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<title>Biological Psychology NewsLink</title>
<link>http://www.biopsychology.com/news/</link>
<description>
Recent news articles related to the field of Biological Psychology.  
A companion to the textbook Biological Psychology by S. Marc Breedlove, Mark R. Rosenzweig, Neil V. Watson.
Published by Sinauer Associates
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<title>Biological clock began ticking 2.5 billion years ago</title>
<link>http://www.newscientist.com/article/mg21428653.900-biological-clock-began-ticking-25-billion-years-ago.html</link>
<description>
  by Debora MacKenzie

OUR core physiology relies on subtle organic timers: disrupt them, and effects range from jet lag to schizophrenia. Exactly how and when life began keeping time is unclear, but a candidate for the original biological clock may solve the mystery.

Biological clocks are ubiquitous in nature, so the first clock should pre-date the evolutionary parting of the ways that led to modern groups of organisms. All the clocks found so far are unique to different groups of organisms, though. Not so the clock discovered by Akhilesh Reddy at the University of Cambridge and colleagues. In an enzyme called peroxiredoxin (PRX), they seem to have found a grandfather clock - one that is common to nearly all life.

PRX gets rid of poisonous, highly reactive oxygen (ROS), which is produced by oxygen-based metabolism. And the enzyme oscillates: it flits between an active and inactive state, depending on whether oxygen is bound to the active site. Using antibodies that bind only to the oxidised enzyme, the team found that PRX oxidation keeps cycling independently on a 24-hour cycle, even when organisms were kept in constant light or constant dark.

Moreover, they found this PRX cycle in mice, fruit flies, a plant, a fungus, an alga, bacteria and even in archaea - the most primitive of all cellular life (Nature, DOI: 10.1038/nature11088). That suggests PRX evolved early in life's history. A gene sequence analysis suggests it did so 2.5 billion years ago, during the Great Oxygenation Event (GOE) - a critical interval when the oxygen released by photosynthesis began to accumulate in the atmosphere.

&amp;Acirc;&amp;copy; Copyright Reed Business Information Ltd.
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<title>Explosions cause brain damage through head movement</title>
<link>http://www.newscientist.com/article/dn21819-explosions-cause-brain-damage-through-head-movement.html</link>
<description>
 by Jamie Condliffe

Soldiers experience high-pressure shock waves and immense forces during explosions in the field, but research suggests brain trauma is caused merely by the sudden head movements.

It has been unclear whether trauma from explosions is caused through high-pressure shock waves penetrating the skull, or through another mechanism. Now a team of researchers from Boston University have performed post mortems on soldiers to establish how traumatic brain injury occurs during explosions.

Many blast victims develop symptoms consistent with chronic traumatic encephalopathy (CTE), a degenerative brain disease that can cause memory problems, depression and learning difficulties. However, CTE is usually caused by repeated concussions such as those experienced by American football players &amp;acirc; not one-off blasts.

&amp;quot;The damage in football players has been linked to acceleration forces due to head impact,&amp;quot; explains Robin Cleveland, a medical engineer who worked on the project at Boston University before moving to the University of Oxford. &amp;quot;Our goal was to see if the same mechanism was responsible for blast injury.&amp;quot;

Cleveland and his colleagues performed a post mortem analysis of brains from four soldiers who had experienced blasts. They compared the brains to those of American footballers and a wrestler who all had a history of repetitive concussive injury, as well as with a person with no brain trauma. They found firm evidence of CTE, as indicated by abnormal deposits of the protein tau in the brain of the soldiers, which was indistinguishable from CTE in the athletes.

&amp;Acirc;&amp;copy; Copyright Reed Business Information Ltd.
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<title>Afghanistan, Like Football, May Be Bad for the Brain</title>
<link>http://news.sciencemag.org/sciencenow/2012/05/afghanistan-like-football-may-be.html?ref=hp</link>
<description>
by Greg Miller

Autopsies of four U.S. military veterans who served in Iraq and Afghanistan reveal features of the same neurodegenerative disease found previously in athletes, researchers report. Experiments with mice suggest that the underlying mechanisms may be similar.

