1. Study tests the ‘three-hit’ theory of autism

    March 27, 2017 by Ashley

    From the Rockefeller University press release:

    Since the first case was documented in the United States in 1938, the causes of autism have remained elusive. Hundreds of genes, as well as environmental exposures, have been implicated in these brain disorders. Sex also seems to have something to do with it: About 80 percent of children diagnosed with an autism spectrum disorder are boys.

    This striking bias caught the attention of Rockefeller University’s Donald W. Pfaff. A neurobiologist who studies hormone effects and sex differences in the brain, Pfaff wondered if maleness might somehow amplify the genetic and environmental risk factors for the disease.

    In collaboration with colleagues specializing in child neurology and psychology, he has proposed a “three-hit” theory of autism, which suggests that a genetic predisposition in combination with early stress is more detrimental to boys than to girls, and more likely to produce the social avoidance that is a hallmark of autism disorders. Now, a team in his lab has found evidence in mice supporting this theory.

    “Together, these three hits — genes, environment, and sex — build on one another, such that their combined effect on behavior is much greater than the sum of the three individually,” says Pfaff, head of the Laboratory of Neurobiology and Behavior.

    A test run

    Pfaff and his colleagues formulated the three-hit theory based on studies of animals suggesting that the male hormone testosterone may sensitize the developing brain to stress in a way that can lead to social avoidance, a behavior characteristic of autism. Mice, like humans, are social animals, and in experiments, described in the Proceedings of the National Academy of Sciences, Pfaff’s team looked to see if male mice were more prone to problems with social responses than females when the other two risk factors were present.

    The theory and these experiments focus on the primary aspect of autism spectrum disorders, social problems, but there are others. In addition to social avoidance, autism is associated with difficulties in communication, as well as unusually restricted interests.

    To achieve a genetic hit, the team, led by Sara Schaafsma, a postdoc in the lab, used mice lacking a gene that is frequently mutated in people diagnosed with autism. To evoke stress in the as-yet unborn mice, the researchers prompted the immune systems of their pregnant mothers to react as though under attack from bacteria.

    Changes in brain and behavior

    The researchers later tested the social behavior of these mice in a series of experiments. The most compelling evidence for the three-hit theory came from a test of social recognition. Most of the animals, even those with two risk factors, showed signs of recognizing a once-unfamiliar mouse over multiple encounters. Only mice with all three hits — those that were male, were genetically predisposed to autism, and had experienced stress as embryos — seemed unable to recognize new acquaintances after encountering them multiple times.

    Next, the researchers looked for molecular changes within these rodents’ brains that might help to explain the differences in behavior. They found an increase in the expression of a gene that helps to kick off stress responses, in a brain region called the left hippocampus. With help from C. David Allis’s lab, they looked for chemical alterations in the packaging of DNA that might explain this uptick in gene activity. This effort revealed one particular chemical change in the nerve cell nucleus that encourages the expression of this stress-relevant gene.

    “Neurodevelopmental disorders, including autism, are often attributed to an interaction between genetic ‘nature’ and environmental ‘nurture.’ Our work indicates how male sex comes to be an important component of this dynamic, at least for one major aspect of autism,” Pfaff says. “By collecting a variety of evidence, we have begun to uncover one molecular mechanism, of many, by which these three hits alter sociability.”


  2. New risk factors for anxiety disorders

    March 20, 2017 by Ashley

    From the University of Würzburg press release:

    Mental, social and inherited factors all play a role in anxiety disorders. In the journal Molecular Psychiatry, a research team from Julius-Maximilians-Universität Würzburg (JMU) in Bavaria, Germany, describes a hitherto unknown genetic pathway for developing such diseases: They pinpointed at least four variants of the GLRB gene (glycine receptor B) as risk factors for anxiety and panic disorders. More than 5000 voluntary participants and 500 patients afflicted by panic disorder took part in the study that delivered these results.

