Western University-led research debunks the IQ myth

After conducting the largest online intelligence study on record, a Western University-led research team has concluded that the notion of measuring one’s intelligence quotient or IQ by a singular, standardized test is highly misleading.

The findings from the landmark study, which included more than 100,000 participants, were published in the journal Neuron.

Utilizing an online study open to anyone, anywhere in the world, the researchers asked respondents to complete 12 cognitive tests tapping memory, reasoning, attention and planning abilities, as well as a survey about their background and lifestyle habits.

"The uptake was astonishing," says Owen, the Canada Excellence Research Chair in Cognitive Neuroscience and Imaging and senior investigator on the project. "We expected a few hundred responses, but thousands and thousands of people took part, including people of all ages, cultures and creeds from every corner of the world."

The results showed that when a wide range of cognitive abilities are explored, the observed variations in performance can only be explained with at least three distinct components: short-term memory, reasoning and a verbal component.

No one component, or IQ, explained everything. Furthermore, the scientists used a brain scanning technique known as functional magnetic resonance imaging (fMRI), to show that these differences in cognitive ability map onto distinct circuits in the brain.

With so many respondents, the results also provided a wealth of new information about how factors such as age, gender and the tendency to play computer games influence our brain function.

"Regular brain training didn’t help people’s cognitive performance at all yet aging had a profound negative effect on both memory and reasoning abilities," says Owen.

Hampshire adds, “Intriguingly, people who regularly played computer games did perform significantly better in terms of both reasoning and short-term memory. And smokers performed poorly on the short-term memory and the verbal factors, while people who frequently suffer from anxiety performed badly on the short-term memory factor in particular”.

To continue the groundbreaking research, the team has launched a new version of the tests at http://www.cambridgebrainsciences.com/theIQchallenge

"To ensure the results aren’t biased, we can’t say much about the agenda other than that there are many more fascinating questions about variations in cognitive ability that we want to answer," explains Hampshire.

(Image by Lasse Kristensen/Shutterstock)

The empathy machine

…Let’s dwell for a moment on ‘Silver Blaze’ (1892), Arthur Conan Doyle’s story of the gallant racehorse who disappeared, and his trainer who was found dead, just days before a big race. The hapless police are stumped, and Sherlock Holmes is called in to save the day. And save the day he does — by putting himself in the position of both the dead trainer and the missing horse. Holmes speculates that the horse is ‘a very gregarious creature’. Surmising that, in the absence of its trainer, it would have been drawn to the nearest town, he finds horse tracks, and tells Watson which mental faculty led him there. ‘See the value of imagination… We imagined what might have happened, acted upon that supposition, and find ourselves justified.’

Holmes takes an imaginative leap, not only into another human mind, but into the mind of an animal. This perspective-taking, being able to see the world from the point of view of another, is one of the central elements of empathy, and Holmes raises it to the status of an art.

Usually, when we think of empathy, it evokes feelings of warmth and comfort, of being intrinsically an emotional phenomenon. But perhaps our very idea of empathy is flawed. The worth of empathy might lie as much in the ‘value of imagination’ that Holmes employs as it does in the mere feeling of vicarious emotion. Perhaps that cold rationalist Sherlock Holmes can help us reconsider our preconceptions about what empathy is and what it does.

Though the scientific literature on empathy is complex, a recent review in Nature Neuroscience by a team of researchers from Harvard and Columbia including Jamil Zaki and Kevin Ochsner has distilled the phenomenon into three central stages. The first stage is ‘experience sharing’, or feeling someone else’s emotions as if they were your own — scared when they are scared, happy when they are happy, and so on. The second stage is ‘mentalising’, or consciously considering those states and their sources, and trying to work through understanding them. The final stage is ‘prosocial concern’, or being motivated to act — wanting, for example, to reach out to someone in pain. However, you don’t need all three to experience empathy. Instead, you can view these as three points on an empathetic continuum: first, you feel; then, you feel and you understand; and finally, you feel, understand, and are compelled to act on your understanding. It seems that the defining thing here is the feeling that accompanies all those stages.

