News Psychology

Allowing native language in school benefits Mexican-American students, researcher finds

A new University of Missouri study shows that Mexican-American students who identify and practice speaking their native language have higher grades than those who are put in English-only environments in their schools.

"A real educational disparity exists because Mexican-Americans, along with other Latinos, are now the largest minority; yet, they still have the lowest high school and college graduation rates," said David Aguayo, a doctoral student in the Department of Educational, School and Counseling Psychology in the College of Education. "I understand the reasons behind English-only efforts, but the research shows that if we don't accept the cultural identity of these students in our schools, such as tolerating their native language, Mexican-Americans may not succeed."

Aguayo compared survey results of 408 Mexican-American students. He examined whether the students were born in the U.S. or Mexico; the students' grade point averages; and the students' abilities to perform college-related tasks. Aguayo found that students who embraced their cultural heritage and spoke in their native languages had higher grade point averages than those that only spoke English while in school and at home.

"It's a simple correlation, but living and learning within your cultural heritage is a benefit," Aguayo said. "It could be speaking the language in school, eating certain foods, or interacting with other people who share your heritage. The stress level of being in a new culture will decrease if these students have a support system in school, while they are adjusting to other cultures."

In the future, Aguayo will study the motivations of Mexican-American students who move to the U.S. Statistics show these students have more success in school than Mexican-American students who have lived in the U.S. their entire lives.

"Educators need to be aware of students' home lives," Aguayo said. "Immigrant parents, in particular, tend to put more trust in educators, rather than being involved in the child's education like we normally see in the U.S. If educators can take the time to learn about the parents' culture, the educators can have a positive impact on the students' future."

Journal Reference:

David Aguayo, Keith Herman, Lizette Ojeda, Lisa Y. Flores. Culture predicts Mexican Americans' college self-efficacy and college performance. Journal of Diversity in Higher Education, 2011; 4 (2): 79 DOI: 10.1037/a0022504

YouTube videos can inaccurately depict Parkinson’s disease and other movement disorders, study finds

Looking online for medical information? Viewers beware, doctors caution. After reviewing the most frequently watched YouTube videos about movement disorders, a group of neurologists found that the people in the videos often do not have a movement disorder.

As described in a Letter to the Editor in this week's New England Journal of Medicine, such medical misinformation may confuse patients suffering from devastating neurological disorders and seeking health information and advice online.

Many people use the Internet as a primary resource for medical information, and YouTube, the third most visited website on the Internet, is a popular platform for patients to share personal medical stories and experiences on video.

Dozens of YouTube videos show people who believe they have movement disorders such as Parkinson's disease demonstrating and talking about their symptoms. In January 2011, neurologists at University College London began a study when patients alerted them that online videos often proposed a diagnosis and suggested therapies.

Seven neurologists from different countries and medical institutions searched YouTube using six keywords: "dystonia," "Parkinsonism," "chorea," "myoclonus," "tics" and "tremor," and found videos allegedly depicting various movement disorders. They then independently reviewed the top three percent most-watched videos that were of sufficient quality to review patient symptoms. Out of 29 videos, the majority (66 percent) were identified as showing "psychogenic" movement disorders, meaning that the abnormal movement originates from a psychological condition or mental state rather than a disease with a physical cause, such as Parkinson's. Of these videos, more than half contained advice about specific therapies to treat the movement disorder. Furthermore, the doctors reviewing the videos did so independently, yet their diagnoses agreed in 87 to 100 percent of all cases.

"Patients and doctors have to be very thoughtful and careful when looking for information on YouTube, as well as the Internet in general," commented Mark Hallett, M.D., senior investigator at the National Institute of Neurological Disorders and Stroke (NINDS) at the National Institutes of Health. "There is a great deal of good information on the Internet, but one has to be careful."

Dr. Hallett was one of two U.S.-based investigators who reviewed and rated the videos, and co-authored the letter. The video review was initiated by neurologists Kailash P. Bhatia, M.D. (principal corresponding author), Maria Stamelou, M.D., Ph.D., and Mark J. Edwards. M.D., Ph.D. at University College London. The other video raters and co-authors were: Alberto J. Espay, M.D. (University of Cincinnati, Ohio), Victor S.C. Fung, Ph.D., F.R.A.C.P. (Sydney Medical School, Australia), Anthony E. Lang, M.D. (University of Toronto, Canada), and Marina A.J. Tijssen, M.D., Ph.D. (Academic Medical Center, Amsterdam, the Netherlands).

