Injuries From Teen Fighting Deal a Blow to IQ

New study explores connection between physical fights, cognitive decline

A new Florida State University study has found that adolescent boys who are hurt in just two physical fights suffer a loss in IQ that is roughly equivalent to missing an entire year of school. Girls experience a similar loss of IQ after only a single fighting-related injury.

The findings are significant because decreases in IQ are associated with lower educational achievement and occupational performance, mental disorders, behavioral problems and even longevity, the researchers said.

“It’s no surprise that being severely physically injured results in negative repercussions, but the extent to which such injuries affect intelligence was quite surprising,” said Joseph A. Schwartz, a doctoral student who conducted the study with Professor Kevin Beaver in FSU’s College of Criminology and Criminal Justice.

Their findings are outlined in the paper, “Serious Fighting-Related Injuries Produce a Significant Reduction in Intelligence,” which was published in the Journal of Adolescent Health. The study is among the first to look at the long-term effects of fighting during adolescence, a critical period of neurological development.

About 4 percent of high school students are injured as a result of a physical fight each year, the researchers said.

Schwartz and Beaver used data from the National Longitudinal Study of Adolescent Health collected between 1994 and 2002 to examine whether serious fighting-related injuries resulted in significant decreases in IQ over a 5- to 6-year time span. The longitudinal study began with a nationally representative sample of 20,000 middle and high school students who were tracked into adulthood through subsequent waves of data collection. At each wave of data collection, respondents were asked about a wide variety of topics, including personality traits, social relationships and the frequency of specific behaviors.

Perhaps not surprisingly, boys experienced a higher number of injuries from fighting than girls; however, the consequences for girls were more severe, a fact the researchers attributed to physiological differences that give males an increased ability to withstand physical trauma.

The researchers found that each fighting-related injury resulted in a loss of 1.62 IQ points for boys, while girls lost an average of 3.02 IQ points, even after controlling for changes in socio-economic status, age and race for both genders. Previous studies have indicated that missing a single year of school is associated with a loss of 2 to 4 IQ points.

The impact on IQ may be even greater when considering only head injuries, the researchers said. The data they studied took into account all fighting-related physical injuries.

The findings highlight the importance of schools and communities developing policies aimed at limiting injuries suffered during adolescence whether through fighting, bullying or contact sports, Schwartz said.

“We tend to focus on factors that may result in increases in intelligence over time, but examining the factors that result in decreases may be just as important,” he said. “The first step in correcting a problem is understanding its underlying causes. By knowing that fighting-related injuries result in a significant decrease in intelligence, we can begin to develop programs and protocols aimed at effective intervention.”

Study finds night owls more likely to be psychopaths

People who stay up late at night are more likely to display anti-social personality traits such as narcissism, Machiavellianism, and psychopathic tendencies, according to a study published by a University of Western Sydney researcher.

Dr Peter Jonason, from the UWS School of Social Sciences and Psychology, assessed over 250 people’s tendency to be a morning- or evening-type person to discover whether this was linked to the ‘Dark Triad’ of personality traits.

The results, published in Personality and Individual Differences, found students who were awake in the twilight hours displayed greater anti-social tendencies than those who went to bed earlier.

“Those who scored highly on the Dark Triad traits are, like many other predators such as lions and scorpions, creatures of the night,” he says.

"For people pursuing a fast life strategy like that embodied by the Dark Triad traits, it’s better to occupy and exploit a lowlight environment where others are sleeping and have diminished cognitive functioning."

Dr Jonason says there may be an evolutionary basis for the link between anti-social behaviour and a preference to being awake late at night.

“There is likely to be a co-evolutionary arms race between cheaters and those who wish to detect and punish them, and the Dark Triad traits may represent specialized adaptations to avoid detection,” he says.

“The features of the night - a low-light environment where others are sleeping - may facilitate the casual sex, mate-poaching, and risk-taking the Dark Triad traits are linked to.”

“Indeed, most crimes and most sexual activity peak at night, suggesting just such a link.”

Dr Jonason adds that far more work is needed, but these results represent an important advance in behavioural ecological and evolutionary psychological models of the Dark Triad, as well as ‘darker’ aspects of human nature and personality.