    In Germany, around 15 percent of adults suffer from anxiety and panic disorders. Some people may have an extreme fear of spiders or other objects while others have breathing difficulties and accelerated heart beat in small rooms or large gatherings of people. With some afflicted persons, the anxiety attacks occur for no apparent cause. Many patients suffer from the detrimental impacts on their everyday lives — they often have problems at work and withdraw from social contacts.

    How are fear and anxiety triggered? How do anxiety disorders arise and evolve?

    Scientists from Münster, Hamburg and Würzburg have looked into these questions within the scope of Collaborative Research Center (CRC) TR 58 funded by Deutsche Forschungsgemeinschaft. Their goal is to develop new therapies that are better tailored to the individual patients. Anxiety disorders can be treated with drugs and behaviour therapy for instance.

    Gene triggers hyperekplexia

    The discovery that different variants of the GLRB gene are associated with anxiety disorders might also contribute to the development of improved therapies. The gene had been known to the researchers for some time, albeit only in connection with a different disease:

    “Some mutations of the gene cause a rare neurological disorder called hyperekplexia,” explains Professor Jürgen Deckert, member of the CRC and Director of the Department of Psychiatry at the JMU University Hospital. The patients are permanently hypertonic and show pronounced startle responses, which may even cause sufferers to fall involuntarily. Similar to persons suffering from anxiety disorders, these patients develop behaviour to avoid potentially frightening situations.

    The “fear network” in the brain is activated

    But the GLRB gene variants that have recently been associated with anxiety and panic disorders for the first time are different from the ones described above. They occur more frequently and presumably entail less severe consequences. But they, too, trigger overshooting startle responses, and as a result may excessively activate the brain’s “fear network.” High-resolution images of the brain activities of study participants provided the clues for the Würzburg scientists.

    “The results point to a hitherto unknown pathway of developing an anxiety disorder,” Deckert says. He believes that further investigations are now necessary to determine whether these findings can be harnessed to develop new or individual therapies. For example, it is conceivable to bring the “fear network” that is misregulated by the GLRB gene back on track by administering drugs.


  3. Study suggests social phobia may be affected by genes

    March 14, 2017 by Ashley

    From the University of Bonn press release:

    People with social anxiety avoid situations in which they are exposed to judgment by others. Those affected also lead a withdrawn life and maintain contact above all on the Internet. Around one in ten people is affected by this anxiety disorder over the course of their life. Researchers at the University of Bonn have now found evidence for a gene that is believed to be linked to the illness. It encodes a serotonin transporter in the brain. Interestingly, this messenger suppresses feelings of anxiety and depressiveness. The scientists want to investigate this cause more precisely and are thus looking for more study participants. The results will be published in the journal Psychiatric Genetics.

    Heart palpitations, trembling and shortness of breath: those who suffer from social phobia avoid larger groups. Verbal tests or everyday arrangements are filled with fear — after all, other people could make a negative judgement. Those affected often avoid such situations for this reason. Contact is often easier over social media or anonymously over the Internet. Social phobias are among the psychiatric disorders that are triggered simultaneously by genetic and environmental factors. “There is still a great deal to be done in terms of researching the genetic causes of this illness,” says Dr. Andreas Forstner from the Institute of Human Genetics at the University of Bonn. “Until now, only a few candidate genes have been known that could be linked to this.”

    Individual base pairs can vary in the DNA

    Together with the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Bonn, Dr. Forstner is conducting a study into the genetic causes of social phobia. The research team investigated the DNA of a total of 321 patients and compared it with 804 control individuals. The focus of the scientists lay on what are known as single nucleotide polymorphisms (SNPs). “There are variable positions in the DNA that can exist to various degrees in different people,” explains Dr. Forstner.