The National Institutes of Health provides peer-reviewed, research-based health information on its website at http://health.nih.gov/. Accurate information on movement disorders can be found at http://www.ninds.nih.gov/disorders/parkinsons_disease/parkinsons_disease.htm.

Journal Reference:

Maria Stamelou, Mark J. Edwards, Alberto J. Espay, Victor S.C. Fung, Mark Hallett, Anthony E. Lang, Marina A.J. Tijssen, Kailash P. Bhatia. Movement Disorders on YouTube — Caveat Spectator. New England Journal of Medicine, 2011; 365 (12): 1160 DOI: 10.1056/NEJMc1107673

Do women's voices really allow men to detect ovulation? No, says new study

The voice can reveal a lot about a person — their sex, their age, how they are feeling — and recent studies have even suggested that women's voices might also contain cues that men can read about how close they are to ovulation. A new study, however, published in the journal PLoS ONE, challenges the view that women broadcast reproductive information in their voice.

Previous studies in this area have typically relied on the comparison of voices recorded in just two phases in the cycle: high conception risk vs. low conception risk. This new work, on the other hand, looked at variation in the voice throughout the entire menstrual cycle — a crucial step to evaluate the potential information contained in any observed voice changes.

Their results showed that the overall variation in women's vocal quality throughout the whole cycle precludes unequivocal identification of the period with the highest conception risk. Specifically, while they found that the women studied spoke with the highest tone (suggested by previous studies to be associated with attractiveness) just prior to ovulation, the tone rose again to levels indistinguishable from pre-ovulation shortly after ovulation, making it a very poor mating clue. Furthermore, they found that the men studied showed only a very slight preference for pre-ovulation voices relative to voices recorded during ovulation.

The authors conclude that women's voices do not provide reliable information about the timing of ovulation, confirming the view that information about reproductive state is 'leaked' rather than broadcast. In an interesting further finding, the study found that women's voice were harsher and more irregular during menstruation, providing scientific data to explain why female opera singers may be granted 'grace days' during menstruation.

The international collaborative study was led by Prof Julia Fischer (German Primate Centre), Dr Stuart Semple (Roehampton University, London) and Dr Ofer Amir (Tel-Aviv University).

Journal Reference:

Julia Fischer, Stuart Semple, Gisela Fickenscher, Rebecca Jürgens, Eberhard Kruse, Michael Heistermann, Ofer Amir. Do Women's Voices Provide Cues of the Likelihood of Ovulation? The Importance of Sampling Regime. PLoS ONE, 2011; 6 (9): e24490 DOI: 10.1371/journal.pone.0024490

Large study finds genetic 'overlap' between schizophrenia, bipolar disorder

Knowledge about the biological origin of diseases like schizophrenia, bipolar disorder and other psychiatric conditions is critical to improving diagnosis and treatment.

In an effort to push the field forward, three UCLA researchers, along with scientists from more than 20 countries, have been taking part in one of the largest collaborative efforts in psychiatry — a genome-wide study involving more than 50,000 study participants aimed at identifying which genetic variants make people susceptible to psychiatric disease.

This collaborative, the Psychiatric Genome-Wide Association Study Consortium (PGC), now reports in the current online edition of the journal Nature Genetics that it has discovered that common genetic variants contribute to a person's risk of schizophrenia and bipolar disorder.

The PGC's studies provide new molecular evidence that 11 regions on the genome are strongly associated with these diseases, including six regions not previously observed. The researchers also found that several of these DNA variations contribute to both diseases.

The findings, the researchers say, represent a significant advance in understanding the causes of these chronic, severe and debilitating disorders.

The UCLA researchers who contributed to the schizophrenia study are Roel A. Ophoff, a professor of psychiatry and human genetics and one of the founding principal investigators of the schizophrenia portion of the study; Dr. Nelson Freimer, a professor of psychiatry and director of the Center for Neurobehavioral Genetics at the Semel Institute for Neuroscience and Human Behavior at UCLA; and Rita Cantor, a professor of psychiatry and human genetics.

