kennedy’s disease impairs the body’s ability to degrade, remove and recycle clumps of “trash” proteins that may otherwise build up on neurons, progressively impairing their ability to control muscle contraction. This mechanism, called autophagy, is akin to a garbage disposal system and is the only way for the body to purge itself of non-working, misshapen trash proteins.

“We’ve known since the mid-1990s that Alzheimer’s disease, Parkinson’s disease and Huntington’s disease are caused by the accumulation of misfolded proteins that should have been degraded, but cannot be turned over,” said senior author Albert La Spada, M.D., Ph.D. and professor of pediatrics, cellular and molecular medicine, and neurosciences. “The value of this study is that it identifies a target for halting the progression of protein build-up, not just in this rare disease, but in many other diseases that are associated with impaired autophagy pathway function.”

Of the 400 to 500 men in the U.S. with Kennedy’s disease, the slow but progressive loss of motor function results in about 15 to 20 percent of those with the disease becoming wheelchair bound during later stages of the disease.

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Gaining insights into the nervous system


Rita Allen Foundation Scholarship supports brain imaging studies.

Neuron picture: synaptic terminal of cortical layer2/3 neurons labeled with targeted genetically encoded sensors of neural activity.

Lin Tian’s fascination with neuroscience stems from a deep curiosity about the complexity and elegance of the human brain. As one of only five scientists in the U.S. and Canada — and the first at UC Davis — to be named a 2014 Rita Allen Foundation Scholar, Tian will be developing optical sensors and applications to acquire fundamental insights about how the nervous system functions in health and disease.

“The functioning brain receives thousands of chemical and electrical signals at the synapse, the area of connection between neurons,” Tian said. “Understanding how neurons integrate these multiple inputs to transmit information and to shape and refine the neural circuitry itself is an important area of research that can shed light on an array of neurological disorders, including depression, addiction, autism, schizophrenia and epilepsy.”

With a five-year, $500,000 grant from the Rita Allen Foundation, Tian will develop imaging tools to obtain a comprehensive view of both excitatory and inhibitory synapses in action at the cellular, tissue and whole-animal levels. She also will apply these tools to uncover the functional organization of cortical layer1 (L1) interneurons in shaping long-range interactions and their link to behavior, which can’t be done with current technology, Tian said.

“Understanding how information is transferred across neural circuitry and systems is the key to innovation in the treatment of neurological disorders,” she said.

Tian is an assistant professor of biochemistry and molecular medicine at UC Davis. She holds a bachelor’s degree in neuroscience from the University of Science and Technology of China and a doctorate in biochemistry, molecular and cell biology from Northwestern University. She completed her postdoctoral training at Howard Hughes Medical Institute Janelia Farm.

Since 1976, more than one hundred young leaders in biomedical science have been selected as Rita Allen Foundation Scholars. The program embraces innovative research with above-average risk and promise. Scholars have gone on to win the Nobel Prize in Physiology or Medicine, the National Medal of Science, the Wolf Prize in Medicine, and the Breakthrough Prize in Life Sciences.

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