    The cause of genetic illnesses often lies in the SNPs. It is estimated that more than thirteen million such changes exist in the human DNA. The scientists investigated a total of 24 SNPs that are suspected in the widest sense of being the cause of social phobias and other mental disorders. “This is the largest association study so far into social phobia,” says associate professor (Privatdozent) Johannes Schumacher from the Institute of Human Genetics at the University of Bonn.

    Patients provided information about their symptoms

    Over the course of the study, scientists at the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at the University Hospital Bonn will ask the patients about their symptoms and the severity of their social phobia. Their DNA is also examined using a blood sample. Whether there is a link between the signs of the illness and the genes is being investigated by the scientists using statistical methods. The evaluation of the previously collected data indicated that an SNP in the serotonin transporter gene SLC6A4 is involved in the development of social phobia.

    This gene encodes a mechanism in the brain that is involved in transporting the important messenger serotonin. This substance suppresses, among other things, feelings of fear and depressive moods. “The result substantiates indications from previous studies that serotonin plays an important role in social phobia,” says associate professor (Privatdozent) Dr. Rupert Conrad from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy. Medications that block serotonin reuptake and increase the concentration of the messenger in the tissue fluid in the brain have already long been used to treat anxiety disorders and depression.

    Subjects can participate in expanded study

    The scientists now want to investigate more closely what the links are between the DNA and social phobia. “In order to achieve this goal, we need many more study participants who suffer from social anxiety,” says the psychologist and study coordinator Stefanie Rambau from the Clinic and Policlinic for Psychosomatic Medicine and Psychotherapy at University Hospital Bonn. Information about the study is available at http://www.SocialPhobiaResearch.de. “Those who take part will help to research social phobia. This is the basis of better diagnosis and treatment procedures in the future,” says Stefanie Rambau.


  4. MRIs predict which high-risk babies will develop autism as toddlers

    February 16, 2017 by Ashley

    From the University of North Carolina Health Care media release:

    autism_stairsUsing magnetic resonance imaging (MRI) in infants with older siblings with autism, researchers from around the country were able to correctly predict 80 percent of those infants who would later meet criteria for autism at two years of age.

    The study, published in Nature, is the first to show it is possible to identify which infants — among those with older siblings with autism — will be diagnosed with autism at 24 months of age.

    “Our study shows that early brain development biomarkers could be very useful in identifying babies at the highest risk for autism before behavioral symptoms emerge,” said senior author Joseph Piven, MD, the Thomas E. Castelloe Distinguished Professor of Psychiatry at the University of North Carolina-Chapel Hill. “Typically, the earliest an autism diagnosis can be made is between ages two and three. But for babies with older autistic siblings, our imaging approach may help predict during the first year of life which babies are most likely to receive an autism diagnosis at 24 months.”

    This research project included hundreds of children from across the country and was led by researchers at the Carolina Institute for Developmental Disabilities (CIDD) at the University of North Carolina, where Piven is director. The project’s other clinical sites included the University of Washington, Washington University in St. Louis, and The Children’s Hospital of Philadelphia. Other key collaborators are McGill University, the University of Alberta, the University of Minnesota, the College of Charleston, and New York University.

    This study could not have been completed without a major commitment from these families, many of whom flew in to be part of this,” said first author Heather Hazlett, PhD, assistant professor of psychiatry at the UNC School of Medicine and a CIDD researcher. “We are still enrolling families for this study, and we hope to begin work on a similar project to replicate our findings.”

    People with Autism Spectrum Disorder (or ASD) have characteristic social deficits and demonstrate a range of ritualistic, repetitive and stereotyped behaviors. It is estimated that one out of 68 children develop autism in the United States. For infants with older siblings with autism, the risk may be as high as 20 out of every 100 births. There are about 3 million people with autism in the United States and tens of millions around the world.

    Despite much research, it has been impossible to identify those at ultra-high risk for autism prior to 24 months of age, which is the earliest time when the hallmark behavioral characteristics of ASD can be observed and a diagnosis made in most children.

