News and Announcements from the Semel Institute and Department of Psychiatry at UCLA

First-time Internet users find boost in brain function after just one week

Rob — Mon, 19 Oct 2009 17:00:00 +0000

You can teach an old dog new tricks, say UCLA scientists who found that middle-aged and older adults with little Internet experience were able to trigger key centers in the brain that control decision-making and complex reasoning after just one week of surfing the Web. The findings, presented Oct. 19 at the 2009 meeting of the Society for Neuroscience, suggest that Internet training can stimulate neural activation patterns and could potentially enhance brain function and cognition in older adults.

As the brain ages, a number of structural and functional changes occur, including atrophy, reductions in cell activity and increases in deposits of amyloid plaques and tau tangles, which can impact cognitive function. Research has shown that mental stimulation similar to that which occurs in individuals who frequently use the Internet may affect the efficiency of cognitive processing and alter the way the brain encodes new information.

"We found that for older people with minimal experience, performing Internet searches for even a relatively short period of time can change brain activity patterns and enhance function," said study author Dr. Gary Small, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA and the author of "iBrain," a book that describes the impact of new technology on the brain and behavior. The UCLA team worked with 24 neurologically normal volunteers between the ages of 55 and 78. Prior to the study, half the participants used the Internet daily, while the other half had very little experience. Age, educational level and gender were similar between the two groups. Study participants performed Web searches while undergoing functional magnetic resonance imaging (fMRI) scans, which recorded the subtle brain-circuitry changes experienced during this activity. This type of scan tracks brain activity by measuring the level of cerebral blood flow during cognitive tasks.

After the initial brain scan, participants went home and conducted Internet searches for one hour a day for a total of seven days over a two-week period. These practice searches involved using the Internet to answer questions about various topics by exploring different websites and reading information. Participants then received a second brain scan using the same Internet simulation task but with different topics. The first scan of participants with little Internet experience demonstrated brain activity in regions controlling language, reading, memory and visual abilities, which are located in the frontal, temporal, parietal, visual and posterior cingulate regions, researchers said. The second brain scan of these participants, conducted after the practice Internet searches at home, demonstrated activation of these same regions, as well as triggering of the middle frontal gyrus and inferior frontal gyrus — areas of the brain known to be important in working memory and decision-making. Thus, after Internet training at home, participants with minimal online experience displayed brain activation patterns very similar to those seen in the group of savvy Internet users — after just a brief period of time.

"The results suggest that searching online may be a simple form of brain exercise that might be employed to enhance cognition in older adults," said Teena D. Moody, the study's first author and a senior research associate at the Semel Institute at UCLA. When performing an Internet search, the ability to hold important information in working memory and to extract the important points from competing graphics and words is essential, Moody noted. Previous research by the UCLA team found that searching online resulted in a more than twofold increase in brain activation in older adults with prior experience, compared with those with little Internet experience. According to Small, the new findings suggest that it may take only days for those with minimal experience to match the activity levels of those with years of experience. Additional studies may address the impact of the Internet on younger individuals and help identify aspects of online searching that generate the greatest levels of brain activation.

The study was funded by the Parvin Foundation. Susan Y. Bookheimer, professor of psychiatry and biobehavioral sciences at the Semel Institute at UCLA, was also an author of this study. Himaja Gaddipati, a UCLA neuroscience student, and Jennifer Brace, a UCLA doctoral student in neuroscience, contributed to the work.

For more news, visit the UCLA Newsroom or follow us on Twitter.

Author:

Rachel Champeau

Center on Aging

Where religious belief and disbelief meet in the brain

Rob — Thu, 01 Oct 2009 00:00:00 +0000

When it comes to religion, believers and nonbelievers appear to think very differently. But at the level of the brain, is believing in God different from believing that the sun is a star or that 4 is an even number? While religious faith remains one of the most significant features of human life, little is known about its relationship to ordinary belief. Nor is it known whether religious believers differ from nonbelievers in how they evaluate statements of fact. In the first neuroimaging study to systematically compare religious faith with ordinary cognition, UCLA and University of Southern California researchers have found that while the human brain responds very differently to religious and nonreligious propositions, the process of believing or disbelieving a statement, whether religious or not, seems to be governed by the same areas in the brain. The study also found that devout Christians and nonbelievers use the same brain regions to judge the truth of religious and nonreligious propositions. The results, the study authors say, represent a critical advance in the psychology of religion. The paper appears Sept. 30 in the journal PLoS ONE (www.plosone.org). Sam Harris, who recently completed his doctoral dissertation in the lab of Mark Cohen, a professor of psychiatry at the UCLA Staglin Center for Cognitive Neuroscience, was a lead author on the study. Jonas Kaplan, a research assistant professor at the USC's Brain and Creativity Institute, was the co-lead author. The study involved 30 adults — 15 committed Christians and 15 nonbelievers — who underwent three functional MRI (fMRI) scans while evaluating religious and nonreligious statements as "true" or "false." The statements were designed to produce near perfect agreement between the two groups during nonreligious trials (e.g., "Eagles really exist") and near perfect disagreement during religious trials (e.g., "Angels really exist"). Contrasting belief and disbelief yielded increased activity in the ventromedial prefrontal cortex (VMPFC), an area of the brain thought to be involved in reward and in judgments of self-relevance. "This region showed greater activity whether subjects believed statements about God, the Virgin Birth, etc., or statements about ordinary facts," the authors said. The case for belief being content-independent was further bolstered by the fact that while the trial statements accepted by religious believers were rejected by nonbelievers, and vice versa, the brains of both showed the same pattern of activity for belief and disbelief. A comparison of all religious with all nonreligious statements suggested that religious thinking is more associated with brain regions that govern emotion, self-representation and cognitive conflict in both believers and nonbelievers, while thinking about ordinary facts is more reliant upon memory retrieval networks. Activity in the brain's anterior cingulate cortex, an area associated with cognitive conflict and uncertainty, suggested that both believers and nonbelievers experienced greater uncertainty when evaluating religious statements. The study raises the possibility that the differences between belief and disbelief may one day be reliably distinguished by neuroimaging techniques. "Despite vast differences in the underlying processing responsible for religious and nonreligious modes of thought," the authors write, "the distinction between believing and disbelieving a proposition appears to transcend content. These results may have many areas of application — ranging from the neuropsychology of religion, to the use of 'belief-detection' as a surrogate for 'lie-detection,' to understanding how the practice of science itself, and truth-claims generally, emerge from the biology of the human brain." Harris is the author of two New York Times best-sellers, "The End of Faith" and "Letter to a Christian Nation," which have been published in more than 15 languages, and is the co-founder and CEO of the The Reason Project. His writing has appeared in Newsweek, the New York Times, the Los Angeles Times, the Times of London, the Boston Globe, the Atlantic and many other journals. Other authors on the study included Cohen, Susan Y. Bookheimer and Marco Iacoboni, of UCLA, and Ashley Curiel, of Pepperdine University. The authors report no conflict of interest. Work in Dr. Cohen's lab is funded by grants from the National Institutes of Health. The UCLA Staglin Center for Cognitive Neuroscience is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders. In addition to conducting fundamental research, the institute's faculty seeks to develop effective treatments for neurological and psychiatric disorders, improve access to mental health services, and shape national health policy regarding neuropsychiatric disorders. For more news, visit the UCLA Newsroom or follow us on Twitter.

Author:

Mark Wheeler

Staglin Center for Cognitive Neuroscience

UCLA researchers develop biomarker for rapid relief of major depression

Rob — Thu, 10 Sep 2009 16:30:00 +0000

UCLA hosts conference on successful aging in a high-tech world Oct. 30

Rob — Tue, 08 Sep 2009 18:50:00 +0000

Why sleep? UCLA scientist delves into one of science's great mysteries

Rob — Thu, 20 Aug 2009 17:50:00 +0000

Sexual minorities more likely to seek mental health services, study finds

Rob — Fri, 14 Aug 2009 00:15:00 +0000

Researchers find genetic link to placebo response in depressive disorder

mood3 — Mon, 20 Jul 2009 07:00:00 +0000

Placebos are a sham — usually mere sugar pills designed to represent "no treatment" in a clinical treatment study. The effectiveness of the actual medication is compared with the placebo to determine if the medication works. And yet, for some people, the placebo works nearly as well as the medication. How well placebos work varies widely among individuals. Why that is so, and why they work at all, remains a mystery, thought to be based on some combination of biological and psychological factors.

Now, researchers at UCLA have found a new explanation: genetics. Dr. Andrew Leuchter, a professor of psychiatry at the UCLA Semel Institute for Neuroscience and Human Behavior, and colleagues report that in people suffering from major depressive disorder, or MDD, genes that influence the brain's reward pathways may modulate the response to placebos. The research appears in the August edition of the Journal of Clinical Psychopharmacology (currently available online by subscription).