In the past 10 years, the widely reported suicides and accidental deaths of professional football players and other athletes&amp;acirc;such as that of Junior Seau earlier this month -- have sparked inquiries into whether even seemingly minor blows to the head can cause personality changes, dementia, and brain degeneration later in life. Autopsies of dozens of former players have revealed a condition known as chronic traumatic encephalopathy (CTE). Its hallmark is the abnormal accumulation of a protein called tau. Many of the athletes diagnosed with CTE on autopsy (currently the only definitive test) had a history of problems with anger, rash and risky decision-making, impairments of memory and attention, and alcohol or drug abuse.

Clinicians and researchers working with troops returning from Iraq and Afghanistan have seen similar symptoms. The new study, led by Lee Goldstein, a physician-scientist who focuses on neurodegenerative disease at Boston University, and Ann McKee, a neuropathologist at the Bedford Veterans Affairs Medical Center in Massachusetts, ties these troublesome threads together.

McKee examined the brains of four veterans, men between the ages of 22 and 45, who suffered from various combinations of cognitive, emotional, and impulse-control problems before dying from suicide or other causes.

&amp;Acirc;&amp;copy; 2010 American Association for the Advancement of Science. </description>
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<title>Trials highlight worrying flaws in psychiatry 'bible'</title>
<link>http://www.newscientist.com/article/mg21428653.600-trials-highlight-worrying-flaws-in-psychiatry-bible.html</link>
<description>
 by Peter Aldhous

HOW reliable is reliable enough? When it comes to diagnosing mental illness, most people would want the bar set pretty high, which is why the latest revision of psychiatry's diagnostic manual has become mired in controversy - again.

Last week, at its annual meeting in Philadelphia, Pennsylvania, the American Psychiatric Association revealed results from &amp;quot;field trials&amp;quot; of diagnoses proposed for the next edition of the APA's Diagnostic and Statistical Manual of Mental Disorders, or DSM-5. Essentially, the trials asked whether doctors would come to the same conclusions when assessing the same patients using the new diagnostic criteria.

While for some diagnoses reliability was good, others yielded scores little better than chance. Already, the results have led to two proposed disorders being relegated to the volume's appendix, which lists conditions that require further study. Critics argue that more might have joined them had the APA not adopted a low threshold for what is considered an acceptable score for reliability.

The conditions with questionable reliability include subtly altered descriptions of two of the most common diagnoses in psychiatry: major depressive disorder and generalised anxiety disorder. That has opened a can of worms, leaving some mental health professionals wondering about the reliability of even established psychiatric diagnoses.

&amp;Acirc;&amp;copy; Copyright Reed Business Information Ltd.
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<title>Paralyzed woman grips, sips coffee with robot arm</title>
<link>http://www.sciencenews.org/view/generic/id/340728/title/Paralyzed_woman_grips%2C_sips_coffee_with_robot_arm</link>
<description>
By Rachel Ehrenberg

Directing a robotic arm with her thoughts, a paralyzed woman named Cathy can pick up a bottle of coffee and sip it through a straw, a simple task that she hasn&amp;acirc;t done on her own for nearly 15 years. The technology that brought about the feat is a brain-computer interface system: A computer decodes signals from a tiny chip implanted in the woman&amp;acirc;s brain, translating her thoughts into actions that are carried out by the robot arm.

The seemingly mundane task of bringing a drink to one&amp;acirc;s mouth is the first published demonstration that severely paralyzed people can conduct directed movements in three-dimensional space using a brain-controlled robotic device. This latest application of the system, called BrainGate, is described in the May 17 Nature.  

&amp;acirc;Much has been demonstrated in terms of laboratory work and monkeys, but this is the first time showing something that&amp;acirc;s going to be useful for patients,&amp;acirc; says neuroscientist Andrew Jackson, of Newcastle University in England. A commentary by Jackson on the new developments appears in the same issue of Nature.

There&amp;acirc;s still a lot of work to do before BrainGate can be used outside a lab. In the current design, the tiny sensor that sits in the patient&amp;acirc;s brain is attached to a mini fridge&amp;acirc;sized computer via ungainly wires. So making the system wireless is one goal. The researchers hope that within a decade the BrainGate system will be available and affordable for people who are paralyzed or have prosthetic limbs. Eventually, similar technology might restore function to a natural limb that no longer works.