Baby owls sleep like baby humans

Researchers at the Max Planck Institute for Ornithology and the University of Lausanne have discovered that the sleeping patterns of baby birds are similar to that of baby mammals. What is more, the sleep of baby birds appears to change in the same way as it does in humans. Studying barn owls in the wild, the researchers discovered that this change in sleep is strongly correlated with the expression of a gene involved in producing dark, melanic feather spots, a trait known to covary with behavioral and physiological traits in adult owls. These findings raise the intriguing possibility that sleep-related developmental processes in the brain contribute to the link between melanism and other traits observed in adult barn owls and other animals.

Sleep in mammals and birds consists of two phases, REM sleep (“Rapid Eye Movement Sleep”) and non-REM sleep. We experience our most vivid dreams during REM sleep, a paradoxical state characterized by awake-like brain activity. Despite extensive research, REM sleep’s purpose remains a mystery. One of the most salient features of REM sleep is its preponderance early in life. A variety of mammals spend far more time in REM sleep during early life than when they are adults. For example, as newborns, half of our time asleep is spent in REM sleep, whereas last night REM sleep probably encompassed only 20-25% percent of your time snoozing.Although birds are the only non-mammalian group known to clearly engage in REM sleep, it has been unclear whether sleep develops in the same manner in baby birds. Consequently, Niels Rattenborg of the MPIO, Alexandre Roulin of Unil, and their PhD student Madeleine Scriba, reexamined this question in a population of wild barn owls. They used an electroencephalogram (EEG) and movement data logger in conjunction with minimally invasive EEG sensors designed for use in humans, to record sleep in 66 owlets of varying age. During the recordings, the owlets remained in their nest box and were fed normally by their parents. After having their sleep patterns recorded for up to five days, the logger was removed. All of the owlets subsequently fledged and returned at normal rates to breed in the following year, indicating that there were no long-term adverse effects of eves-dropping on their sleeping brains.

Despite lacking significant eye movements (a trait common to owls), the owlets spent large amounts of time in REM sleep. “During this sleep phase, the owlets’ EEG showed awake-like activity, their eyes remained closed, and their heads nodded slowly”, reports Madeleine Scriba from the University of Lausanne (see video). Importantly, the researchers discovered that just as in baby humans, the time spent in REM sleep declined as the owlets aged.

In addition, the team examined the relationship between sleep and the expression of a gene in the feather follicles involved in producing dark, melanic feather spots. “As in several other avian and mammalian species, we have found that melanic spotting in owls covaries with a variety of behavioral and physiological traits, many of which also have links to sleep, such as immune system function and energy regulation”, notes Alexander Roulin from the University of Lausanne. Indeed, the team found that owlets expressing higher levels of the gene involved in melanism had less REM sleep than expected for their age, suggesting that their brains were developing faster than in owlets expressing lower levels of this gene. In line with this interpretation, the enzyme encoded by this gene also plays a role in producing hormones (thyroid and insulin) involved in brain development.

Although additional research is needed to determine exactly how sleep, brain development, and pigmentation are interrelated, these findings nonetheless raise several intriguing questions. Does variation in sleep during brain development influence adult brain organization? If so, does this contribute to the link between behavioral and physiological traits and melanism observed in adult owls? Do sleep and pigmentation covary in adult owls, and if so how does this influence their behavior and physiology? Finally, Niels Rattenborg from the Max Planck Institute for Ornithology in Seewiesen hopes that “this naturally occurring variation in REM sleep during a period of brain development can be used to reveal exactly what REM sleep does for the developing brain in baby owls, as well as humans.”

Largest neuronal network simulation achieved using K computer

By exploiting the full computational power of the Japanese supercomputer, K computer, researchers from the RIKEN HPCI Program for Computational Life Sciences, the Okinawa Institute of Technology Graduate University (OIST) in Japan and Forschungszentrum Jülich in Germany have carried out the largest general neuronal network simulation to date.

The simulation was made possible by the development of advanced novel data structures for the simulation software NEST. The relevance of the achievement for neuroscience lies in the fact that NEST is open-source software freely available to every scientist in the world.