Placebos are thought to act by stimulating the brain's central reward pathways by releasing a class of neurotransmitters called monoamines, specifically dopamine and norepinephrine. These are the brain chemicals that make us "feel good." Because the chemical signaling done by monoamines is under strong genetic control, the scientists reasoned that common genetic variations between individuals — called genetic polymorphisms — could influence the placebo response. Researchers took blood samples from 84 people diagnosed with MDD; 32 were given medication and 52 a placebo.

The researchers looked at the polymorphisms in genes that coded for two enzymes that regulate monoamine levels: catechol-O-methyltransferase (COMT) and monoamine oxidase A (MAO-A). Subjects with the highest enzyme activity within the MAO-A polymorphism had a significantly lower placebo response than those with other genotypes. With respect to COMT, those with lower enzyme activity within this polymorphism had a lower placebo response.

"Our findings suggest that patients with MDD who have specific MAO-A and COMT genotypes may be biologically advantaged or disadvantaged in mounting a placebo response, because of the activity of these two enzymes," said Leuchter, who directs the Laboratory of Brain, Behavior and Pharmacology at the UCLA Semel Institute. "To our knowledge, this is the first study to examine the association between MAO-A and COMT polymorphisms and a response to placebo in people who suffer from major depressive disorder," he said. Leuchter noted that this is not the sole explanation for a response to a placebo, which is likely to be caused by many factors, both biological and psychosocial. "But the data suggests that individual differences in response to placebo are significantly influenced by individual genotypes," he said. Including the influence of genotype in the design of clinical trials could facilitate more powerful testing of future treatments, Leuchter said.

Funding for the study was provided by the National Center for Complementary and Alternative Medicine of the National Institutes of Health, Eli Lilly and Co., and Pfizer Inc. Other authors included James McCracken, Aimee Hunter and Ian Cook, all of UCLA, and Jonathan Alpert of Massachusetts General Hospital and Harvard University.

Author disclosure information:

Dr. Andrew Leuchter has provided scientific consultation or served on advisory boards of a number of companies, including Eli Lilly and Co., where he has also served in the speakers bureau. He has received research/grant support from the National Center for Complementary and Alternative Medicine, Eli Lilly and Co., and Pfizer Inc., among others.
Dr. James T. McCracken has served as an adviser and consultant for Eli Lilly and Co. and other companies and receives research support from, among others, Eli Lilly and Co. Aimee M. Hunter has nothing to disclose financially.
Dr. Ian A. Cook has served in the speakers bureau for Pfizer Pharmaceuticals Inc. and other companies and has received research support from, among others, Eli Lilly and Co. and Pfizer Inc.
Dr. Jonathan E. Alpert has served as an adviser and consultant for Eli Lilly and Co. and other companies and has served in the speakers bureau for Eli Lilly and Co. He receives research support from, among others, Eli Lilly and Co. and Pfizer Inc.

The Semel Institute for Neuroscience and Human Behavior is an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders. In addition to conducting fundamental research, institute faculty seek to develop effective treatments for neurological and psychiatric disorders, improve access to mental health services and shape national health policy regarding neuropsychiatric disorders.

Semel Institute for Neuroscience and Human Behavior

UCLA receives grant to study the impact of music on children with autism

mood3 — Mon, 20 Jul 2009 07:00:00 +0000

In June 2009, newspapers reported that archaeologists in Germany had discovered a 35,000-year-old flute made of bird bone. It represented, one paper said, "the earliest known flowering of music-making in Stone Age culture." And we have been tapping our toes, humming along, singing and dancing ever since. The power of music affects all of us and has long appealed to our emotions. It is for this reason that UCLA researchers are using music to help children with autism spectrum disorders (ASD), for whom understanding emotions is a very difficult task. This inability robs them of the chance to communicate effectively and make friends and can often lead to social isolation and loneliness.

Thanks to a grant from the NAMM Foundation, the trade association of the international music products association, Istvan Molnar-Szakacs, a researcher at the UCLA Tennenbaum Center for the Biology of Creativity and member of the of the Help Group–UCLA Autism Research Alliance, and colleagues have developed a music education program designed to help children with ASD better understand emotions and learn to recognize emotions in others. "This is a 'naturalistic study,' in that it takes place not in a lab but in the child's classroom at the Help Group's Village Glen School for children with autism, where they are engaged in music-making," Molnar-Szakacs said. Specifically, the children are using a method of music education known as the Orff-Schulwerk approach.

Developed by 20th-century German composer Carl Orff ("schulwerk" is German for schooling), it is a unique approach to music learning that is supported by movement and based on things that kids intuitively like to do, such as sing, chant rhymes, clap, dance and keep a beat or play a rhythm on anything near at hand. Orff called this music and movement activity "elemental" — basic, unsophisticated and concerned with the fundamental building blocks of music. The 12-week program uses elements from the Orff method — including games, instruments and teamwork — and combines them with musical games. The idea is to pair emotional musical excerpts with matching displays of social emotion (happy with happy, sad with sad, etc.) in a social, interactive setting.

"Music is a birthright of all children. To be able to listen and appreciate, sing or participate in music-making are as essential to development as mathematical or linguistic learning," Molnar-Szakacs said. "The purpose of this work is to provide a means for awakening the potential in every child for being 'musical' — that is, to be able to understand and use music and movement as forms of expression and, through that, to develop a recognition and understanding of emotions." In fact, he said, participating in musical activities has the potential to scaffold and enhance all other learning and development, from timing and language to social skills. "Beyond these more concrete intellectual benefits, the extraordinary power of music to trigger memories and emotions and join us together as an emotional, empathic and compassionate humanity are invaluable," Molnar-Szakacs said.

The goal of the research is to evaluate the effect of the music education program on outcomes in social communication and emotional functioning, as well as the children's musical development, according to Molnar-Szakacs. "Hopefully this will be a fun, engaging and cost-effective therapeutic intervention to help children with ASD recognize and understand emotions in daily life interactions," he said. "An improved ability to recognize social emotions will allow these children to form more meaningful social relationships and hopefully greatly improve their quality of life."

Molnar-Szakacs is collaborating on the grant with Elizabeth A. Laugeson, a UCLA clinical instructor of psychiatry and director of the Help Group–UCLA Autism Research Alliance. The alliance is an innovative partnership between the Help Group and the UCLA Semel Institute for Neuroscience and Human Behavior that is dedicated to enhancing and expanding clinical research in the education and treatment of ASD and contributing to the development, greater understanding and use of best-practice models by researchers, educators and clinicians. The investigators report no conflicts of interest.

The NAMM Foundation is a nonprofit organization dedicated to advancing active participation in music-making across the lifespan by supporting scientific research, philanthropic giving and public service programs from the international music products industry. The Help Group, founded in 1975, serves children with a wide range of special needs and is the largest and most comprehensive nonprofit of its kind in the United States. Recognized as a leader in the field of autism, it offers extensive special education, therapy and assessment services.
The Help Group educates more than 850 students between the ages of 3 and 22 on a daily basis in its highly specialized autism day schools.
The UCLA Tennenbaum Center for the Biology of Creativity has as its mission the study of the molecular, cellular, systems and cognitive mechanisms that result in cognitive enhancements and explain unusual levels of performance in gifted individuals, including extraordinary creativity. It is part of the Semel Institute for Neuroscience and Human Behavior, an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders.

For more news, visit the UCLA Newsroom.

Tennenbaum Center for the Biology of Creativity

UCLA collaboration identifies immune system link to schizophrenia

mood3 — Wed, 01 Jul 2009 07:00:00 +0000

Disruptions also found in cellular pathways involved in memory and cognition

Schizophrenia is a devastating mental disease, thought to be caused by the interaction of both genetic and environmental factors. Because there is no biochemical test that can identify the disorder, physicians rely upon the recognition of its symptoms — which can include auditory hallucinations and paranoia — in order to make their diagnosis.

Now following on their earlier work that identified three gene locations that may be implicated in schizophrenia, researchers at UCLA and colleagues from around the world have, for the first time, identified additional genes that confirm what scientists have long suspected — that the immune system may play a role in the development of the disorder. Further, they have also identified genetic anomalies that disrupt the cellular pathways involved in brain development, memory and cognition, all markers of schizophrenia.

The research appears in the July 1 online edition of the journal Nature. Roel Ophoff, the co-lead author and an assistant professor at the Center for Neurobehavioral Genetics at the UCLA Semel Institute for Neuroscience and Human Behavior, and his collaborators from nearly 50 institutions worldwide, performed a genome-wide scan of 2,663 people diagnosed with schizophrenia and 13,498 controls from eight European locations They were looking for single nucleotide polymorphisms (SNP), genetic variations that are commonly present in the general population but more often present in those suffering from the disorder. In total, nearly 314,000 SNPs were included in their analysis. They found significant associations with genetic markers on the Major Histocompatibility Complex (MHC), a group of genes that controls several aspects of the immune response. Further, they discovered additional variations in two other genes, called NRGN and TCF4, which points to perturbation of pathways involved in brain development, memory and cognition.