 &amp;Acirc;&amp;copy; Society for Science &amp;amp; the Public 2000 - 2012</description>
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<title>Best illusions of 2012: Making Brad Pitt look ugly</title>
<link>http://www.newscientist.com/blogs/nstv/2012/05/best-illusions-of-the-year-making-brad-pitt-look-ugly.html</link>
<description>
Sandrine Ceurstemont, editor, New Scientist TV

Brad Pitt may look attractive when seen head on. But an illusion that presents photos viewed in your peripheral vision shows how pretty faces can quickly look ugly.

The effect was discovered accidentally by psychology student Sean Murphy from the University of Queensland in Australia while looking at photos for another experiment. He went on to study the illusion with colleagues who discovered that the distortion occurs when the eyes of a series of photos are aligned and presented quickly in succession. The transformation is caused by differences between faces that follow each other, for example big eyes will seem to bulge if preceded by squinting eyes.

The illusion was published last year but now the team has created this new video that shows the effect more dramatically. The illusion has won second prize in this year's Best Illusion of the Year contest.

&amp;Acirc;&amp;copy; Copyright Reed Business Information Ltd.
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<title>Coffee gives jolt to life span</title>
<link>http://www.sciencenews.org/view/generic/id/340733/title/Coffee_gives_jolt_to_life_span</link>
<description>
By Nathan Seppa

It&amp;acirc;s the news that coffee addicts have been waiting for: Drinking several cups of coffee every day may help you live longer. A study of more than 400,000 people finds that drinking coffee reduces the risk of death from heart disease, stroke and even infections, researchers report in the May 17 New England Journal of Medicine.

Scientists have long puzzled over the notion that a stimulant could provide a health benefit. &amp;acirc;There&amp;acirc;s been a concern for a long time&amp;acirc; that coffee could even be detrimental, says study coauthor Neal Freedman, an epidemiologist at the National Cancer Institute in Bethesda, Md. &amp;acirc;Our results might provide some reassurance for long-term coffee drinkers.&amp;acirc;

Since the study volunteers weren&amp;acirc;t randomly assigned to drink coffee or not, the research has the limitations of being observational in nature. But with data from 402,260 participants, the results are &amp;acirc;very powerful&amp;acirc; and unlikely to be superseded by another coffee study anytime soon, says Roy Ziegelstein, a cardiologist at the Johns Hopkins Bayview Medical Center. &amp;acirc;This might be as good as it gets,&amp;acirc; he says.

Freedman and his colleagues analyzed data provided by men and women who completed a detailed questionnaire that included information about coffee intake as part of a medical study in the mid-1990s. The researchers excluded people who had previously had cancer, heart disease or some other serious illness and recorded the remaining volunteers&amp;acirc; mortality status through 2008 by checking death records.

 &amp;Acirc;&amp;copy; Society for Science &amp;amp; the Public 2000 - 2012</description>
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<title>NIH-funded research provides new clues on how ApoE4 affects Alzheimer's risk</title>
<link>http://www.nih.gov/news/health/may2012/ninds-16.htm</link>
<description>
Common variants of the ApoE gene are strongly associated with the risk of developing late-onset Alzheimer's disease, but the gene's role in the disease has been unclear. Now, researchers funded by the National Institutes of Health have found that in mice, having the most risky variant of ApoE damages the blood vessels that feed the brain.

The researchers found that the high-risk variant, ApoE4, triggers an inflammatory reaction that weakens the blood-brain barrier, a network of cells and other components that lines brain's brain vessels. Normally, this barrier allows nutrients into the brain and keeps harmful substances out.

The study appears today in Nature, and was led by Berislav Zlokovic, M.D., Ph.D., director of the Center for Neurodegeneration and Regeneration at the Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles.

&amp;acirc;Understanding the role of ApoE4 in Alzheimer's disease may be one of the most important avenues to a new therapy,&amp;quot; Dr. Zlokovic said. &amp;quot;Our study shows that ApoE4 triggers a cascade of events that damages the brain's vascular system,&amp;quot; he said, referring to the system of blood vessels that supply the brain.

