TAG: "Neuroscience"

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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Kids with autism, SPD show brain wiring differences


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

Pratik Mukherjee, UC San Francisco

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

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

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

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

Elysa Marco, UC San Francisco

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

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

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Aging brain influenced by experiences throughout life


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

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

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

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

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

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

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Study links autistic behaviors to enzyme


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

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

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

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

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

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

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$1M grant funds study into neurochemistry behind addiction


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

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

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

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

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