    For this Nature study, Piven, Hazlett, and researchers from around the country conducted MRI scans of infants at six, 12, and 24 months of age. They found that the babies who developed autism experienced a hyper-expansion of brain surface area from six to 12 months, as compared to babies who had an older sibling with autism but did not themselves show evidence of the condition at 24 months of age. Increased growth rate of surface area in the first year of life was linked to increased growth rate of overall brain volume in the second year of life. Brain overgrowth was tied to the emergence of autistic social deficits in the second year.

    Previous behavioral studies of infants who later developed autism — who had older siblings with autism -revealed that social behaviors typical of autism emerge during the second year of life.

    The researchers then took these data — MRIs of brain volume, surface area, cortical thickness at 6 and 12 months of age, and sex of the infants — and used a computer program to identify a way to classify babies most likely to meet criteria for autism at 24 months of age. The computer program developed the best algorithm to accomplish this, and the researchers applied the algorithm to a separate set of study participants.

    The researchers found that brain differences at 6 and 12 months of age in infants with older siblings with autism correctly predicted eight out of ten infants who would later meet criteria for autism at 24 months of age in comparison to those infants with older ASD siblings who did not meet criteria for autism at 24 months.

    “This means we potentially can identify infants who will later develop autism, before the symptoms of autism begin to consolidate into a diagnosis,” Piven said.

    If parents have a child with autism and then have a second child, such a test might be clinically useful in identifying infants at highest risk for developing this condition. The idea would be to then intervene ‘pre-symptomatically’ before the emergence of the defining symptoms of autism.

    Research could then begin to examine the effect of interventions on children during a period before the syndrome is present and when the brain is most malleable. Such interventions may have a greater chance of improving outcomes than treatments started after diagnosis.

    “Putting this into the larger context of neuroscience research and treatment, there is currently a big push within the field of neurodegenerative diseases to be able to detect the biomarkers of these conditions before patients are diagnosed, at a time when preventive efforts are possible,” Piven said. “In Parkinson’s for instance, we know that once a person is diagnosed, they’ve already lost a substantial portion of the dopamine receptors in their brain, making treatment less effective.

    Piven said the idea with autism is similar; once autism is diagnosed at age 2-3 years, the brain has already begun to change substantially.

    “We haven’t had a way to detect the biomarkers of autism before the condition sets in and symptoms develop,” he said. “Now we have very promising leads that suggest this may in fact be possible.”


  5. Brain neurons help keep track of time

    December 14, 2016 by Ashley

    From the American Association for the Advancement of Science media release:

    memory neuronsTurning the theory of how the human brain perceives time on its head, a novel analysis in mice reveals that dopamine neuron activity plays a key role in judgment of time, slowing down the internal clock. As Patrick Simen and Matthew Matell note in a related Perspective, “The results suggest the need to reassess the leading theory of dopamine function in timing — the dopamine clock hypothesis.”

    Organisms’ ability to accurately estimate periods of time is variable and depends on circumstances, including motivation, attention, and emotions. Dopamine (DA) neurons residing in the midbrain have been implicated as regulators of this complex process.

    However, a direct link between the signals carried by DA neurons and timekeeping is lacking. What’s more, current studies in which timing behavior is disrupted have demonstrated conflicting results — in some cases, increased DA release speeds up the subjective sense of time, while in other instances, it is slowed down or unaffected.

    To make sense of DA’s involvement in time approximation, Sofia Soares and colleagues tracked DA activity in mice performing timed tasks. The mice were presented with two audible tones, and trained to classify the interval between each as shorter or longer.

    Soares et al. observed bursts of activity in mouse DA neurons that synchronized exclusively to the second noise, reflecting the rodents’ anticipation of an upcoming reward, combined with their surprise about the arrival time of the sound. The authors discovered the transient activation or inhibition of dopamine neurons was sufficient to slow down or speed up time estimation, respectively. Simen and Matell emphasize the brain’s fine-tuned ramping up and down of DA signals may prove essential in resolving previous experimental inconsistencies, and identifying novel DA functions that help shape behavior.