The ApoE gene encodes a protein that helps regulate the levels and distribution of cholesterol and other lipids in the body. The gene exists in three varieties. ApoE2 is thought to play a protective role against both Alzheimer's and heart disease, ApoE3 is believed to be neutral, and ApoE4 confers a higher risk for both conditions. Outside the brain, the ApoE4 protein appears to be less effective than other versions at clearing away cholesterol; however,inside the brain, exactly how ApoE4 contributes to Alzheimer's disease has been a mystery.
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<title>Schizophrenia&acirc;s core genetic features proposed</title>
<link>http://www.sciencenews.org/view/generic/id/340699/title/Schizophrenia%E2%80%99s_core_genetic_features_proposed_</link>
<description>
By Laura Sanders

Schizophrenia&amp;acirc;s elusive genetic roots may finally be within grasp. A new, wide-ranging effort has uncovered a set of DNA signatures that are shared by people with the disease consistently enough that the set can be used to reliably predict whether someone has the disease. If replicated, the results may point out ways to diagnose schizophrenia and suggest new targets for treatment.

By analyzing a battery of 542 genetic variants, researchers could predict who had schizophrenia in a group of European Americans and African Americans. The confirmation of the result in people of varying ancestry suggests that the set of genes truly does detect the core features of the disorder, scientists report online May 15 in Molecular Psychiatry.

&amp;acirc;Genetic studies in psychiatry tend to produce initial excitement but are then not reproduced in independent populations, which is the most important proof that a finding is solid and real,&amp;acirc; says study coauthor Alexander Niculescu of the Indiana University School of Medicine in Indianapolis.

Niculescu and his colleagues created their gene panel by assessing a slew of earlier studies on schizophrenia: Data from humans and animals on gene variation and gene behavior all fed into the team&amp;acirc;s analysis. If a gene popped out of several different datasets, the reasoning went, it is probably important to schizophrenia. Niculescu compares this method &amp;acirc; called convergent functional genomics &amp;acirc; to an Internet search: &amp;acirc;The more links to a web page, the higher it comes up on your search list.&amp;acirc;

 &amp;Acirc;&amp;copy; Society for Science &amp;amp; the Public 2000 - 2012</description>
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<title>Even moderate noise may harm hearing</title>
<link>http://www.sciencenews.org/view/generic/id/340704/title/Even_moderate_noise_may_harm_hearing</link>
<description>
By Rebecca Cheung

Constant low-level noise might cause hearing problems, a new study in rats finds. The discovery, published online May 15 in Nature Communications, suggests that extended exposure to noise at levels usually deemed safe for human ears could actually impair sound perception.

The findings are &amp;acirc;definitely a warning flag,&amp;acirc; says study coauthor Michael Merzenich, an integrative neuroscientist at the University of California, San Francisco. He adds that it will be important to find out whether people employed at factories where continuous low-intensity noise is emitted throughout the workday experience similar consequences.

&amp;acirc;The big picture is that there is no safe sound,&amp;acirc; says Jos Eggermont, an auditory neuroscientist at the University of Calgary in Canada. Even sounds considered safe can cause damage if delivered in a repetitive way, he says. &amp;acirc;There might be not-so-subtle effects that accumulate and affect communication and speech understanding.&amp;acirc;

It&amp;acirc;s common knowledge that sustained exposure to louder noises &amp;acirc; such as that above 85 decibels &amp;acirc; or brief exposures to very loud noises above 100 decibels can cause inner ear damage and hearing impairments. But until recently, the impact of chronic, quieter sound hasn&amp;acirc;t been well studied.

In the new study, Merzenich and his colleague Xiaoming Zhou of East China Normal University in Shanghai exposed adult mice to 65 decibel sound &amp;acirc; roughly at the higher end of normal human speech volume &amp;acirc; for 10 hours daily. 