"This is another step forward in understanding the biological basis of this disorder, one that robs people of their lives," said Ophoff, who holds a joint appointment at the University of Utrecht, The Netherlands. "It also shows the importance of worldwide collaborations for the study of schizophrenia genetics, because it allows us to do very large numbers of scans." The findings are significant yet not without challenge, said Ophoff, since the study aimed at the "common variants" in the human genome. "In other words," he said, "these are not rare mutations present in only a few individuals, but these genetic variants are abundantly present in the population. Anybody could carry this variant, but that doesn't mean they will necessarily develop the disease. Yet, when you look at the population at large, these variants are more often present in patients than in healthy control subjects." And that’s important, he noted, in developing new techniques to thwart the disease. "Knowing these specific genes are involved in the pathway leading to schizophrenia provides unique clues as to which molecular mechanisms are involved," he said. While the association between schizophrenia and the immune system has long been suspected, the evidence for it has, until now, been mostly circumstantial. And impaired cognitive and memory functions are increasingly being recognized as core features of schizophrenia, which are poorly addressed by current medications. "The three common genetic variants we describe, then, which we feel predisposes certain individuals to schizophrenia, have the potential to be translated into targets for the development of new and novel medications," Ophoff said.

Some 40 other authors and institutions contributed to the paper, and there were multiple funding sources; for UCLA, funding was provided by the National Institute of Mental Health. Other UCLA authors included Dr. Nelson Freimer, director of the Center for Neurobehavioral Genetics and professor of psychiatry, and Rita Cantor, professor of human genetics, both members of the David Geffen School of Medicine. The UCLA authors report no conflicts of interest.

For more news, see UCLA Newsroom.

Center for Neurobehavioral Genetics

Alterations in brain's white matter key to schizophrenia

mood3 — Fri, 19 Jun 2009 07:00:00 +0000

White matter 'integrity' may be predictive of functional outcome

Schizophrenia, a chronic and debilitating disorder marked in part by auditory hallucinations and paranoia, can strike in late adolescence or early adulthood at a time when people are ready to stand on their own two feet as fully independent adults.

Now scientists at UCLA think they are beginning to understand one important piece of this puzzle. In the first study of its kind, the researchers used a novel form of brain imaging to discover that white matter in the brains of adolescents at risk of developing schizophrenia does not develop at the same rate as healthy people. Further, the extent of these alterations can be used to predict how badly patients will or will not deteriorate functionally over time.

Reporting in the online edition of the journal Biological Psychiatry, lead author Katherine Karlsgodt, a postdoctoral fellow in UCLA's Department of Psychology, and senior authors Tyrone Cannon and Carrie Bearden, professors at the UCLA Semel Institute for Neuroscience and Human Behavior, focused on the brain's white matter — which forms the major connections between different brain regions — because it is known that white matter is disrupted in people who already have schizophrenia.

"We found that healthy subjects showed a normal and expected increase in measures indexing white matter integrity in the temporal lobe as they age," said Karlsgodt, "but young people at high-risk for psychosis showed no such increase — that is, they fail to show the normal developmental pattern."

While there is growing evidence that schizophrenics show changes in white matter, and there is increasing evidence that white matter connectivity may be highly relevant to the development of psychosis, there is very little known about how these changes arise, said Karlsgodt. Historically, looking at white matter has been hard to do. But in recent years, she said, researchers have begun to use a relatively new technique, diffusion tensor imaging (DTI) that uses the movement of water molecules along white matter tracts to map out the brain's pathways. In the last few years, these techniques have been applied to research schizophrenia and other disorders.

The researchers studied a control group of 25 healthy individuals and 36 teens and young adults, aged 12 to 26, at very high risk for developing schizophrenia, and followed them over a two-year period. The adolescents were identified as high risk due to genetic factors (i.e., being close relatives of someone with schizophrenia), or because they showed very early clinical symptoms of the disease. All of the subjects underwent a DTI scan at the start of the trial, along with clinical and functional assessments. Follow-up assessments of clinical and functional outcome were done at different periods over the next two years.

Failing to find a normal increase in white matter integrity over time in the at-risk subjects, said Karlsgodt, "suggests there is a fundamental difference in how typically developing young people and high-risk adolescents develop during this period right before the disease would be expected to manifest. Something may go awry with the developmental process during this period that might contribute to the onset of the disorder."

The other important finding, she said, was that by looking at white matter integrity in the temporal lobe at people's first appointment, "we could predict how well they would be functioning 15 months later at work, school and home.

"This is a very exciting finding, because it means we might be closer to being able to identify people who will need more or different treatments in the future, so that we can get them the help they need."

Research was carried out in the Clinical Neuroscience Lab of Tyrone D. Cannon of UCLA, with additional contribution from co-author Tara A. Niendam of the University of California, Davis. Research was supported by the National Institutes of Health, the National Alliance for Research on Schizophrenia and Affective Disorders, and a gift to UCLA by Garen and Shari Staglin. The authors reported no known biomedical financial interests or other potential conflicts of interest.

Karlsgodt, Bearden and Cannon are members of the Center for the Assessment and Prevention of Prodromal States (CAPPS) at the Semel Institute. CAPPS provides clinical, psychosocial and neuropsychological assessments, and psychological and psychiatric treatment. It also conducts other research aimed at early identification and prevention of these at-risk mental states.

The Semel Institute for Neuroscience and Human Behavior is a world-leading, interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders.

For more news, visit the UCLA Newsroom.

Staglin Center for Cognitive Neuroscience

UCLA scientists identify new gene linked to autism risk

mood3 — Thu, 21 May 2009 20:34:49 +0000

Discovery may explain why disorder strikes boys four times more than girls

UCLA scientists have discovered a variant of a gene called CACNA1G that may increase children's risk of developing autism, particularly boys. The journal Molecular Psychiatry publishes the findings in its May 19 advance online edition.

Classic autism strikes four times as many boys as girls. When including the entire spectrum of autism disorders, such as the milder Asperger syndrome, boys are 10 times more likely to be diagnosed than girls. "This is a strong finding," said Dr. Stanley Nelson, professor of human genetics at the David Geffen School of Medicine at UCLA and the study's principal investigator. "No one has scrutinized the role that CACNA1G plays in autism. "We found that a common form of the gene occurs more frequently in the DNA of families that have two or more sons affected by autism but no affected daughters," he said. "Our study may explain why boys are more susceptible to the disorder than girls."

Nelson and his colleagues zeroed in on a region of chromosome 17 that previous studies have tied to autism. The research team scoured the DNA of 1,046 members of families with at least two sons affected by autism for common gene variants. A variant is a gene that has undergone subtle changes from the normal DNA yet is shared by a significant portion of the population. The researchers used tools of the Human Genome Project to scan thousands of variants across all genes in the suspicious region of the chromosome and to pluck out the most common forms.

"We wanted to identify what was happening in this region of chromosome 17 that boosts autism risk," Nelson said. "When the same genetic markers kept cropping up in a single region of the DNA, we knew we had uncovered a big clue."

The researchers traced the genetic markers to CACNA1G, which helps move calcium between cells. They discovered that the gene has a common variant that appears in the DNA of nearly 40 percent of the population.

"This alternate form of CACNA1G consistently increased the correlation to autism spectrum disorders, suggesting that inheriting the gene may heighten a child's risk of developing autism," Nelson said. How the gene contributes to higher autism risk remains unclear, but Nelson emphasized that it cannot be considered a risk factor on its own. "This variant is a single piece of the puzzle," he said. "We need a larger sample size to identify all of the genes involved in autism and to solve the whole puzzle of this disease."

The UCLA team's next step will be to sequence the gene in people who possess the altered variant in order to identify the exact change that increases autism risk. These subtle variations offer potential markers for the real mutation causing greater susceptibility to the disease. Nelson's co-authors included Samuel Strom, Jennifer Stone, John ten Bosch, Barry Merriman, Rita Cantor and Daniel Geschwind, all of UCLA. The study was funded by the National Institute of Mental Health and Cure Autism Now, which merged with Autism Speaks in 2007.

The DNA samples and clinical data were provided by families who donated blood to the Los Angeles–based Autism Genetic Resource Exchange (AGRE), a program created and funded by Cure Autism Now. "When parents like me first formed AGRE, this was our dream, that talented scientists would use our gene bank to collaborate and bring us closer to understanding autism," said Jon Shestack, co-founder of Cure Autism Now and a board member of Autism Speaks. "AGRE has played an important role in almost every major autism genetics paper in the past five years."

Autism is a complex brain disorder that strikes in early childhood. The condition disrupts a child's ability to communicate and develop social relationships and is often accompanied by acute behavioral challenges. The Centers for Disease Control and Prevention reports that one in 150 American children is diagnosed with an autism spectrum disorder. The diagnosis of autism has expanded tenfold in the last decade.

For more news, visit the UCLA Newsroom.

Center for Autism Research & Treatment

UCLA study shows traumatic brain injury haunts children for years

mood3 — Wed, 13 May 2009 17:07:03 +0000

The take-home message: helmets and seat belts

Traumatic Brain Injury (TBI) is the single most common cause of death and disability in children and adolescents, according to the Centers for Disease Control. Now, according to a new study by UCLA researchers, the effects of a blow to the head, whether it’s mild or a concussion, can linger for years. Reporting in the May issue of the journal Neuropsychology, Talin Babikian, lead author and a UCLA post-doctoral fellow, and senior author Robert Asarnow, a UCLA professor of psychiatry, analyzed 28 selected articles about TBI that were published between the years 1988 and 2007, quantifying for the first time a summary of all of the available literature on the effects of a traumatic brain injury on the developing brain of a child or adolescent.