     


  6. Physical stature as a teen could predict future stock choices

    November 9, 2016 by Ashley

    From the Cornell University media release:

    tablet computer seniorSocial scientists have long studied the relationship between a person’s height and their success in life. Taller people, studies purport, tend to be better educated, earn more money, and have higher confidence and self-esteem than those who are “vertically challenged.”

    A Cornell researcher and two of his former University of Miami colleagues are authors of a new study that takes that idea a step further — showing that observed physical attributes are related to participation in the stock market.

    Specifically: Individuals who are relatively tall are more likely to hold stocks in their financial portfolios, and those who are relatively overweight or obese are more risk-averse and less likely to participate in the market.

    Jawad Addoum, assistant professor of finance and the Robert R. Dyson Sesquicentennial Fellow in the Charles H. Dyson School of Applied Economics and Management, is co-author of “Stature, Obesity and Portfolio Choice,” which was published online Aug. 1 in the journal Management Science.

    Co-authors are Alok Kumar, Ph.D. ’03, finance department chair at Miami, and George Korniotis, associate professor of finance.

    Addoum, who arrived at Cornell in June after four years as assistant professor of finance at Miami, stresses that it’s not just height as an adult that plays a role in a person’s portfolio decisions.

    It’s really about height during teenage years,” he said. “Those who grow tall early drive most of this effect. People who grow tall early are able to enjoy a sort of social dominance as teens. Tall teens are more likely to play sports and participate in other extracurricular activities, and they tend to have a better overall experience in high school.”

    The researchers posit that people’s physical attributes could evoke environmental responses — and shape personality traits such as optimism, self-esteem and trust — that could in turn play a role in risk-taking behavior.

    Addoum and his team analyzed four sets of data — two from Europe and two from the U.S. — which contained detailed information regarding households’ investment decisions.

    The U.S. data sets included the Health and Retirement Study and the National Longitudinal Survey of Youth (NLSY). The latter sample, which included individuals who were age 14 to 22 in 1979, was analyzed separately from the other three sets; it only contains information about the decision to own stocks, mutual funds and bonds, whereas the other three data sets separated ownership of stocks and mutual funds with that of less risky bonds. However, it also reports height at two points in time: height during teenage years and final height as an adult.

    Noteworthy among the group’s findings:

    Gender-specific effects: Consistent with related studies, the group found that the positive effects of height are stronger for men than for women, and that the negative effects of body mass index (BMI) are greater for women than for men;

    Teen height vs. adult height: The researchers found that while both teen and adult height are important determinants of market participation, teen height appears to be economically more important. What’s more, adult height becomes statistically insignificant when relative current and relative teen BMI are factored in.

    BMI and impatience: Citing a 2015 study that linked BMI and impatience, the group attempted to link obese individuals’ avoidance of stocks to time preferences. However, analysis of NLSY findings suggest that cognitive skills are more telling in portfolio decisions than impatience.

    Addoum said that, in a traditional rational model, someone should be able to decide how to invest based on their current situation and not on physiological factors or experiences during their teen years. But that’s not always the case.

    “Someone should be able to look at this as, “I want to build my wealth, and I should invest,'” he said. “But it turns out that early experiences can lead to hesitance in terms of financial risk-taking. This suggests that social experiences can have long-lasting effects that really matter.”

    The group says its findings could be applied to other behaviors, such as risk-taking among hedge and mutual fund managers, as well as corporate managers. Future work will examine, among other things, the role of physical attributes in managerial decisions.