Schizophrenia and bipolar disorder are common and often devastating brain disorders. Some of the most prominent symptoms of schizophrenia are persistent delusions, hallucinations and cognitive problems. Bipolar disorder is characterized by severe, episodic mood swings. Both affect about 1 percent of the world's population and usually strike in late adolescence or early adulthood.

Despite the availability of treatments, these illnesses are usually chronic, and patients' response to treatment is often incomplete, leading to prolonged disability and personal suffering. Family history, which reflects genetic inheritance, is a strong risk factor for both schizophrenia and bipolar disorder, and it has generally been assumed that dozens of genes, along with environmental factors, contribute to disease risk.

In the schizophrenia study, a total of seven locations on the genome were implicated in the disease, five of which had not been identified before. When similar data from the bipolar disorder study, which ran concurrently, were combined with results from the schizophrenia study, three gene locations were identified that proved to be involved in both disorders, suggesting a "genetic overlap" between schizophrenia and bipolar disorder.

"Genetic factors play an important role in the susceptibility to develop schizophrenia," Ophoff said, "but identifying these genetic factors has been very difficult. We know that schizophrenia is not caused by a single gene that explains everything but an interplay of many genetic and non-genetic factors."

At the same time, he said, the disease itself is not uniform but manifests itself in different ways; currently, there is no objective biological marker or "sign" that can be used for diagnosis.

"This so-called heterogeneity at the genetic and clinical level is the biggest challenge for genetic studies of neuropsychiatric disorders," Ophoff said. "One way to deal with these difficulties is to increase the size of the study so there is sufficient 'power' to detect genetic effects, even amidst this clinical and genetic diversity."

The fact that even this large study resulted in a limited number of schizophrenia and bipolar genes demonstrates once again, he said, the complex nature of the disease.

Formed in 2007, the PGC is the largest consortium ever in psychiatry. Over 250 researchers from more than 20 countries have come together in an unparalleled spirit of cooperation to advance knowledge of the genetic causes of mental illness. Crucial to the success of the project was the willingness of many groups to share genetic data from tens of thousands of patients collected over many years.

The research was funded by numerous European, American and Australian funding bodies. Funds for coordination of the consortium were provided by the National Institute of Mental Health in the U.S.

Journal References:

Schizophrenia Psychiatric Genome-Wide Association Study (GWAS) Consortium. Genome-wide association study identifies five new schizophrenia loci. Nature Genetics, 2011; DOI: 10.1038/ng.940
Psychiatric GWAS Consortium Bipolar Disorder Working Group. Large-scale genome-wide association analysis of bipolar disorder identifies a new susceptibility locus near ODZ4. Nature Genetics, 2011; DOI: 10.1038/ng.943

Biologists discover genes that repair nerves after injury

Biologists at the University of California, San Diego have identified more than 70 genes that play a role in regenerating nerves after injury, providing biomedical researchers with a valuable set of genetic leads for use in developing therapies to repair spinal cord injuries and other common kinds of nerve damage such as stroke.

In the September 22 issue of the journal Neuron, the scientists detail their discoveries after an exhaustive two-year investigation of 654 genes suspected to be involved in regulating the growth of axons — the thread-like extensions of nerve cells that transmit electrical impulses to other nerve cells. From their large-scale genetic screen, the researchers identified 70 genes that promote axon growth after injury and six more genes that repress the re-growth of axons.

"We don't know much about how axons re-grow after they're damaged," said Andrew Chisholm, a professor of biology at UC San Diego. "When you have an injury to your spinal cord or you have a stroke you cause a lot of damage to your axons. And in your brain or spinal cord, regeneration is very inefficient. That's why spinal cord injuries are basically untreatable."

Chisholm and UC San Diego biology professor and HHMI Investigator Yishi Jin headed the collaborative research team, which also included researchers from the University of Oregon.

While scientists in recent decades have gained a good understanding of how nerve cells, or neurons, develop their connections in the developing embryo, much less is known about how adult animals and humans repair — or fail to repair — those connections when axons are damaged.

"There are many processes not involved in early development that are involved in switching the neurons to this re-growth mode," said Chisholm. "In essence what we found are genes that people had not suspected previously to be part of this process."