The key and surprising finding, the authors say, was that over time, children and adolescents with a severe traumatic brain injury appear to fall even farther behind their peers than one would expect, making intervention and monitoring especially important in this group.

Various levels of TBI in children were included in the studies that were reviewed. The extent of a brain injury is typically based on the “Glasgow Coma Scale” or GCS, a standard clinical tool to measure severity of a brain injury. It includes a person's eye/pupil response, motor response, and verbal communication to determine injury severity--mild, moderate, or severe TBI. The children in the studies were sorted by TBI severity and the time since their injury. All three severity levels were examined, and follow-up exams were done on average 0-5 months, 6-23 months, or 24+ months after injury, for 14 key aspects of neurocognition.

Other key points the authors found:

Time didn’t heal all the worse the injury, the worse the neurocognitive outcome over time, especially on measures of general intellectual functioning and brain processing speed. Indeed, the moderate and severe TBI groups were similarly impaired after examination at 24-plus months.
The authors found that while there was modest recovery in intellectual functioning and attention, weaknesses in many children with even moderate TBI persisted even two years after the injury, compared to children in control groups.
For children diagnosed with severe TBI, more help was needed. They showed significant problems within months on IQ, executive functioning (processing speed, attention), and verbal memory (both immediate and delayed). After two or more years, all areas studied were impaired.

“The good news is that the studies showed that children with mild traumatic brain injuries and concussions may show some difficulties in cognition initially, but the effects are subtle and typically diminish over time,” said Babikian. “The bad news, though, is the existence of a subgroup of patients who show persistent neurocognitive problems and need to be screened and followed. “And because younger children have more development ahead of them, the same injury can affect a four-year-old and a 12-year-old very differently,” she said. “Further, children who suffer a severe brain injury may show a slower rate of development as a group, highlighting the importance of targeted treatment developed specifically for children with severe TBI.” Equally important, said Babikian, is the take-home message of prevention. “Because younger children with a traumatic brain injury seem to generally do worse than their older counterparts,” she said, “the public health implication of this research is a reminder of the importance of the use of protective measures to minimize the effects of a brain injury, when one does occur, as well as prevention through consistent use of helmets and seatbelts.”

The research was funded by the National Institute of Neurological Disorders and Stroke, part of the National Institutes of Health, and by the Della Martin Foundation. The authors report no conflict of interest.

The UCLA Department of Psychiatry and Biobehavioral Sciences is the home within the David Geffen School of Medicine for faculty who are expert in the origins of and treatments for disorders of complex human behavior. It is part of the Semel Institute for Neuroscience and Human Behavior, a world leading, interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders.

Semel Institute for Neuroscience and Human Behavior

How to build a bigger brain

mood3 — Tue, 12 May 2009 19:00:00 +0000

Study shows that meditation may increase gray matter

Push-ups, crunches, gyms, personal trainers — people have many strategies for building bigger muscles and stronger bones. But what can one do to build a bigger brain?

Meditate.

That's the finding from a group of researchers at UCLA who used high-resolution magnetic resonance imaging (MRI) to scan the brains of people who meditate. In a study published in the journal NeuroImage and currently available online (by subscription), the researchers report that certain regions in the brains of long-term meditators were larger than in a similar control group. Specifically, meditators showed significantly larger volumes of the hippocampus and areas within the orbito-frontal cortex, the thalamus and the inferior temporal gyrus — all regions known for regulating emotions.

"We know that people who consistently meditate have a singular ability to cultivate positive emotions, retain emotional stability and engage in mindful behavior," said Eileen Luders, lead author and a postdoctoral research fellow at the UCLA Laboratory of Neuro Imaging. "The observed differences in brain anatomy might give us a clue why meditators have these exceptional abilities."

Research has confirmed the beneficial aspects of meditation. In addition to having better focus and control over their emotions, many people who meditate regularly have reduced levels of stress and bolstered immune systems. But less is known about the link between meditation and brain structure. In the study, Luders and her colleagues examined 44 people — 22 control subjects and 22 who had practiced various forms of meditation, including Zazen, Samatha and Vipassana, among others. The amount of time they had practiced ranged from five to 46 years, with an average of 24 years.

More than half of all the meditators said that deep concentration was an essential part of their practice, and most meditated between 10 and 90 minutes every day.

The researchers used a high-resolution, three-dimensional form of MRI and two different approaches to measure differences in brain structure. One approach automatically divides the brain into several regions of interest, allowing researchers to compare the size of certain brain structures. The other segments the brain into different tissue types, allowing researchers to compare the amount of gray matter within specific regions of the brain. The researchers found significantly larger cerebral measurements in meditators compared with controls, including larger volumes of the right hippocampus and increased gray matter in the right orbito-frontal cortex, the right thalamus and the left inferior temporal lobe. There were no regions where controls had significantly larger volumes or more gray matter than meditators. Because these areas of the brain are closely linked to emotion, Luders said, "these might be the neuronal underpinnings that give meditators' the outstanding ability to regulate their emotions and allow for well-adjusted responses to whatever life throws their way." What's not known, she said, and will require further study, are what the specific correlates are on a microscopic level — that is, whether it's an increased number of neurons, the larger size of the neurons or a particular "wiring" pattern meditators may develop that other people don't.

Because this was not a longitudinal study — which would have tracked meditators from the time they began meditating onward — it's possible that the meditators already had more regional gray matter and volume in specific areas; that may have attracted them to meditation in the first place, Luders said. However, she also noted that numerous previous studies have pointed to the brain's remarkable plasticity and how environmental enrichment has been shown to change brain structure.

Other authors of the study included Arthur Toga, director of the UCLA Laboratory of Neuro Imaging; Natasha Lepore of UCLA; and Christian Gaser of the University of Jena in Germany. Funding for the study was provided by the National Institutes of Health. The authors report no conflicts of interest.

The UCLA Laboratory of Neuro Imaging, which seeks to improve understanding of the brain in health and disease, is a leader in the development of advanced computational algorithms and scientific approaches for the comprehensive and quantitative mapping of brain structure and function. The laboratory is part of the UCLA Department of Neurology, which encompasses more than a dozen research, clinical and teaching programs. The department has ranked No. 1 among its peers nationwide in National Institutes of Health funding for the last seven years (2002–08).

For more news, visit the UCLA Newsroom.

Semel Institute for Neuroscience and Human Behavior

World's largest DNA scan for autism uncovers new gene variant for disorder

mood3 — Tue, 28 Apr 2009 19:40:49 +0000

UCLA scientists, in partnership with 30 research institutions across the country, have identified a new gene variant that is highly common in autistic children. And when researchers scrutinized the activity of the gene, known as CDH10, in the fetal brain, they discovered that it is most active in key regions that support language, speech and interpreting social behavior.

Published April 28 in the advance online edition of the journal Nature, the two findings suggest that CDH10 plays a critical role in shaping the developing brain and may contribute to a prenatal risk of autism. A variant is a gene that has undergone subtle changes from the normal DNA yet is shared by a significant portion of the population.

"While this gene variant is common in the general population, we discovered that it occurs about 20 percent more often in children with autism," said study author Dr. Daniel Geschwind, director of the UCLA Center for Autism Treatment and Research. "A major change like this in the genetic code is too common to be a simple mutation it is a risk factor in the origin of the disease."

Using the largest population sample to date, the scientists systematically scanned the DNA of 3,100 individuals from 780 families nationwide. Each family had at least two autistic children. The scan connected autism to a specific region of chromosome 5, which previous studies at UCLA and collaborating institutions had pinpointed as a hub for genetic variations linked to higher autism risk.

To verify the findings, Dr. Hakon Hakonarson at the Children's Hospital of Philadelphia led the team in conducting a second scan on the DNA of 1,200 individuals from families affected by autism, as well as nearly 6,500 healthy controls. All participants shared European ancestry. The scientists evaluated the relationship of more than half a million gene variants to autism and consistently discovered six changes that occurred more frequently in autistic children than in the control group.

These variants sat on chromosome 5 between two genes, CDH9 and CDH10. In the second half of the study, the UCLA team looked at the two genes' presence in the developing human brain. While CDH9's presence appeared minimal, the scientists discovered that CDH10 was most active in the fetal brain's frontal cortex, a region critical to language, social behavior and complex thought processes such as judgment.

"This is a landmark finding," Geschwind said. "It's no coincidence that a gene linked to autism has a higher concentration in key brain regions that regulate speech and the ability to interpret social interaction. Our research suggests that CDH10 is switched on at a very early stage and plays an important role in regulating the developing brain. This prenatal activity somehow makes the infant more susceptible to autism." By influencing the development of important brain structures, CDH10 provides a tangible link between genes, brain circuitry and a child's future behavior, Geschwind noted. The discovery also opens up a number of intriguing next steps for research, including the possibility of an imaging study to explore whether the gene behaves differently in the autistic brain.