  7. ‘Sixth sense’ may be more than just a feeling

    September 29, 2016 by Ashley

    From the National Institutes of Health media release:

    regions of the brain correlated with more severe neurobehavioral symptomsWith the help of two young patients with a unique neurological disorder, an initial study by scientists at the National Institutes of Health suggests that a gene called PIEZO2 controls specific aspects of human touch and proprioception, a “sixth sense” describing awareness of one’s body in space. Mutations in the gene caused the two to have movement and balance problems and the loss of some forms of touch. Despite their difficulties, they both appeared to cope with these challenges by relying heavily on vision and other senses.

    “Our study highlights the critical importance of PIEZO2 and the senses it controls in our daily lives,” said Carsten G. Bönnemann, M.D., senior investigator at the NIH’s National Institute of Neurological Disorders and Stroke (NINDS) and a co-leader of the study published in the New England Journal of Medicine. “The results establish that PIEZO2 is a touch and proprioception gene in humans. Understanding its role in these senses may provide clues to a variety of neurological disorders.”

    Dr. Bönnemann’s team uses cutting edge genetic techniques to help diagnose children around the world who have disorders that are difficult to characterize. The two patients in this study are unrelated, one nine and the other 19 years old. They have difficulties walking; hip, finger and foot deformities; and abnormally curved spines diagnosed as progressive scoliosis.

    Working with the laboratory of Alexander T. Chesler, Ph.D., investigator at NIH’s National Center for Complementary and Integrative Health (NCCIH), the researchers discovered that the patients have mutations in the PIEZO2 gene that appear to block the normal production or activity of Piezo2 proteins in their cells. Piezo2 is what scientists call a mechanosensitive protein because it generates electrical nerve signals in response to changes in cell shape, such as when skin cells and neurons of the hand are pressed against a table. Studies in mice suggest that Piezo2 is found in the neurons that control touch and proprioception.

    “As someone who studies Piezo2 in mice, working with these patients was humbling,” said Dr. Chesler. “Our results suggest they are touch-blind. The patient’s version of Piezo2 may not work, so their neurons cannot detect touch or limb movements.

    Further examinations at the NIH Clinical Center suggested the young patients lack body awareness. Blindfolding them made walking extremely difficult, causing them to stagger and stumble from side to side while assistants prevented them from falling. When the researchers compared the two patients with unaffected volunteers, they found that blindfolding the young patients made it harder for them to reliably reach for an object in front of their faces than it was for the volunteers. Without looking, the patients could not guess the direction their joints were being moved as well as the control subjects could.

    The patients were also less sensitive to certain forms of touch. They could not feel vibrations from a buzzing tuning fork as well as the control subjects could. Nor could they tell the difference between one or two small ends of a caliper pressed firmly against their palms. Brain scans of one patient showed no response when the palm of her hand was brushed.

    Nevertheless, the patients could feel other forms of touch. Stroking or brushing hairy skin is normally perceived as pleasant. Although they both felt the brushing of hairy skin, one claimed it felt prickly instead of the pleasant sensation reported by unaffected volunteers. Brain scans showed different activity patterns in response to brushing between unaffected volunteers and the patient who felt prickliness.

    Despite these differences, the patients’ nervous systems appeared to be developing normally. They were able to feel pain, itch, and temperature normally; the nerves in their limbs conducted electricity rapidly; and their brains and cognitive abilities were similar to the control subjects of their age.

    “What’s remarkable about these patients is how much their nervous systems compensate for their lack of touch and body awareness,” said Dr. Bönnemann. “It suggests the nervous system may have several alternate pathways that we can tap into when designing new therapies.

    Previous studies found that mutations in PIEZO2 may have various effects on the Piezo2 protein that may result in genetic musculoskeletal disorders, including distal arthrogryposis type 5, Gordon Syndrome, and Marden-Walker Syndrome. Drs. Bönnemann and Chesler concluded that the scoliosis and joint problems of the patients in this study suggest that Piezo2 is either directly required for the normal growth and alignment of the skeletal system or that touch and proprioception indirectly guide skeletal development.