Of particular interest to the UC San Diego biologists are the six genes that appear to repress the growth of axons.

"The discovery of these inhibitors is probably the most exciting finding," said Chisholm, because identifying and eliminating the inhibiting factors to the re-growth of axons could be just as essential as the biochemical pathways that promote axon re-growth in repairing spinal cord injuries and other kinds of nerve damage.

The scientists were also surprised to learn that some of the genes they found to be involved in the re-growth of axons were known to have other functions, such as regulating the release of neurotransmitters.

"This was in large part unexpected," said Chisholm. "These genes had not been implicated in the re-growth of axons before."

To find the 76 genes, the researchers conducted painstaking experiments on more than 10,000 tiny laboratory roundworms known as C. elegans. The first step involved developing genetic mutants of these transparent roundworms for each one of 654 genes that were suspected to play a role in the regulation of axon regrowth in worms, fruit flies and mice. They then labeled the roundworm neurons with green fluorescent protein and, with a precise surgical laser, damaged a specific axon.

"The goal was to study this process in its simplest form," said Chisholm. "Because the animals are essentially transparent, we can see the axons expressing this green fluorescent protein."

By examining the re-growth, or lack of growth, of the damaged axon 24 hours later, the scientists were then able to determine which of these 654 genes were actually important to axon re-growth.

Chisholm said that while the 76 genes identified are believed to have similar roles in mammals as well as roundworms, because their functions were "conserved" by the organisms through evolution, he and his research team are now collaborating with other investigators to conduct experiments on mice to verify this connection and determine which of these genes are the most critically important.

"Worms are clearly different from mammals," he added. "But there will be a core of conserved molecules doing the same job."

In addition to Chisholm and Jin, the UC San Diego biologists involved in the study were Lizhen Chen, Zhiping Wang, Anindya Ghosh-Roy, Thomas Hubert, Dong Yan, and Zilu Wu. Sean O'Rourke and Bruce Bowerman from the University of Oregon were also part of the team.

The research project was supported by grants from the National Institutes of Health and the Howard Hughes Medical Institute.

Journal Reference:

Lizhen Chen, Zhiping Wang, Anindya Ghosh-Roy, Thomas Hubert, Dong Yan, Sean O'Rourke, Bruce Bowerman, Zilu Wu, Yishi Jin, Andrew D. Chisholm. Axon Regeneration Pathways Identified by Systematic Genetic Screening in C. elegans. Neuron, Volume 71, Issue 6, 1043-1057, 22 September 2011 DOI: 10.1016/j.neuron.2011.07.009

Looking closely at personality disorders: Should DSM-5 reduce and redefine them?

A newly published paper from Rhode Island Hospital argues against the proposed changes to redefine the number of personality disorders in the upcoming Diagnostic Statistical Manual, 5th edition (DSM-5). In their study, the researchers found the current scoring used in the DSM-IV already captures the dimensional nature of personality disorders.

The paper is published in the Journal of Clinical Psychiatry and is now available online in advance of print.

The DSM-IV currently defines 10 different personality disorders. One of the proposed changes for DSM-5 would introduce a dimensional model to the categorical system, noted Mark Zimmerman, M.D., director of outpatient psychiatry at Rhode Island Hospital and lead author of the paper. Zimmerman and the researchers argue that there already exists a dimensional component in the current DSM-IV that can be used to identify some traits of a disorder even when the full criteria are not met. Thus, according to DSM-IV the personality disorders can be rated on a three-point dimensional scale with a rating of 0 indicating no traits for the disorders are found; 1 indicating sub-threshold traits; and a rating of 2 indicating the disorder is present.

Using this scoring method, Zimmerman and his group studied 2,150 psychiatric outpatients and evaluated them with semi-structured diagnostic interviews for DSM-IV defined disorders and measures of psychosocial morbidity.

Zimmerman says, "What we found is that the DSM-IV three-point dimensional approach is an effective method in identifying personal disorders and these findings raise questions as to whether or not there is a need to modify the DSM-IV for personality disorders at all. We propose, instead, that we call more attention to the fact that there is a quasi-dimensional approach already built into the existing DSM-IV."