Using NEST, the team, led by Markus Diesmann in collaboration with Abigail Morrison both now with the Institute of Neuroscience and Medicine at Jülich, succeeded in simulating a network consisting of 1.73 billion nerve cells connected by 10.4 trillion synapses. To realize this feat, the program recruited 82,944 processors of the K computer.  The process took 40 minutes to complete the simulation of 1 second of neuronal network activity in real, biological, time.

Although the simulated network is huge, it only represents 1% of the neuronal network in the brain. The nerve cells were randomly connected and the simulation itself was not supposed to provide new insight into the brain - the purpose of the endeavor was to test the limits of the simulation technology developed in the project and the capabilities of K. In the process, the researchers gathered invaluable experience that will guide them in the construction of novel simulation software.

This achievement gives neuroscientists a glimpse of what will be possible in the future, with the next generation of computers, so called exa-scale computers.

“If peta-scale computers like the K computer are capable of representing 1% of the network of a human brain today, then we know that simulating the whole brain at the level of the individual nerve cell and its synapses will be possible with exa-scale computers hopefully available within the next decade,” explains Diesmann.

Memory of 250.000 PCs

Simulating a large neuronal network and a process like learning requires large amounts of computing memory.  Synapses, the structures at the interface between two neurons, are constantly modified by neuronal interaction and simulators need to allow for these modifications.

More important than the number of neurons in the simulated network is the fact that during the simulation each synapse between excitatory neurons was supplied with 24 bytes of memory. This enabled an accurate mathematical description of the network.

In total, the simulator coordinated the use of about 1 petabyte of main memory, which corresponds to the aggregated memory of 250.000 PCs.

NEST

NEST is a widely used, general-purpose neuronal network simulation software available to the community as open source. The team ensured that their optimizations were of general character, independent of a particular hardware or neuroscientific problem. This will enable neuroscientists to use the software to investigate neuronal systems using normal laptops, computer clusters or, for the largest systems, supercomputers, and easily exchange their model descriptions.

A large, international project

Work on optimizing NEST for the K computer started in 2009 while the supercomputer was still under construction. Shin Ishii, leader of the brain science projects on K at the time, explains that: “Having access to the established supercomputers at Jülich, JUGENE and JUQUEEN, was essential, to prepare for K and cross-check results.”

Mitsuhisa Sato, of the RIKEN Advanced Institute for Computer Science, points out that: “Many researchers at many different Japanese and European institutions have been involved in this project, but the dedication of Jun Igarashi now at OIST, Gen Masumoto now at the RIKEN Advanced Center for Computing and Communication, Susanne Kunkel and Moritz Helias now at Forschungszentrum Jülich was key to the success of the endeavor.”

Paving the way for future projects

Kenji Doya of OIST, currently leading a project aiming to understand the neural control of movement and the mechanism of Parkinson’s disease, says: “The new result paves the way for combined simulations of the brain and the musculoskeletal system using the K computer. These results demonstrate that neuroscience can make full use of the existing peta-scale supercomputers.”

The achievement on K provides new technology for brain research in Japan and is encouraging news for the Human Brain Project (HBP) of the European Union, scheduled to start this October. The central supercomputer for this project will be based at Forschungszentrum Jülich.

The researchers in Japan and Germany are planning on continuing their successful collaboration in the upcoming era of exa-scale systems.

2 dimensions of value: Dopamine neurons represent reward but not aversiveness

To make decisions, we need to estimate the value of sensory stimuli and motor actions, their “goodness” and “badness.” We can imagine that good and bad are two ends of a single continuum, or dimension, of value. This would be analogous to the single dimension of light intensity, which ranges from dark on one end to bright light on the other, with many shades of gray in between. Past models of behavior and learning have been based on a single continuum of value, and it has been proposed that a particular group of neurons (brain cells) that use dopamine as a neurotransmitter (chemical messenger) represent the single dimension of value, signaling both good and bad.

The experiments reported here show that dopamine neurons are sensitive to the value of reward but not punishment (like the aversiveness of a bitter taste). This demonstrates that reward and aversiveness are represented as two discrete dimensions (or categories) in the brain. “Reward” refers to the category of good things (food, water, sex, money, etc.), and “punishment” to the category of bad things (stimuli associated with harm to the body and that cause pain or other unpleasant sensations or emotions).