    Our study demonstrates that bench and bedside research are connected by a two-way street,” said Dr. Chesler. “Results from basic laboratory research guided our examination of the children. Now we can take that knowledge back to the lab and use it to design future experiments investigating the role of PIEZO2 in nervous system and musculoskeletal development.”

    This work was supported by the NCCIH and NINDS intramural research programs.


  8. ADHD may emerge after childhood for some people, according to new study

    September 21, 2016 by Ashley

    From the King’s College London media release:

    man_eating_appleWhile it is well established that childhood ADHD may continue into adulthood, new research by King’s College London suggests that for some people the disorder does not emerge until after childhood.

    Attention-deficit/hyperactivity disorder (ADHD) is a developmental disorder marked by inattention, hyperactivity and impulsivity and is one of the most common behavioural disorders in children. It is widely believed that adult ADHD is the continuation of the disorder from childhood.

    However, researchers from the Institute of Psychiatry, Psychology & Neuroscience (IoPPN) at King’s found that nearly 70 per cent of the young adults with ADHD in their study did not meet criteria for the disorder at any of the childhood assessments. Adults with this ‘late-onset’ ADHD had high levels of symptoms, impairment and other mental health disorders.

    Published in JAMA Psychiatry, these findings have important implications for our understanding of ADHD, as ADHD that onsets in adulthood could have different causes to childhood ADHD.

    Findings from this UK cohort are confirmed by evidence for adult-onset ADHD world-wide: a study from Brazil will be published by JAMA Psychiatry alongside this research, which also identified a large proportion of adults with ADHD as not having the disorder in childhood. Both the UK and Brazilian studies support previous findings from a New Zealand cohort.

    The research sample in the King’s College London study included more than 2,200 British twins from the Environmental Risk (E-Risk) Longitudinal Twin Study. Symptoms of childhood ADHD were measured at the ages of 5, 7, 10 and 12 through mother and teacher reports. Young adults were interviewed at the age of 18 to assess ADHD symptoms and any associated impairments, as well as the existence of other mental health disorders.

    As the study was a cohort of twins, the researchers were also able to examine the genetic basis of ADHD. They found that adult ADHD was less heritable than childhood ADHD, and that having a twin with childhood ADHD did not place individuals at a higher risk of developing late-onset ADHD.

    Dr Jessica Agnew-Blais from the IoPPN at King’s College London said: ‘We were very interested by this large ‘late-onset’ ADHD group, as ADHD is generally seen as a childhood-onset neurodevelopmental disorder. We speculated about the nature of late-onset ADHD: the disorder could have been masked in childhood due to protective factors, such as a supportive family environment. Or it could be entirely explained by other mental health problems. Alternatively, late-onset ADHD could be a distinct disorder altogether. We think it is important that we continue to investigate the underlying causes of late-onset ADHD.

    Although ADHD occurs in approximately 4 per cent of adults, relatively few adults receive a diagnosis or treatment for the disorder. It is crucial that we take a developmental approach to understanding ADHD, and that the absence of a childhood diagnosis should not prevent adults with ADHD from receiving clinical attention.’

    Professor Louise Arseneault, also from the IoPPN at King’s College London, said: ‘Our research sheds new light on the development and onset of ADHD, but it also brings up many questions about ADHD that arises after childhood. How similar or different is ‘late-onset’ ADHD compared with ADHD that begins in childhood? How and why does late-onset ADHD arise? What treatments are most effective for late-onset ADHD? These are the questions we should now be seeking to answer.’


  9. Altruism is favored by chance

    August 9, 2016 by Ashley

    From the University of Bath media release:

    sharing childrenWhy do we feel good about giving to charity when there is no direct benefit to ourselves, and feel bad about cheating the system? Mathematicians may have found an answer to the longstanding puzzle as to why we have evolved to cooperate.

    An international team of researchers, publishing in the Proceedings of the National Academy of Sciences, has found that altruism is favoured by random fluctuations in nature, offering an explanation to the mystery as to why this seemingly disadvantageous trait has evolved.