In their study, the researchers found the three-point dimensional convention embodied in DSM-IV was more strongly associated with measures of psychosocial morbidity than categorical diagnosis, and that there was no difference between the three-point, a 5-point and a criterion count method of scoring the DSM-IV personality dimensions. This argues against changing DSM-IV to the dimensional approach proposed for DSM-5.

Journal Reference:

Mark Zimmerman, Iwona Chelminski, Diane Young, Kristy Dalrymple, Jennifer Martinez. DoesDSM-IVAlready Capture the Dimensional Nature of Personality Disorders?The Journal of Clinical Psychiatry, 2011; DOI: 10.4088/JCP.11m06974

Gene for Lou Gehrig's disease and frontotemporal dementia identified

Frontotemporal dementia and amyotrophic lateral sclerosis, also known as Lou Gehrig's disease — two fatal neurodegenerative disease with distinct symptoms — are triggered by a common mutation in many cases, according to researchers who say they have identified the mutated gene.

In the study, reported in the September 21 online issue of Neuron, the scientists described the discovery of a genetic mutation that is accountable for almost 12 percent of familial FTD and more than 22 percent of familial ALS samples studied.

They also report that the defect is the strongest genetic risk factor found to date for the more common, non-inherited, sporadic forms of these diseases. It was found in 3 percent of sporadic FTD and 4 percent of sporadic ALS samples in the largest clinical patient series.

The study was led by scientists at the Mayo Clinic in Florida, in collaboration with researchers at UCSF, the University of British Columbia and UCLA. The finding emerged from the identification and study of a family stricken by both ALS and FTD, reported last year. In that study, led by the UCSF scientists and published in the Journal of Neurology, Neurosurgery and Psychiatry, the researchers honed in on the region in which the gene was located.

"Both clinically and at the molecular level this discovery is going to significantly improve our understanding of these diseases," said co-author Adam Boxer, MD, PhD, of the UCSF Memory and Aging Center, the lead author on the 2010 paper. The discovery makes it possible to develop a diagnostic test for the mutation, as well as to create animal models that may be used to help unravel the molecular mysteries connecting the mutation to the diseases, he said.

In the current study, a detailed molecular genetic characterization of the family that Boxer described was done in the laboratory of senior author Rosa Rademakers, PhD, from the Mayo Clinic. She and colleagues identified the gene and the specific mutation within it.

The mutation consists of from hundreds to thousands of extra copies of a six-letter DNA sequence GGGGCC strung end to end within a region of human chromosome nine. The mutation occurs within a gene of unknown function called C9ORF72.

After identifying the mutation, the Mayo researchers searched for it in DNA from other patients with both familial and sporadic forms of the diseases, where they found the strong associations.

FTD is characterized by disturbances in decision making, language skills, behavior and emotional expression, and is as common as Alzheimer's disease in people younger than 65, according to Boxer. ALS is a neuromuscular disease, leading to muscle paralysis and respiratory failure, often within three to five years. However, it is not unusual for patients diagnosed with one of the two diseases to exhibit symptoms of the other.

Since 2006, six separate groups have reported evidence for a genetic link between the disorders and the same chromosomal region. In the study led by Boxer last year, the researchers described clinical aspects of the disease within the family, and homed in more closely to the gene than others had.

The pattern of protein deposition in the brains of family members in the study may eventually shed light on common aspects of the neurodegenerative process that occurs in both diseases, Boxer said.

There is only one standard medical treatment for ALS, riluzole, which extend life for about six months, he said.

There is no known effective treatment to slow FTD. However, neurologists have generally become much better at recognizing the degenerative disorder, according to Boxer.

Boxer and Bruce Miller, MD, the director of the UCSF Memory and Aging Center and a co-author of both studies, are leaders in FTD research, diagnosis and patient care.

"Ten years ago some neurologists did not acknowledge the existence of FTD," Boxer says. "Today we are much better at diagnosing the disease, although sometimes it still takes an expert to distinguish it from Alzheimer's or from psychiatric disorders.

"We're actively trying to develop treatments for FTD, and we believe this discovery will pave the way for major advances in these efforts."