 &amp;Acirc;&amp;copy; Society for Science &amp;amp; the Public 2000 - 2012</description>
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<title>How Neuroscientists and Magicians Are Conjuring Brain Insights</title>
<link>http://blogs.scientificamerican.com/observations/2012/05/14/how-neuroscientists-and-magicians-are-conjuring-brain-insights/</link>
<description>
By Mariette DiChristina 

&amp;acirc;I see you have a watch with a buckle.&amp;acirc; Standing at my side, Apollo Robbins held my wrist lightly as he turned my hand over and back.

I knew exactly what was coming but I fell for it anyway. &amp;acirc;Yes,&amp;acirc; I said, trying to keep an eye on him, &amp;acirc;that looks pretty easy for you to take off, but my rings would be harder.&amp;acirc; He agreed, politely, while looking down at my hands and then up into my eyes: &amp;acirc;Which one do you think would be hardest to remove?&amp;acirc;

While I considered the answer, he had already removed my watch and put it on his own wrist behind his back, unseen. He isn&amp;acirc;t called the &amp;acirc;The Gentleman Thief&amp;acirc; for nothing.

Robbins had just skillfully managed my attentional spotlight&amp;acirc;that is, the focus of awareness at any given moment. To conceal his pilfering, Robbins had employed what is generally called &amp;acirc;misdirection&amp;acirc;: he got me to attend to the wrong things, added to my brain&amp;acirc;s cognitive load with his humorous patter, created a distracting internal dialogue in me by giving me a question to answer, and generally flummoxed me all the while by pressing here and there on a shoulder or wrist. Adding insult to injury, Robbins had just described what he does&amp;acirc;and shown his techniques while swiftly lifting another watch and emptying the pockets of the amiable Flip Phillips of Skidmore College. Still, I never stood a chance. My response to being fooled so easily? I laughed out loud. 

&amp;Acirc;&amp;copy; 2012 Scientific America</description>
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<title>Searching for the Onset of Autism</title>
<link>http://blogs.scientificamerican.com/observations/2012/05/15/searching-for-the-onset-of-autism/</link>
<description>
By Mariette DiChristina 

Early behavioral intervention has shown some promise as a way to help children with autism. But it&amp;acirc;s difficult to see the hallmarks of autism before two years of age with today&amp;acirc;s diagnostic criteria. Could we find other methods?

Seeking to answer that question is Jed Elison at the California Institute of Technology, who is working with Ralph Adolphs at Caltech and Joe Piven at the University of North Carolina among other colleagues around the U.S. and Canada. Elison provided some preliminary findings at the Neuromagic 2012 conference held from May 7 to 10, 2012 on San Sim&amp;Atilde;&amp;sup3;n, the Island of Thought, near Vigo, Spain.

Today&amp;acirc;s criteria, from the psychiatric bible called the DSM-IV, include attributes of social impairments, communication deficits, and repetitive patterns of behavior and restricted interests (either in intensity or content). &amp;acirc;There&amp;acirc;s a biological reality,&amp;acirc; said Elison, &amp;acirc;that you can&amp;acirc;t capture perfectly with a classification system like this.&amp;acirc; Nevertheless, there&amp;acirc;s &amp;acirc;no question that the classification system serves a very important role in identifying kids who require specialized clinical services&amp;acirc; Recognizing the condition early can help. &amp;acirc;There&amp;acirc;s some evidence that early intervention alleviates&amp;acirc; some of the behavioral challenges for these children, he added.

Elison and collaborative partners of the Infant Brain Imaging Study Network are recruiting families who have a child with autism and an infant sibling under six months of age. 

&amp;Acirc;&amp;copy; 2012 Scientific American</description>
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<title>Not-So-Quick Fix: ADHD Behavioral Therapy May Be More Effective Than Drugs in Long Run</title>
<link>http://www.scientificamerican.com/article.cfm?id=adhd-behavioral-therapy-more-effective-drugs-long-term</link>
<description>
By SciCurious 

Before stimulant drugs such as Ritalin, Concerta and Adderall began their rise to popularity in the 1970s, treatment for attention-deficit hyperactivity disorder (ADHD) focused on behavioral therapy. But as concerns build over the mounting dosages and extended treatment periods that come with stimulant drugs, clinical researchers are revisiting behavioral therapy techniques. Whereas stimulant medications may help young patients focus and behave in the classroom, research now suggests that behaviorally based changes make more of a difference in the long-term.