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Orangutans Have a Big Idea

Even when they are very young, orangutans may start to form ideas about their world—specifically, how and when to use certain tools. That’s the conclusion of a new study, which indicates that ape cultural traditions may not be that different from our own.

Like humans, orangutans have behavioral traditions that vary by region. Orangutans in one area use tools, for example, whereas others don’t. Take the island of Sumatra, in western Indonesia. By the age of 6 or 7, orangutans from swampy regions west of Sumatra’s Alas River use sticks to probe logs for honey. Yet researchers have never observed this “honey-dipping” among orangutans in coastal areas east of the water.

How do such differences arise? Many experts say that social learning is key—that the apes figure out how to honey-dip by watching others. But even the most careful field researcher can have difficulty proving this, says Yale University anthropologist David Watts. Wild apes are always responding to their environment, he says. And it may be influencing their behavior far more than social learning.

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MRIs Reveal Signs of Brain Injuries Not Seen in CT Scans

Hospital MRIs may be better at predicting long-term outcomes for people with mild traumatic brain injuries than CT scans, the standard technique for evaluating such injuries in the emergency room, according to a clinical trial led by researchers at UCSF and the San Francisco General Hospital and Trauma Center (SFGH).

Published this month in the journal Annals of Neurology, the study led by UCSF neuroradiologist Esther Yuh, MD, PhD, followed 135 people treated for mild traumatic brain injuries over the past two years at one of three urban hospitals with level-one trauma centers: SFGH, the University of Pittsburgh Medical Center and University Medical Center Brackenridge in Austin, Texas. The study was called the NIH-funded TRACK-TBI (Transforming Research and Clinical Knowledge in Traumatic Brain Injury).

All 135 patients with mild traumatic brain injuries received CT scans when they were first admitted, and all were given MRIs about a week later. Most of them (99) had no detectable signs of injury on a CT scan, but more than a quarter (27/99) who had a “normal” CT scans also had detectable spots on their MRI scans called “focal lesions,” which are signs of microscopic bleeding in the brain.

Spotting these focal lesions helped the doctors predict whether the patients were likely to suffer persistent neurological problems. About 15 percent of people who have mild traumatic brain injuries do suffer long-term neurological consequences, but doctors currently have no definitive way of predicting whether any one patient will or not.

“This work raises questions of how we’re currently managing patients via CT scan,” said the study’s senior author Geoff Manley, MD, PhD, the chief of neurosurgery at SFGH and vice-chair of the Department of Neurological Surgery at UCSF. “Having a normal CT scan doesn’t, in fact, say you’re normal,” he added.

Better Precision Tools Needed for Head Injuries

At least 1.7 million Americans seek medical attention every year for acute head injuries, and three-quarters of them have mild traumatic brain injuries – which generally do not involve skull fractures, comas or severe bleeding in the brain but have a variety of more mild symptoms, such as temporary loss of consciousness, vomiting or amnesia.

The U.S. Centers for Disease Control and Prevention estimates that far more mild traumatic brain injuries may occur each year in the United States but the true number is unknown because only injuries severe enough to bring someone to an emergency room are counted.

Most of those who do show up at emergency rooms are treated and released without being admitted to the hospital. In general, most people with mild traumatic brain injuries recover fully, but about one in six go on to develop persistent, sometimes permanent, disability.

The problem, Manley said, is that there is no way to tell which patients are going to have the poor long-term outcomes. Some socioeconomic indicators can help predict prolonged disability, but until now there were no proven imaging features, or blood tests for predicting how well or how fast a patient will recover. Nor is there a consensus on how to treat mild traumatic brain injuries.

“The treatment’s all over the place – if you’re getting treatment at all,” Manley said.

The new work is an important step toward defining a more quantitative way of assessing patients with mild traumatic brain injuries and developing more precision medical tools to detect, monitor and treat them, he added.