The researchers used a technique called linkage analysis to narrow the search for the gene by comparing affected and unaffected family members. Another group of scientists — reporting in the same online edition of Neuron on the same gene — found that C9ORF72 emerged as being significantly associated with FTD and ALS in a genome-wide scan of patients in Finland.

The Mayo portion of the study was funded by the National Institutes of Health and the ALS association (ALSA). The UCSF portion was funded by the NIH, the John Douglas French Foundation; the Hellman Family Foundation and the Tau Research Consortium and the Larry Hillblom Foundation and the state of California.

Journal Reference:

Mariely DeJesus-Hernandez, Ian R. Mackenzie, Bradley F. Boeve, Adam L. Boxer, Matt Baker, Nicola J. Rutherford, Alexandra M. Nicholson, NiCole A. Finch, Heather Flynn, Jennifer Adamson, Naomi Kouri, Aleksandra Wojtas, Pheth Sengdy, Ging-Yuek R. Hsiung, Anna Karydas, William W. Seeley, Keith A. Josephs, Giovanni Coppola, Daniel H. Geschwind, Zbigniew K. Wszolek, Howard Feldman, David S. Knopman, Ronald C. Petersen, Bruce L. Miller, Dennis W. Dickson, Kevin B. Boylan, Neill R. Graff-Radford, and Rosa Rademakers. Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS. Neuron, 2011; DOI: 10.1016/j.neuron.2011.09.011

Stressed and strapped: Caregivers for friends, relatives suffer emotional and financial strain

Family members or friends caring for aging or disabled individuals in California are under both financial and emotional strain and are likely to face even greater burdens, given recent cuts in state support for programs and services that support in-home care, write the authors of a new policy brief by the UCLA Center for Health Policy Research.

The study looked at California's estimated 6 million-plus informal caregivers of all ages and found higher levels of serious psychological distress and negative health behaviors, such as smoking, compared with the general population. Of particular concern are an estimated 2.6 million caregivers between the ages of 45 and 64 who may be setting themselves up for an unhealthy future due to higher rates of poor health behaviors, compared with both non-caregivers in the same age range and older caregivers.

"This is the 'sandwich generation,' the group of people struggling to meet the needs of both growing children and aging parents, often alone and while holding down full-time jobs," said Geoffrey Hoffman, the brief's lead author. "Caregivers need help, especially as baby boomers age and place even greater strains on their and their families' abilities to cope."

Using data from the 2009 California Health Interview Survey (CHIS), the authors found that California caregivers provide an average of 20 hours of care per week for a friend or relative who can no longer do certain things for themselves, such as bathing, shopping, managing medications or paying bills.

Few caregivers are paid for their work or use state services that might help alleviate both financial and psychological burdens. And with the U.S. Census projecting that the population of those 65 and older will more than double in the next 30 years, the magnitude of largely uncompensated care by family and friends will rapidly increase.

"We may be seeing an association between caregiving and stress, where caregivers are both more likely to be seriously depressed and to exhibit certain health behaviors that put them at risk," Hoffman said. "These effects on caregivers' overall health merit attention from policymakers."

Among the findings:

Caregivers under stress
Mental health: More than 1 million caregivers report moderate or serious distress levels, with almost one-third reporting that their emotions interfere a lot with their household chores (29.9 percent) or their social lives (32.9 percent).

Middle-aged caregivers struggling: Compared with both older caregivers and non-caregivers of the same age, middle-aged caregivers are more likely to binge drink (25.5 percent), smoke (15.9 percent) and/or be obese (30.1 percent).

Stress and smoking: Caregivers of all ages who reported serious psychological distress were 208 percent more likely to smoke than non-caregivers with serious psychological distress — an exceptional amount.
Middle-aged caregivers lack support Nearly one-third (29.0 percent) of middle-aged caregivers are single, divorced or widowed, and more than two-thirds (67.1 percent) hold down full- or part-time jobs. Nearly one-quarter (22.5 percent) are low-income.
Caregiving is time-intensive Approximately one-third of caregivers who live with care recipients spend an average of 36 hours on caregiving — almost as much as a full-time job. A majority (62.0 percent) of caregivers of all ages work full or part time.
Caregivers of all ages under financial strain Only 7.4 percent of informal caregivers reported being paid for the help they provide. Moreover, nearly 20 percent spent $250 or more of their own money on caregiving in the past month. The strains of caregiving may be alleviated by respite services (short-term temporary relief from duties), yet only 13.5 percent of caregivers report ever using any respite care.