    The researchers, from the Universities of Bath, Manchester and Princeton (USA), developed a mathematical model to predict the path of evolution when altruistic “cooperators” live alongside “cheats” who use up resources but do not themselves contribute.

    Humans are not the only organisms to cooperate with one another. The scientists used the example of Brewer’s yeast, which can produce an enzyme called invertase that breaks down complex sugars in the environment, creating more food for all. However, those that make this enzyme use energy that could instead have been used for reproduction, meaning that a mutant “cheating” strain that waits for others to do the hard work would be able to breed faster as a result.

    Darwinian evolution suggests that their ability to breed faster will allow the cheats (and their cheating offspring) to proliferate and eventually take over the whole population. This problem is common to all altruistic populations, raising the difficult question of how cooperation evolved.

    Dr Tim Rogers, Royal Society University Research Fellow at the University of Bath, said: “Scientists have been puzzled by this for a long time. One dominant theory was that we act more favourably towards genetic relatives than strangers, summed up by J. S. Haldane’s famous claim that he would jump into a river to save two brothers or eight cousins.

    What we are lacking is an explanation of how these behaviours could have evolved in organisms as basic as yeast. Our research proposes a simple answer — it turns out that cooperation is favoured by chance.”

    The key insight is that the total size of population that can be supported depends on the proportion of cooperators: more cooperation means more food for all and a larger population. If, due to chance, there is a random increase in the number of cheats then there is not enough food to go around and total population size will decrease. Conversely, a random decrease in the number of cheats will allow the population to grow to a larger size, disproportionally benefitting the cooperators. In this way, the cooperators are favoured by chance, and are more likely to win in the long term.

    Dr George Constable, soon to join the University of Bath from Princeton, uses the analogy of flipping a coin, where heads wins £20 but tails loses £10:

    Although the odds winning or losing are the same, winning is more good than losing is bad. Random fluctuations in cheat numbers are exploited by the cooperators, who benefit more then they lose out.”


  10. Researchers identify new autism blood biomarker

    May 4, 2016 by Ashley

    From the UT Southwestern Medical Center media release:

    autism metaphorResearchers at UT Southwestern Medical Center have identified a blood biomarker that may aid in earlier diagnosis of children with autism spectrum disorder, or ASD.

    Early intervention is the key to the best treatment for ASD, which affects about 1 in 70 children. Unfortunately, most children are not diagnosed until about age 4, when communication and social disabilities become apparent. This neurodevelopmental disorder is characterized by social interaction and communication challenges, and restricted and repetitive patterns of behavior.

    In a recent edition of Scientific Reports, UT Southwestern researchers reported on the identification of a blood biomarker that could distinguish the majority of ASD study participants versus a control group of similar age range. In addition, the biomarker was significantly correlated with the level of communication impairment, suggesting that the blood test may give insight into ASD severity.

    “Numerous investigators have long sought a biomarker for ASD,” said Dr. Dwight German, study senior author and Professor of Psychiatry at UT Southwestern. “The blood biomarker reported here along with others we are testing can represent a useful test with over 80 percent accuracy in identifying ASD.”

    Since other studies have found abnormalities in the immune systems of autistic children, researchers set out to search for antibodies in the blood related to ASD. In this study, researchers found that boys with ASD had significantly reduced levels of a serum IgG1 antibody. Investigating further, researchers analyzed 25 peptoid compounds that bound to IgG1 and zeroed in on one — ASD1 — that was 66 percent accurate in diagnosing ASD. When combined with thyroid stimulating hormone level measurements, the ASD1-binding biomarker was 73 percent accurate at diagnosis.

    More testing, including analysis of blood samples from girls with ASD, is needed to further validate the findings, Dr. German said. Girls made up a small ratio of the study group, and the biomarker did not correlate as strongly with ASD diagnosis as with boys.