The DNA samples and clinical data were provided by families who donated blood to the Los Angeles-based Autism Genetic Resource Exchange (AGRE), a program created and funded by Cure Autism Now, which merged with Autism Speaks in 2007. "When parents like me first formed AGRE, this was our dream, that talented scientists would use our gene bank to collaborate and bring us closer to understanding autism," said Jon Shestack, co-founder of Cure Autism Now and a board member of Autism Speaks. "AGRE has played an important role in almost every major autism genetics paper in the past five years." Autism is a complex brain disorder that strikes in early childhood. The condition disrupts a child's ability to communicate and develop social relationships and is often accompanied by acute behavioral challenges.

The Centers for Disease Control and Prevention report that one in 150 American children is diagnosed with an autism spectrum disorder; the disorder affects four times as many boys as girls. The diagnosis of autism has expanded tenfold in the last decade. The UCLA portion of the study was supported primarily with funding from the National Institute of Mental Health. Geschwind's UCLA colleagues included Brett Abrahams, Rita Cantor, Hongmei Dong, Edward Herman, Ted Hutman, Ana Alvarez Retuerto, Marian Sigman and Lisa Sonnenblick. Additional co-authors included scientists from the Children's Hospital of Philadelphia, USC, Autism Speaks, the University of Pennsylvania, the University of Miami, Mount Sinai School of Medicine, the University of Washington, the University of North Carolina, UC Davis, Yale University, the University of Illinois, the University of Utah, Indiana University, Vanderbilt University and the University of Pittsburgh.

The UCLA Center for Autism Research and Treatment provides diagnosis, family counseling and treatment for patients with autism. UCLA is one of eight centers in the National Institutes of Health–funded Studies to Advance Autism Research and Treatment network and one of 10 original Collaborative Programs for Excellence in Autism.

http://newsroom.ucla.edu/portal/ucla/world-s-largest-dna-scan-uncovers-8...

Center for Autism Research & Treatment

Teaching autistic teens to make friends

mood3 — Tue, 07 Apr 2009 23:31:21 +0000

During the first week of class, the teens' eyes were downcast, their responses were mumbled and eye contact was almost nonexistent. By Week 12, though, these same kids were talkative, responsive and engaged.
That's the result of a special class designed at UCLA to help teens with autism spectrum disorders (ASD) learn to interact appropriately with their peers. ASD includes a range of pervasive developmental disorders characterized by problems with communication and socialization; it's estimated that one in 150 children born in the United States has some form of ASD.
In a study appearing in the April edition of the Journal of Autism and Developmental Disorders, UCLA clinical instructor of psychiatry Elizabeth Laugeson and colleagues report that in comparison with a control group, the treatment group taking the class significantly improved their overall social skills and interactions with their peers.
"Although, typically, developing teens often learn basic social rules through observation of peer behavior and specific instruction from parents," Laugeson said, "adolescents with autism spectrum disorders often require further instruction.
"It's hard enough to be a teenager," she said, "but it's harder still for adolescents with autism because they typically lack the ability to pick up on all the social cues most of us take for granted — things like body language, hand gestures and facial expressions, along with speech inflections like warmth, sarcasm or hostility.
"Lack of these basic social skills may lead to rejection, isolation or bullying from their peers. And sadly, that isolation can carry into their adult life."
Laugeson and her colleagues developed the class, called PEERS (Program for the Education and Enrichment of Relational Skills), to give high-functioning teens with ASD a set of specific social skills.
"How do you have a successful get-together with someone? How do you go up to a group of teens and join their conversation? What do you say as a comeback when someone teases you? Without these core social skills, it becomes very difficult for teenagers to make and keep friends," Laugeson said.
In the study, 33 teens with ASD — 28 males and five females — attended the PEERS classes. All the participants had a previous diagnosis of high-functioning autism, Asperger's Disorder or Pervasive Developmental Disorder–Not Otherwise Specified (PDD-NOS). The teens met once a week for 12 weeks; each session lasted 90 minutes. Instruction was conducted in a small-group format, with seven to 10 teens, using established strategies for teaching social skills to adolescents with ASD.
Parents were also required to attend separate, concurrent sessions where they were provided direct instruction and guidance to support their child's development.
"Parental involvement was mandatory and important," said Laugeson, who is also associate director of the UCLA Parenting and Children's Friendship Program and director of the Help Group–UCLA Autism Research Alliance. "Other research has shown us that parent involvement can have significant positive effects upon children's friendships, both in terms of direct instruction and supervision, as well as supporting a child's development of an appropriate peer network."
The class focused on teaching rules of social etiquette to the teens, while their parents were given information about how to supervise the implementation of these newly learned skills. These included: how to comfortably join and exit a group of peers; how to pick the right peer group (such as jocks, nerds or gamers); learning good sportsmanship; learning good host behavior during get-togethers; changing bad reputations by changing one's "look" and owning up to a previously bad reputation; and handling teasing, bullying and arguments.
Each class included brief didactic instruction, role-playing exercises in which appropriate social skills were modeled, behavioral rehearsal for teens to practice newly learned skills, coaching with performance feedback, and weekly "homework" assignments supervised by parents, such as inviting a friend over to the home for a get-together.
"The class is very structured, and the skills are broken into small steps that give the teens specific actions they can take in response to a social situation," Laugeson said. "This method of instruction is very appealing to teens with autism because they tend to think concretely and often learn by rote. So if they are teased, for example, we teach them to give a short comeback — like saying 'whatever' or 'so what?' They learn not to take the bait."
Results of testing show that teens who have been through the PEERS program were having more peer interactions with their friends outside of school, and parents reported significant improvement in overall social skills, as measured by a standardized test of social functioning.
Results were encouraging, as improvement was demonstrated on a number of outcome measures. Teens in the treatment group demonstrated improved knowledge of rules of social etiquette relevant to making and keeping friends. They and their parents also reported a significant increase in the frequency of hosted get-togethers and a significantly better quality of friendships at the end of treatment, in comparison with the control group.
"For me, the most important outcome of this research is that we're able to have a direct impact on the quality of lives for teenagers with ASD," Laugeson said. "Helping them to develop meaningful relationships and feel more comfortable within their social world — these are essential ingredients to living a happy life, and what could be more important than that?"

The classes are continuing and currently enrolling. For more information, visit www.semel.ucla.edu/socialskills/ or call the UCLA Parenting and Children's Friendship Program at 310-825-0142.

Other authors of the study were Dr. Fred Frankel, Dr. Catherine Mogil and Ashley Dillon, all of UCLA. Funding was provided by the National Institutes of Health and the National Institute of Mental Health. The authors report no conflict of interest.

The Program for the Education and Enrichment of Relational Skills (PEERS) is part of the UCLA Semel Institute for Neuroscience and Human Behavior, an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders.

Center for Autism Research & Treatment

Study details strategy for boosting ranks of black HIV/AIDS researchers

mood3 — Tue, 31 Mar 2009 23:11:40 +0000

African Americans, who make up 13 percent of the U.S. population, are disproportionately affected by AIDS, accounting for nearly 49 percent of newly diagnosed HIV/AIDS cases nationwide. About 500,000 African Americans are now living with HIV/AIDS.

Yet there are very few African American HIV/AIDS researchers, due to historical, social and other factors that prevent them from training in the biomedical, behavioral and social aspects of HIV/AIDS research.

In response to the shortage, researchers from the UCLA Center for Culture, Trauma and Mental Health Disparities and the UCLA AIDS Institute have developed a series of recommendations that could reverse the trend and lead more African American researchers into the field. The recommendations are outlined in an article published in a supplement to the April issue of the American Journal of Public Health (available online at www.ajph.org/cgi/content/full/99/S1/S48).

"The most effective behavior-change policies allow for individuals to be part of the solution and not the problem," said lead author Dr. Gail Wyatt, professor of psychiatry and biobehavioral sciences at the Semel Institute for Neuroscience and Human Behavior at UCLA. "We need African American experts who are at the forefront of HIV/AIDS prevention."

The researchers have identified four institutional factors, as well as two individual factors, that limit the number of African Americans pursuing HIV/AIDS research.

Institutional factors include limitation of early career decisions and a lack of exposure to research, research socialization and mentoring. For example, African American college students often don't receive research training early in their careers, so they may not be experienced in pulling together a team of strong research collaborators. In addition, some department chairs may think it is "too late" for doctoral graduates to move into a research career, and there are few senior African Americans to mentor and encourage a new generation of African American HIV/AIDS investigators.

Compounding this situation are individual factors. Given the scarcity of role models, African American students may have negative perceptions about their own competence as HIV/AIDS investigators, and there is limited support for culturally congruent research.