The authors note that recent cuts to California's In-Home Supportive Services program and the scheduled Dec 1. elimination of the Adult Day Health Care program will likely place even greater burdens on informal caregivers.

"Family members and friends supporting loved ones in need provide the bulk of personal assistance services and often absorb the high costs of caregiving, both financially and emotionally," said Dr. Bruce Chernof, president and CEO of The SCAN Foundation, which provided funding for the analysis. "Programs that support family caregivers can help them create and sustain vulnerable elders in community settings, which promotes the values of dignity, choice and independence as loved ones grow older."

The authors urge support for the Community Living Assistance and Supports (CLASS) program, a voluntary, consumer-funded long-term care insurance program proposed under health reform, which would provide a cash benefit that could be used to compensate informal caregivers and to purchase needed respite or mental health services.

Other provisions in the health reform law also offer a range of initiatives to provide in-home care to seniors and people with disabilities and reduce dependence on high-cost Medicaid nursing homes, according to the authors. Programs like the Community First Choice Option, which provides community-based attendant supports and services to disabled individuals requiring an institutional level of care, as well as proposed new Medicaid funding for Aging and Disability Resource Centers, could significantly lift the burden off of family and other informal caregivers, the researchers say.

Hedging your bets: How the brain makes decisions based on related information

When making decisions based on multiple, interdependent factors, we choose based on how these factors correlate with each other, and not based on an ad hoc rule of thumb or through trial and error as was previously thought, according to research funded by the Wellcome Trust.

The study, published September 21 in the journal Neuron, identifies the regions of the brain involved in tracking this correlation, which include the insula and the anterior cingulate cortex, both of which have previously been associated with decision making, emotions and awareness.

Decision-making is an extremely complex process, particularly when it involves a number of interdependent factors. How we make sense of these factors has until now been unclear. But researchers at the Wellcome Trust Centre for Neuroimaging at UCL, together with collaborators at the California Institute of Technology have now shown that our brains learn the correlation between events. This allows us to observe the outcome of just one action and then infer the outcomes of other actions without having to sample them individually.

Dr Klaus Wunderlich from the Wellcome Trust Centre for Neuroimaging explains: "Imagine our ancestors foraging for food in the woods. They could spend their time either collecting berries or hunting deer. But they have previously observed that deer eat berries. So, as they are foraging, if they notice a lack of fresh berries, they can infer that there are lots of deer around and instead focus on hunting."

The majority of the research into learning and decision-making over the past decade has focused on the direct relationship between actions and rewards. The scientific understanding was hitherto that we learn about each of a number of multiple rewards separately and then use trial and error or a rule of thumb to predict outcomes.

In the above example, this would mean that the hunter could only predict the success of hunting deer after having tried it and observed the actual outcome. In an ever-changing natural environment it is likely the case that the key correlations are more stable than the relationship between individual actions and reward. In other words, the fact that deer eat berries is always true, but the success at hunting deer can vary from year to year. Learning about the correlations therefore has immediate benefits for efficient choices.

To investigate how humans learn correlations between outcomes, the researchers scanned the brains of sixteen subjects using functional magnetic resonance imaging (fMRI), which measures activity in the brain, while the subjects performed a game involving managing resources. This involved a scenario whereby a power company generates fluctuating amounts of electricity from two renewable energy sources, a solar plant and a wind park.

The researchers instructed subjects to create an energy portfolio under a specific goal constraint which necessitated keeping the total energy output as constant as possible by adjusting weights that determined how the two resources were combined. The best performance was achievable by finding a solution that exploited knowledge of the interdependence of the resources, a task similar to a simple portfolio problem in finance. Importantly, the outcomes of the two resources co-varied with each other and this correlation between the two outcomes changed probabilistically over time, requiring subjects to continuously update their estimate of the current correlation.

The researchers found that the brain represents information about how much the two resources are correlated with each other in the insula and the anterior cingulate cortex, and uses a mechanism based on measuring how accurate the prediction was to update this information each time new information becomes available.