Rather than having one neurotransmitter (dopamine) to represent a single dimension of value, the present results imply the existence of four neurotransmitters to represent two dimensions of value. Dopamine signals evidence for reward (“gains”) and some other neurotransmitter presumably signals evidence against reward (“losses”). Likewise, there should be a neurotransmitter for evidence of danger and another for evidence of safety. It is interesting that there are three other neurotransmitters that are analogous to dopamine in many respects (serotonin, norepinephrine, and acetylcholine), and it is possible that they could represent the other three value signals.

Burnt sugar-derivative reduces muscle wasting in fly and mouse models of muscular dystrophy

A trace substance in caramelized sugar, when purified and given in appropriate doses, improves muscle regeneration in a mouse model of Duchenne muscular dystrophy. The findings are published today (Aug. 1) in the journal Skeletal Muscle.

Morayma Reyes, professor of pathology and laboratory medicine, and Hannele Ruohola-Baker, professor of biochemistry and associate director of the Institute for Stem Cell and Regenerative Medicine, headed the University of Washington team that made the discovery. The first authors of the paper were Nicholas Ieronimakis, UW Department of Pathology; and Mario Pantoja, UW Department of Biochemistry.

They explained that the mice in their study, like boys with the gender-linked inherited disorder, are missing the gene that produces dystrophin, a muscle-repair protein. Neither the mice nor the affected boys can replace enough of their routinely lost muscle cells. In people, muscle weakness begins when the boys are toddlers, and progresses until, as teens, they can no longer walk unaided. During early adulthood, their heart and respiratory muscles weaken. Even with ventilators to assist breathing, death usually ensues before age 30. No cure or satisfactory treatment is available. Prednisone drugs relieve some symptoms, but at the cost of severe side effects.

The disabling, then lethal, nature of the rare disease in young men presses scientists to search for better therapeutic agents. Reyes and Ruohola-Baker are seeking ways to suppress the disorder’s characteristic functional and structural muscle defects.

Ruohola-Baker’s lab originally identified the sphingosine 1-phosphate (S1P) pathway as a critical player in ameliorating muscular dystrophy in flies. Her lab did this through a large genetic suppressor screen using the fruit fly, Drosophila melanogaster. Sphingosine 1-phosphate is found in the cells of most living beings from yeasts to mammals. Named after the enigmatic sphinx, this cell signal is important in many activities of living cells, from migration to proliferation. The multi-talented, bioactive lipid is essential, Reyes said, in turning stem cells into specific types of cells, in regenerating damaged tissue, and in inhibiting cell death. Without cell receptors for sphingosine 1-phosphate, an embryo would fail to develop.

Other scientists had observed that levels of sphingosine 1-phosphate are lower in the muscles of mice with the muscular dystrophy mutation, and that certain cell repair pathways involving this signal are impaired. However, sphingosine 1-phosphate couldn’t be administered as a drug because it is rapidly used up.

Instead, Reyes and Ruohola-Baker sought to prevent the sphingosine 1-phosphate occurring naturally in the body from degrading. A fruit fly model of Duchenne muscular dystrophy allowed Ruohola-Baker’s lab to rapidly score small molecule therapy candidates for raising the level of sphingosine 1-phosphate. Flies with the genetic defect act normally after they hatch and fly around, but in a few weeks, due to muscle degeneration, they are flightless. By using insect activity monitors, the scientists assessed the effects of drug and gene therapy candidates on the flies’ ability to move.

This screening tool led to the discovery that a small molecule with a long name, 2-acetyl4 (5)-tetrahydroxybutyl imidazole, or THI for short, blocks an enzyme that breaks down sphingosine 1-phosphate.

“It’s interesting to note that THI is a trace component of Caramel Color III, which the U.S. Food and Drug Administration categories as ‘generally recognized as safe’,” said Reyes. The substance is also found in very tiny amounts in burnt sugar, brown sugar, beer, cola and some candies.