To boost the ranks of African American HIV/AIDS researchers, the study authors make the following seven recommendations to universities and other institutions of higher learning, and private and government funders of research and training:

Fund research that encourages partnerships with historically African American and minority-serving institutions, such as the National Medical Association and the Association of Black Psychologists, so that clinically trained professionals can participate in and learn more about HIV/AIDS research.
Provide for retraining of established researchers who wish to shift their focus to HIV/AIDS.
Continue to offer loan-repayment programs for graduate education.
Incorporate mentorships into graduate and professional training programs.
Encourage universities and training programs to recognize mentors whose students pursue HIV/AIDS research, and establish awards that recognize the work of African American investigators in the field.
Develop and use culturally congruent theories and measures in HIV/AIDS research.
Require training in cultural competence for federal staff, reviewers and mentors.

"HIV/AIDS research conducted by highly trained African Americans should be the norm and not the exception," the authors conclude. "Such researchers add an important voice and level of expertise to HIV prevention that can only be enhanced by implementing programs to increase the representation of African American investigators in NIH-funded research. A concerted effort to remove barriers to funding and career trajectories to ensure that HIV/AIDS research addresses the most affected populations is needed."

In addition to Wyatt, study authors included John K. Williams, Tina Henderson and LeKeisha Sumner, all of the UCLA Department of Psychiatry and Biobehavioral Sciences.

The National Institute of Mental Health (NIMH) and the UCLA AIDS Institute funded this study.

The UCLA Center for Culture, Trauma and Mental Health Disparities is a unique new interdisciplinary, center funded by the NIMH that promotes research into the behavioral, biological, psychological and social factors associated with trauma among ethnic minorities. The Center faculty aim to understand how depression, post-traumatic stress disorder, and other mental health outcomes affect men and women who may not seek or receive effective care. This understanding would help healthcare professionals create new strategies to reduce mental health disparities among these groups.

The UCLA AIDS Institute, established in 1992, is a multidisciplinary think tank drawing on the skills of top-flight researchers in the worldwide fight against HIV and AIDS, the first cases of which were reported in 1981 by UCLA physicians. Institute members include researchers in virology and immunology, genetics, cancer, neurology, ophthalmology, epidemiology, social science, public health, nursing, and disease prevention. Their findings have led to advances in treating HIV, as well as other diseases, such as hepatitis B and C, influenza and cancer.

Semel Institute for Neuroscience and Human Behavior

Bad news for insomniacs: 'hunger hormones' affected by poor sleep

mood3 — Wed, 25 Mar 2009 19:00:00 +0000

Insomnia has long been associated with poor health, including weight gain and even obesity. Now researchers at UCLA have found out why. In a study to be published in the May issue of the journal Psychoneuroendocrinology and currently available online by subscription, Sarosh Motivala, an assistant professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA, and colleagues looked at two hormones that are primarily responsible for regulating the body's energy balance, telling the body when it is hungry and when it is full. The study found that chronic insomnia disrupts one of these two hormones.

To date, no study has evaluated nocturnal levels of the two hormones, ghrelin and leptin, in primary insomnia patients. Ghrelin, a peptide secreted by the stomach, stimulates appetite and increases before meals. Leptin, which affects body weight and is secreted primarily by fat cells, signals the hypothalamus regarding the degree of fat storage in the body; decreased leptin tells the body there is a calorie shortage and promotes hunger, while increased levels promote energy expenditure.

In the study, researchers compared healthy sleepers with those suffering from chronic insomnia and measured the levels of the two hormones at various times throughout the night. They found that while leptin levels averaged out over the night to be roughly the same between the two groups, levels of ghrelin were 30 percent lower in insomnia sufferers.

On the face of it, a decreased level of ghrelin would seem to inhibit weight gain; it is an increase in ghrelin, after all, that stimulates appetite. But Motivala compared his findings with other, earlier studies on sleep deprivation and speculates that a switch may occur during the day: Sleep loss leads to increased ghrelin and decreased leptin, a "double whammy" that stimulates appetite. Motivala is currently working on a study to examine this switch. "The current study shows that insomnia patients have a dysregulation in energy balance that could explain why these patients gain weight over time," said Motivala, who is also a member of the Cousins Center for Psychoneuroimmunology at UCLA. "This is an exciting finding because it highlights how diverse behaviors like sleep and eating are connected. We are just beginning to explore the possible consequences of these connections, but it is another example of the importance of a good night's sleep for the body."

For the study, 38 male participants were divided into two groups — 14 insomnia sufferers and 24 healthy subjects. Both groups had similar ages and body weight. Both groups underwent polysomnography sleep studies that monitor brain waves. Circulating levels of ghrelin and leptin were measured at 11 p.m., 2 a.m. and 6 a.m. Ghrelin levels across the night were significantly lower in insomnia patients, while leptin were not significantly different between the two groups.

The UCLA Cousins Center for Psychoneuroimmunology encompasses an interdisciplinary network of scientists working to advance the understanding of psychoneuroimmunology by linking basic and clinical research programs and by translating findings into clinical practice. The center is affiliated with the Semel Institute for Neuroscience and Human Behavior and the David Geffen School of Medicine at UCLA.

Cousins Center for Psychoneuroimmunology

Study gives more proof that intelligence is largely inherited

mood3 — Tue, 17 Mar 2009 18:58:22 +0000

They say a picture tells a thousand stories, but can it also tell how smart you are? Actually, say UCLA researchers, it can. In a study published in the Journal of Neuroscience Feb. 18, UCLA neurology professor Paul Thompson and colleagues used a new type of brain-imaging scanner to show that intelligence is strongly influenced by the quality of the brain's axons, or wiring that sends signals throughout the brain. The faster the signaling, the faster the brain processes information. And since the integrity of the brain's wiring is influenced by genes, the genes we inherit play a far greater role in intelligence than was previously thought.

Genes appear to influence intelligence by determining how well nerve axons are encased in myelin — the fatty sheath of "insulation" that coats our axons and allows for fast signaling bursts in our brains. The thicker the myelin, the faster the nerve impulses. Thompson and his colleagues scanned the brains of 23 sets of identical twins and 23 sets of fraternal twins. Since identical twins share the same genes while fraternal twins share about half their genes, the researchers were able to compare each group to show that myelin integrity was determined genetically in many parts of the brain that are key for intelligence. These include the parietal lobes, which are responsible for spatial reasoning, visual processing and logic, and the corpus callosum, which pulls together information from both sides of the body.

The researchers used a faster version of a type of scanner called a HARDI (high-angular resolution diffusion imaging) — think of an MRI machine on steroids — that takes scans of the brain at a much higher resolution than a standard MRI. While an MRI scan shows the volume of different tissues in the brain by measuring the amount of water present, HARDI tracks how water diffuses through the brain's white matter — a way to measure the quality of its myelin. "HARDI measures water diffusion," said Thompson, who is also a member of the UCLA Laboratory of Neuro-Imaging. "If the water diffuses rapidly in a specific direction, it tells us that the brain has very fast connections. If it diffuses more broadly, that's an indication of slower signaling, and lower intelligence."

"So it gives us a picture of one's mental speed," he said.

Because the myelination of brain circuits follows an inverted U-shaped trajectory, peaking in middle age and then slowly beginning to decline, Thompson believes identifying the genes that promote high-integrity myelin is critical to forestalling brain diseases like multiple sclerosis and autism, which have been linked to the breakdown of myelin. "The whole point of this research," Thompson said, "is to give us insight into brain diseases."He said his team has already narrowed down the number of gene candidates that may influence myelin growth.

And could this someday lead to a therapy that could make us smarter, enhancing our intelligence?

"It's a long way off but within the realm of the possible," Thompson said.

Graphics from the study can be found at www.loni.ucla.edu/~thompson/HARDI/PDF/hardi3.jpg.

The UCLA Department of Neurology encompasses more than a dozen research, clinical and teaching programs. These programs cover brain mapping and neuroimaging, movement disorders, Alzheimer's disease, multiple sclerosis, neurogenetics, nerve and muscle disorders, epilepsy, neuro-oncology, neurotology, neuropsychology, headaches and migraines, neurorehabilitation, and neurovascular disorders. The department ranked No. 1 in 2005 and 2006 among its peers nationwide in National Institutes of Health funding.

Semel Institute for Neuroscience and Human Behavior

Teenage stress has implications for adult health

mood3 — Tue, 10 Mar 2009 21:47:44 +0000

Most of us remember our teenage years with a mix of fondness and relief. Fondness for the good memories, and relief that all that teenage stress, angst and drama — first love, gossip, SATs, fights with parents — is behind us. Or is it? It turns out, say UCLA researchers, that even stressful times from the teenage years exact a physical toll that could have implications for health during adulthood.

Andrew J. Fuligni, a professor of psychiatry at the Semel Institute for Neuroscience and Human Behavior at UCLA, and colleagues report that in a study of otherwise healthy, normal teens who self-reported various negative interpersonal interactions, researchers found that a greater frequency of such stress was associated with higher levels of an inflammatory marker called C-reactive protein, or CRP. CRP has been identified as an indicator for the later development of cardiovascular disease (CVD).

The study will appear in an upcoming issue of the journal Psychosomatic Medicine and is currently available online (subscription only).