"It may be possible that such an evolved mechanism works best if the correlation is learnt through multiple observations, but this learning mechanism is still unable to make sense of complex statistics from tables or charts," says Dr Wunderlich. "This might explain why humans often utterly fail at making financial decisions that are based on understanding correlations."

Co-author Peter Bossaerts, a Professor of Finance at the California Institute of Technology, takes an economist's view of the research.

"When investing in more than one asset, such as stocks and bonds, it is important that one does so with the right mix, which is determined by the correlation between the returns on the assets." But how do we actually make this judgement?

"We are often presented with rough rules of thumb depending on our risk aversion — the more risk averse, the more bonds we invest in. In fact, from the point of view of financial returns, the mix between stocks and bonds should not depend on risk aversion at all, but on how correlated the two are. And, as we show in this research, in fact we do combine sources in an optimal way, taking into account explicitly how the outputs are correlated."

Journal Reference:

Klaus Wunderlich, Mkael Symmonds, Peter Bossaerts, Raymond J. Dolan. Hedging Your Bets by Learning Reward Correlations in the Human Brain. Neuron, 2011; 71 (6): 1141 DOI: 10.1016/j.neuron.2011.07.025

Zinc regulates communication between brain cells

Zinc has been found to play a critical role in regulating communication between cells in the brain, possibly governing the formation of memories and controlling the occurrence of epileptic seizures.

A collaborative project between Duke University Medical Center researchers and chemists at the Massachusetts Institute of Technology has been able to watch zinc in action as it regulates communication between neurons in the hippocampus, where learning and memory processes occur — and where disrupted communication may contribute to epilepsy.

"We discovered that zinc is essential to control the efficiency of communication between two critical populations of nerve cells in the hippocampus," said James McNamara, M.D., senior author and chair of the Department of Neurobiology at Duke. "This addresses a longstanding controversy in the field."

The study appeared in Neuron Journal online on Sept. 21.

McNamara noted that zinc supplements are commonly sold over the counter to treat several different brain disorders, including depression. It isn't clear whether these supplements modify zinc content in the brain, or modify the efficiency of communication between these nerve cells. He emphasized that people taking zinc supplements should be cautious, pending needed information on the desired zinc concentrations and how oral supplements affect them.

More than 50 years ago scientists discovered that high concentrations of zinc are contained in a specialized compartment of nerve cells, called vesicles, that package the transmitters which enable nerve cells to communicate. The highest concentrations of brain zinc were found among the neurons of the hippocampus, the center of learning and memory.

Zinc's presence in these vesicles suggested that zinc played some role in communication between nerve cells, but whether it actually did so remained controversial.

To address this controversy, McNamara and his colleagues at Duke teamed up with Dr. Steve Lippard and colleagues in the Department of Chemistry at the Massachusetts Institute of Technology.

The Lippard team synthesized a novel chemical that bound zinc far more rapidly and selectively than previously available compounds. Use of this chemical let the Duke team rapidly bind the zinc released by nerve cells, taking it out of circulation and preventing enhanced communication.

The Duke team went on to confirm that eliminating zinc from the vesicles of mutant mice also prevented enhanced communication. They also found that increases in the transmitter glutamate seemed to increase zinc-mediated enhancement of communication.

Interestingly, the nerve cells in which the high concentrations of zinc reside are critical for a particular type of memory formation. Excessive enhancement of communication by the zinc-containing nerve cells occurs in epileptic animals and may worsen the severity of the epilepsy.

"Carefully controlling zinc's regulation of communication between these nerve cells is critical to both formation of memories and perhaps to occurrence of epileptic seizures," McNamara said.

McNamara also noted that the scientific collaboration between the Duke and MIT scientists was critical to the success of this work. The availability of the novel chemical provided a critical tool that allowed the neuroscientists to unravel the puzzle.

Journal Reference:

Enhui Pan, Xiao-an Zhang, Zhen Huang, Artur Krezel, Min Zhao, Christine E. Tinberg, Stephen J. Lippard, James O. McNamara. Vesicular Zinc Promotes Presynaptic and Inhibits Postsynaptic Long-Term Potentiation of Mossy Fiber-CA3 Synapse. Neuron, 2011; 71 (6): 1116 DOI: 10.1016/j.neuron.2011.07.019