A new synthesis of behavioral, cognitive and pharmacological findings emerged at the recent Experimental Biology meeting, held last month in San Diego, where experts in ADHD research and treatment gathered to present their work. Their findings suggest that behavioral and cognitive therapies focused on reducing impulsivity and reinforcing positive long-term habits may be able to replace current high doses of stimulant treatment in children and young adults.

Recent surveys indicate that 9 percent of all children in the U.S. have been diagnosed with ADHD. The condition's core symptoms include hyperactivity, inattention, inability to perform monotonous tasks and lack of impulse control. Children with ADHD have trouble in school and forming relationships, and 60 percent will continue to suffer from the disorder well into adulthood.

As of 2007, 2.7 million U.S. children and adolescents with ADHD were being treated with stimulant drugs. But new research reveals that these drugs are not necessarily the panacea they have been thought to be. Psychologist Claire Advokat of Louisiana State University has been looking at the effects of stimulant medications in college students to see what improves with medication and what does not. 

&amp;Acirc;&amp;copy; 2012 Scientific American</description>
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<title>Do Psychedelics Expand the Mind by Reducing Brain Activity?</title>
<link>http://www.scientificamerican.com/article.cfm?id=do-psychedelics-expand-mind-reducing-brain-activity</link>
<description>
By Adam Halberstadt and Mark Geyer 

What would you see if you could look inside a hallucinating brain? Despite decades of scientific investigation, we still lack a clear understanding of how hallucinogenic drugs such as LSD (lysergic acid diethylamide), mescaline, and psilocybin (the main active ingredient in magic mushrooms) work in the brain. Modern science has demonstrated that hallucinogens activate receptors for serotonin, one of the brain&amp;acirc;s key chemical messengers. Specifically, of the 15 different serotonin receptors, the 2A subtype (5-HT2A), seems to be the one that produces profound alterations of thought and perception. It is uncertain, however, why activation of the 5-HT2A receptor by hallucinogens produces psychedelic effects, but many scientists believe that the effects are linked to increases in brain activity. Although it is not known why this activation would lead to profound alterations of consciousness, one speculation is that an increase in the spontaneous firing of certain types of brain cells leads to altered sensory and perceptual processing, uncontrolled memory retrieval, and the projection of mental &amp;acirc;noise&amp;acirc; into the mind&amp;acirc;s eye.

The English author Aldous Huxley believed that the brain acts as a &amp;acirc;reducing valve&amp;acirc; that constrains conscious awareness, with mescaline and other hallucinogens inducing psychedelic effects by inhibiting this filtering mechanism. Huxley based this explanation entirely on his personal experiences with mescaline, which was given to him by Humphrey Osmond, the psychiatrist who coined the term psychedelic. Even though Huxley proposed this idea in 1954, decades before the advent of modern brain science, it turns out that he may have been correct. Although the prevailing view has been that hallucinogens work by activating the brain, rather than by inhibiting it as Huxley proposed, the results of a recent imaging study are challenging these conventional explanations.

&amp;Acirc;&amp;copy; 2012 Scientific American, </description>
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<title>Best illusion of 2012: Floating star drifts into final</title>
<link>http://www.newscientist.com/blogs/shortsharpscience/2012/05/floating-star.html</link>
<description>
Caroline Morley, online picture researcher

On the edge of your vision as you read this, the water swirls but the starfish turns in the other direction, floating above the background.

The image itself is, of course, still: the movement is created in your head. It uses the phenomenon of periphery drift to make us see movement where there is none. The different contrasts between the colours are the key to making us see the star and the background move in opposite directions.

This image was created by Kaia Nao, an alternative identity for wildlife painter Joe Hautman. It is a finalist in the 2012 Best Illusion of the Year Contest, run by the Neural Correlate Society to encourage and publicise the work of researchers in the field of visual illusions. See the winning video in our New Scientist TV post &amp;quot;Best illusion of 2012: The disappearing hand trick&amp;quot;.

&amp;Acirc;&amp;copy; Copyright Reed Business Information Ltd.
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