"Although most research on stress and inflammation has focused upon adulthood, these results show that such links can occur as early as the teenage years, even among a healthy sample of young men and women," Fuligni said. "That suggests that alterations in the biological substrates that initiate CVD begin before adulthood."

Those everyday kinds of stressors, such as a fight with a parent or peer, are among the most frequent and powerful predictors of psychological distress among individuals, he said. That led the researchers to wonder: If stress could have a powerful psychological influence, could it have a physiological influence as well?

The study looked at a total of 69 adolescents, average age 17, from Latin American and European backgrounds, who completed a daily diary checklist each night for 14 days. In it, they reported any experiences of negative interpersonal interaction with family, peers or school personnel — for example, conflicts with family and friends, peer harassment or any kind of punishment by parents or teachers. Blood samples were obtained an average of eight months later and assayed for circulating levels of the CRP protein; the research protocol took into account such factors as socioeconomic status, major stressful life events and being overly sensitive to rejection or daily psychological distress.

The researchers found that daily interpersonal stress experienced during the high school years was associated with elevated levels of inflammation, as measured by higher levels of CRP, even among normal, healthy teens. "Our findings are consistent with the emerging body of evidence that points to the link between stress and increased inflammation, which places individuals at risk for the later development of cardiovascular disease," said Fuligni, who is also a member of the UCLA Cousins Center for Psychoneuroimmunology and the UCLA Center for Culture and Health.

The results are also interesting because they suggest that the association of interpersonal stress with inflammation exists regardless of individual teens' psychological appraisal of stressful experiences or any tendency to be particularly sensitive to social rejection, he said.Fuligni suggests the results of this research show the importance of focusing on actual daily stressful experiences when examining the implications of psychological and social factors for the development of risk for CVD during the teenage years. "Although the frequency of some of these experiences may be low, they could have a significant impact upon long-term physical health during adulthood," Fulgini said.

Other authors included Julienne Bower, Steve W. Cole, senior author Michael R. Irwin and Eva H. Telzer, all of UCLA, and Lisa Kiang, of Wake Forest University. The authors report no conflicts of interest. Support for this project was provided by the Russell Sage Foundation and the UCLA Cousins Center, and by the UCLA Older Americans Independence Center Inflammatory Biology Core.

The Cousins Center for Psychoneuroimmunology at UCLA encompasses an interdisciplinary network of scientists working to advance the understanding of psychoneuroimmunology by linking basic and clinical research programs and by translating findings into clinical practice. The center is affiliated with the Semel Institute for Neuroscience and Human Behavior and the David Geffen School of Medicine at UCLA. The Semel Institute is an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders.

Cousins Center for Psychoneuroimmunology

UCLA Confers Mani Bhaumik Award to Harvard medical school physician Herbert Benson, a pioneer in mind/body medicine

mood3 — Wed, 04 Mar 2009 05:21:43 +0000

The Cousins Center for Psychoneuroimmunology at UCLA has named Harvard University’s Dr. Herbert Benson as this year’s recipient of the Mani Bhaumik Award. The award has been established to support investigators in the international community who advance the understanding of the brain and the conscious mind in healing through visionary research, books, and education.

Benson, the director emeritus of the Benson-Henry Institute (BHI) for Mind Body Medicine at Massachusetts General Hospital, and an associate professor of medicine at the Harvard Medical School, will receive his award in a ceremony at 5 p.m. on Wednesday, March18, in the Auditorium of the Semel Institute for Neuroscience and Human Behavior on the UCLA campus. His keynote lecture is titled, "The Relaxation Response: Its Alteration of Gene Expression and how it Counteracts the Harmful Effects of Stress.” Benson’s talk will be followed by a question-and-answer session and a reception. The event is free and open to the public. Parking on campus is $9.00 in Lot 9.

A graduate of Wesleyan University and the Harvard Medical School, Benson is the author or co-author of more than 180 scientific publications and 11 books. A pioneer in mind/body medicine, he is one of the first Western physicians to bring the effect of conscious mind on healing into medicine. In his 35-plus year career, he defined one of the tenets of mind/body medicine, the relaxation response, which leads to a state of deep rest that changes the physical and emotional responses to stress (e.g., decreases in heart rate, blood pressure, rate of breathing, muscle tension, and an overall feeling of well being).He continues to lead teaching and research into the techniques and efficacy of the relaxation response in counteracting the numerous harmful effects of stress.

Benson and his colleagues have shown that a mind-body approach--one that couples the relaxation response with nutrition, exercise and cognitive therapies--is a useful tool for helping to treat such conditions as chronic pain, infertility, premenstrual syndrome, and insomnia. They also have found that it can alleviate symptoms associated with cancer and AIDS.

“Dr. Benson is truly one of the seminal thinkers in bringing the integrated study of the mind and body to Western medicine,” said Mani Bhaumik. “Even though, as a cardiologist, he was trained in the Western ethos of medicine, he persevered in successfully developing his relaxation response at a time when such practices of alternative medicine were frowned upon in the West.”

"I am deeply honored to receive the Mani Bhaumik award,” said Benson. “It has special meaning to me because of my personal friendship with Norman Cousins. Norman and I often sought each other's advice on how best to ensure the success of psychoneuroimmunology and mind body medicine for the future. He would be delighted with tonight's event."

Bhaumik, co-inventor of the laser technology that made LASIK surgery possible, has funded the annual $15,000 award. His interest in psychoneuroimmunology (PNI) — the investigation of the interactions between the brain and the immune system — springs from the pioneering work of Norman Cousins. Cousins came to UCLA in 1978 as an adjunct professor of medical humanities to harness the energies of top scientists dedicated to the emerging field of PNI. He was particularly interested in the impact of positive emotions and attitudes, such as purpose determination, love, hope, faith, will to live and festivity. His efforts resulted in the creation of the UCLA Program in Psychoneuroimmunology, which now carries his name. Cousins died in 1990.

"It is an honor for me to be associated with the Cousins Center, as I was privileged to know Norman Cousins, whose insights continue to inspire me. With this award, my goal is to educate the public on the important benefits of the research and understanding of psychoneuroimmunology," said Bhaumik.

Bhaumik earned a Ph.D. in physics from the Indian Institute of Technology and a Sloan Foundation Fellowship for postdoctoral work at UCLA. For his valuable contributions to laser technology, he was elected by his scientific peers as a fellow of the American Physical Society and the Institute of Electrical and Electronics Engineers. Bhaumik received the Mahatma Gandhi Humanitarian Award from the Indian American Heritage Foundation for his outstanding contributions to science and humanity and for his international bestselling book, "Code Name God." He is also the creator and one of the executive producers of the new animated series, “Cosmic Quantum Ray,” which has been distributed worldwide for broadcast in 2009. The series is geared towards inspiring children’s interest in science. Most recently, Bhaumik was named the Patron of the International Year of Astronomy (IYA2009) and his just published primer on cosmology, “The Cosmic Detective” (Penguin) has been chosen as an official book of IYA2009.

The Cousins Center encompasses an interdisciplinary network of scientists working to advance the understanding of psychoneuroimmunology by linking basic and clinical research programs and by translating findings into clinical practice. Led by Dr. Michael Irwin, the center is affiliated with the Semel Institute for Neuroscience and Human Behavior and the David Geffen School of Medicine at UCLA, directed by Dr. Peter Whybrow.

Cousins Center for Psychoneuroimmunology

Assessment technique lets scientists see brain aging before symptoms appear

mood3 — Mon, 05 Jan 2009 21:00:00 +0000

Approach combines PET scans with information on patients' Alzheimer's risk

UCLA scientists have used innovative brain-scan technology developed at UCLA, along with patient-specific information on Alzheimer's disease risk, to help diagnose brain aging, often before symptoms appear. Published in the January issue of Archives of General Psychiatry, their study may offer a more accurate method for tracking brain aging.

Researchers used positron emission tomography (PET), which allows a window into the brain of living people and specifically reveals plaques and tangles, the hallmarks of neurodegeneration. The PET scans were complemented by information on patients' age and congnitive status and a genetic profile. Combining key patient information with a brain scan may give us better predictive power in targeting those who may benefit from early interventions, as well as help test how well treatments are working, said study author Dr. Gary Small, who holds UCLA's Parlow-Solomon Chair on Aging and is a professor at the Semel Institute for Neuroscience and Human Behavior at UCLA.

Scientists took PET brain scans of 76 non-demented volunteers after they had been intravenously injected with a new chemical marker called FDDNP, which binds to plaque and tangle deposits in the brain. They reported that older age correlated with higher concentrations of FDDNP in the medial and lateral temporal regions of the brain, areas involved with memory, where plaques and tangles usually collect. This group demonstrated higher FDDNP levels in the frontal region of the brain, also involved in memory, than study participants without allele. We found that for many volunteers, the imaging scans reflected subtle brain changes, which take place before symptoms manifest, said Small, who is also director of the UCLA Center on Aging.