The researchers added a purified, concentrated form of THI to the food of young flies with the muscular dystrophy-like mutation. They confirmed that the THI alleviated muscle wasting in the flies. A few other drugs, including a THI derivative and an unrelated drug now in clinical trials for rheumatoid arthritis, also showed beneficial effects in fruit flies.

The study of THI then switched from insects to mammals. Reyes lab began by treating old dystrophic mice with direct injection of THI. Later, the researchers simply added the compound to the drinking water in the habitats of young dystrophic mice. These mice were comparable in developmental stage to human teens who have muscular dystrophy genetic variation.

“We observed that treatment with THI significantly increased muscle fiber size and muscle-specific force in our affected mice,” Reyes said. “We also saw that other hallmarks of impaired muscle regeneration – fat deposits and fibrosis [scar tissue] accumulation – were also lower in the THI-treated mice.”

The research team linked the desired regenerative effects in the mice to the response of muscle-forming cells and the subsequent regrowth of muscle fibers. A type of sphingosine 1-phosphate, and cell receptors for it, also were observed in the cells in the regenerating muscle fibers. The researchers proposed that sphingosine 1-phosphate turned up the dial on the regulators for the biochemical pathways that mediate skeletal muscle mass and muscle function.

Now that they have shown proof-of-concept, the researchers hope to conduct additional animal studies on THI and other compounds that protect the body’s supply of sphingosine 1-phosphate necessary for muscle cell regeneration. If THI continues to show promise as a nutraceutical or food-based drug, medical scientists will head into pre-clinical studies of effectiveness and safety before advancing to human trials. In addition to muscular dystrophy treatment research, similar studies might also be conducted in the future on loss of muscle strength during normal or accelerated aging.

While excited about the preliminary findings, the scientists cautioned that they are still at the very earliest stages of research, and that much more work needs to be done before any conclusions can be drawn about the potential of THI as a muscular dystrophy treatment.

New Insight Into How Brain ‘Learns’ Cocaine Addiction

A team of researchers says it has solved the longstanding puzzle of why a key protein linked to learning is also needed to become addicted to cocaine. Results of the study, published in the Aug. 1 issue of the journal Cell, describe how the learning-related protein works with other proteins to forge new pathways in the brain in response to a drug-induced rush of the “pleasure” molecule dopamine. By adding important detail to the process of addiction, the researchers, led by a group at Johns Hopkins, say the work may point the way to new treatments.

“The broad question was why and how cocaine strengthened certain circuits in the brain long term, effectively re-wiring the brain for addiction,” says Paul Worley, M.D., a professor in the Solomon H. Snyder Department of Neuroscience at the Johns Hopkins University School of Medicine. “What we found in this study was how two very different types of systems in the brain work together to make that happen.” Cocaine addiction, experts say, is among the strongest of addictions.

Worley did not come to the problem as an addiction researcher, but as an expert in a group of genes known as immediate early genes, which rapidly ramp up production in neurons when the brain is exposed to new information. In 2001, he said, a European group led by François Conquet of GlaxoSmithKline reported that deleting mGluR5, a protein complex that responds to the common brain-signaling molecule glutamate, made mice unresponsive to cocaine. “That finding came out of the blue,” says Worley, who knew mGluR proteins for their interactions with immediate early genes. “I never would have thought this type of protein was linked to dopamine and addiction, because the functions for it that we knew about up to that point were completely unrelated. That’s what scientists love: when you’re pretty sure something is right, but you don’t have a clue why.”

The finding set Worley’s research group on a long search for an explanation. Eventually, in addition to studying the effects of altering genes for the relevant proteins in mice, they partnered with experts in measuring the brain’s electrical signals and in a biophysical technique that detects when chemical bonds are rotated within protein molecules. Using different types of experiments, they pieced together a complex story of how dopamine released in response to cocaine works together with mGluR5 and immediate early genes to switch cells into synapse-strengthening mode.

“The process we identified explains how cocaine exposure can co-opt normal mechanisms of learning to induce addiction,” Worley says. Knowing the details of the mechanism may help researchers identify targets for potential drugs to treat addiction, he adds.

(Image: Milos Jokic)