Currently, the new FDDNP-PET scans are used in a research setting, but clinical trials are in development to bring the technology to wider patient use. The study was funded by both government and nonprofit agencies, including the National Institutes of Health, the U.S. Department of Energy, the Ahmanson Foundation, the Larry L. Hillblom Foundation and the Tamkin Foundation.

Memory & Aging Research Center

Vulnerability to post-traumatic stress disorder runs in families, study shows

mood3 — Fri, 19 Dec 2008 20:00:00 +0000

Research finds genetic connection between PTSD, depression and anxiety:

Earthquakes have aftershocks — not just the geological kind but the mental kind as well. Just like veterans of war, earthquake survivors can experience post-traumatic stress disorder, depression and anxiety.

In 1988, a massive earthquake in Armenia killed 17,000 people and destroyed nearly half the town of Gumri. Now, in the first multigenerational study of its kind, UCLA researchers studying survivors of that catastrophe have discovered that vulnerability to PTSD, anxiety and depression runs in families.

Armen Goenjian, a research psychiatrist in the UCLA Department of Psychiatry and Biobehavioral Sciences, and colleagues studied 200 participants from 12 multigenerational families exposed to the earthquake. Participants suffered from varying degrees of the disorders. The researchers found that 41 percent of the variation of PTSD symptoms was due to genetic factors and that 61 percent of the variation of depressive symptoms and 66 percent of anxiety symptoms were attributable to genetics. Further, they found that a large proportion of the genetic liabilities for the disorders were shared.

The research appears in the December issue of the journal Psychiatric Genetics. "This was a study of multigenerational family members — parents and offspring, grandparents and grandchildren, siblings, and so on — and we found that the genetic makeup of some of these individuals renders them more vulnerable to develop PTSD, anxiety and depressive symptoms," said Goenjian, a member of the UCLA–Duke University National Center for Child Traumatic Stress and lead author of the study. In addition, Goenjian noted, the study suggests that a large percentage of genes are shared between the disorders. "That tracks with clinical experience," he said. "For example, in clinical practice, the therapist will often discover that patients who come in for treatment of depression have coexisting anxiety. Our findings show that a substantial portion of the coexistence can be explained on the basis of shared genes and not just environmental factors such as upbringing."

The researchers used statistical methods to assess heritabilities. One method was used to determine the genetic component of a disorder such as PTSD. Then, a separate analysis was used to see if different phenotypes shared genes. The results showed that a significant amount of genes are shared between PTSD and depression, PTSD and anxiety, and finally depression and anxiety.

Until now, Goenjian said, the only studies that have suggested such a heritability of PTSD have been twin studies. "It's very hard to do family studies on PTSD because typically only single individuals, not whole families, are exposed to a particular trauma," he said. "In our study, we were able to avert this problem since all the subjects were exposed to the same severe trauma at the same time." In fact, he said, the 200 participants all saw destroyed buildings throughout Gumri, 90 percent witnessed dead bodies left lying in the streets and 92 percent witnessed severely injured people.

The findings are promising for the next step in understanding the underlying biology of these disorders, which is locating the specific genes involved, Goenjian said. Other authors on the paper included Julia N. Bailey, Ida S. Karayana, Ernest P. Noble and Terry Ritchie, all of UCLA; David P. Walling from the Collaborative Neuroscience Network; and Haig A. Goenjian from the Tulane University School of Medicine.

Funding for the study was provided by the Collaborative Neuroscience Network. The researchers report no conflicts of interest.

The UCLA Department of Psychiatry and Biobehavioral Sciences within the David Geffen School of Medicine is home to faculty who are experts in the origins of and treatments for disorders of complex human behavior. The department is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, a world-leading interdisciplinary research and education institute devoted to the understanding of complex human behavior and the causes and consequences of neuropsychiatric disorders.

For more news, visit the UCLA Newsroom

Semel Institute for Neuroscience and Human Behavior

Nearly 5% of U.S. population suffers from persistent depression or anxiety

mood3 — Tue, 02 Dec 2008 20:21:00 +0000

Study finds that few receive appropriate treatment for disorders:

Though effective treatments are available for individuals suffering from chronic depression and anxiety, very little is known about how often these treatments are used or how prevalent these conditions are among the nation's general population. But in a first-of-its-kind study, UCLA researchers have developed estimates for both the prevalence of chronic psychiatric illness in the general population and how often individuals suffering from such illnesses receive appropriate treatment.

In the study, published in the December issue of the peer-reviewed journal Psychiatric Services and currently available online, researchers found that approximately 4.7 percent of the nation's population suffers from persistent depression or anxiety disorders, with a minority of those afflicted receiving adequate medication or counseling. The study was based on data from Healthcare for Communities, a nationally representative household survey of adults in the United States. The researchers analyzed responses from 1,642 adults with major depression or anxiety disorders. These surveys, conducted in 1997 and 1998, with follow-ups approximately two-and-a-half years later, assessed diagnosis, quality of life, treatment satisfaction, medical conditions, suicidal thoughts, insurance, and the use of medications and counseling.

From a policy perspective, this study indicates that we have to do much better in terms of helping people in the population and clinicians in primary care, said lead author Dr. Alexander S. Young, a UCLA professor of psychiatry and director of health services for the Department of Veterans Affairs Desert Pacific Mental Illness Research, Education and Clinical Center (MIRECC).

Semel Institute for Neuroscience and Human Behavior

Study IDs three effective treatments for childhood anxiety disorders

mood3 — Tue, 04 Nov 2008 16:00:00 +0000

Treatment that combines a certain type of psychotherapy with an antidepressant medication is most likely to help children with anxiety disorders, but each treatment alone is also effective, according to a new study funded by the National Institute of Mental Health (NIMH), part of the National Institutes of Health. Anxiety disorders are among the most common mental disorders affecting children and adolescents. Untreated anxiety can undermine a child's success in school, jeopardize his or her relationships with family and inhibit social functioning. This study represents a significant advance in the treatment of children and adolescents with anxiety disorders, said study author Dr. John Piacentini, a professor of psychiatry and director of UCLA's Child OCD, Anxiety and Tic Disorders Program.

UCLA was one of 6 study sites. The Child/Adolescent Anxiety Multimodal Study randomly assigned 488 children between the ages of 7 and 17 to one of the following four treatment options for a 12-week period:

Cognitive behavioral therapy - a specific type of therapy that, for this study, taught children about anxiety and helped them face and master their fears by guiding them through structured tasks
The antidepressant sertraline (Zoloft), a selective serotonin reuptake inhibitor
Cognitive behavioral therapy combined with sertraline
A placebo (sugar pill)

The children, recruited from 6 regionally dispersed sites throughout the United States, all had moderate to severe separation anxiety disorder, generalized anxiety disorder or social phobia. Many also had coexisting disorders, including other anxiety disorders, attention-deficit hyperactivity disorder and behavioral problems. Piacentini and colleagues found that 81 percent of the children and adolescents who received the combination treatment improved, compared with 60 percent in the therapy-only group, 55 percent in the sertraline-only group and 24 percent in the placebo group. Results also showed that the treatments were safe. Children taking sertraline alone showed no more side effects than the children taking the placebo, and few children discontinued the trial due to side effects. In addition, no child attempted suicide - a rare side effect sometimes associated with antidepressant medications in children. The study findings echo previous studies in which sertraline and other selective serotonin reuptake inhibitors were found to be effective in treating childhood anxiety disorders. The study's results also provide further evidence that high-quality cognitive behavioral therapy, with or without medication, can effectively treat anxiety disorders in children, according to the researchers.

The study is currently available online in the New England Journal of Medicine.

Semel Institute for Neuroscience and Human Behavior

New candidate genes for schizophrenia identified

mood3 — Tue, 21 Oct 2008 01:00:00 +0000

Schizophrenia is a severe psychiatric disease characterized by disorganized behavior, delusions and hallucinations. Sadly, there is no clear understanding of its cause. Now, in a collaborative study, UCLA and Dutch researchers have identified three new candidate genes for schizophrenia that may contribute to a better understanding of how the disease evolves.

Reporting in the October issue of the American Journal of Human Genetics, Roel A. Ophoff, an assistant professor with the Center for Neurobehavioral Genetics at the Semel Institute for Neuroscience and Human Behavior at UCLA, and his colleagues examined the genetic makeup of 54 Dutch patients diagnosed with deficit schizophrenia, a particularly severe form of the disease that is both chronic and debilitating. Specifically, they looked at a number of large but rare deletions and duplications in the genome of the patients, known as copy number variants, or CNVs. Scientists suspect that such missing or duplicated segments of DNA could be responsible for increased susceptibility to a number of diseases.

In this study, the researchers showed that three of these rare CNVs interrupted genes associated with brain function. Changes in these three genes are rare but seem to dramatically increase the risk of developing schizophrenia, Ophoff said. The identification of these new candidate genes will provide a better insight into the underlying biology of schizophrenia and explain why some individuals are at risk to develop the disease. Another important step will be to assess the inheritance patterns of such CNVs, Ophoff said. Since this is an inherited disease affecting approximately 1 percent of the population, this would be valuable toward establishing the clinical relevance of this important class of genomic variations.

Center for Neurobehavioral Genetics