If doctors knew which patients were at risk of greater disabilities, they could be followed more closely. Being able to identify patients at risk of long-term consequences would also speed the development of new therapeutics because it would allow doctors to identify patients who would benefit the most from treatment and improve their ability to test potential new drugs in clinical trials.

Excessive alcohol when you’re young could have lasting impacts on your brain

Alcohol misuse in young people causes significant changes in their brain function and structure. This and other findings were recently reviewed by Dr Daniel Hermens from the University of Sydney’s Brain and Mind Research Institute in the journal Cortex.

"Young people are particularly vulnerable to the damaging effects of alcohol misuse," said Dr Hermens.

Most people have their first alcoholic drink during adolescence and while they drink less frequently than adults, they tend to drink more on each occasion - binge drinking.

The early functional signs of brain damage from alcohol misuse are visual, learning, memory and executive function impairments. These functions are controlled by the hippocampus and frontal structures of the brain, which are not fully mature until around 25 years of age.

Structural signs of alcohol misuse include shrinking of the brain and significant changes to white matter.

In his review, Dr Hermens notes that changes in a young person’s brain caused by alcohol misuse could either represent a predisposition (genetic or environmental) to alcohol misuse, or a marker for future risk of ongoing misuse. Whichever it is, there is no doubt that the more frequent the alcohol misuse, the greater the damage and the less likely the brain is to recover from that damage.

"When the toxicity of alcohol stops your brain from laying down new memories, you experience a blackout," said Dr Hermens. Young people who binge drink may only drink once a week, but on a massive night out they may have three to four blackouts, which begins to cause serious damage to their brain.

One of the best predictors of a person having problems with alcohol is their earliest age of first use. But changing the legal drinking age is not the answer. In Australia the legal drinking age is 18, three years earlier than in the US. Despite the difference in legal drinking age, the age of first use is the same between the two countries.

Another key factor affecting young people who drink is mental health, “poor mental health more than doubles a young person’s risk of alcohol and other substance misuse” says Dr Hermens.

The solution lies in education, treatment and prevention. Dr Hermens and his team have been working with NSW Health to prepare a set of guidelines for health carers to identify and respond to early stages of brain impairment in young people resulting from alcohol misuse. They are currently working on a set of educational charts that inform young people of the risks of irresponsible drinking.

It may be possible to use cognitive remediation to change the drinking habits of young drinkers and prevent relapse. At the same time, vitamin supplements or other medicines may effectively treat some of the structural changes, and it may be possible to develop protective agents that can prevent young brains from the damaging effects of alcohol.

"More work needs to be done in this area. Excessive alcohol use accounts for 4 percent of the global burden of disease. We would save a lot of money and improve the quality of life for millions of people if we could prevent the mental and physical problems associated with alcohol misuse" said Dr Hermens.

REM sleep enhances emotional memories

Witnessing a car wreck or encountering a poisonous snake are scenes that become etched in our memories.

But how do we process and store these emotional scenes so that they’re preserved more efficiently than other, more neutral memories?

In a new study published recently in “Frontiers in Integrative Neuroscience,” University of Notre Dame researchers Jessica Payne and Alexis Chambers found that people who experienced rapid eye movement (REM) sleep soon after being presented with an emotionally-charged negative scene — a wrecked car on a street, for example — had superior memory for the emotional object compared to subjects whose sleep was delayed for at least 16 hours. This increased memory for the emotional object corresponded with a diminished memory for the neutral background of the scene, such as the street on which the wrecked car was parked.

These results suggest that the sleeping brain preserves in long-term memory only those scenes that are emotionally salient and aid in adaptation.

“Our results suggest that REM sleep, which has long been thought to play a role in emotional processing and emotional memory, helps us selectively preserve in memory only what is most important and perhaps beneficial to survival,” says Payne, a Notre Dame assistant professor of psychology who specializes in sleep’s impact on memory, creativity and the ability to process new ideas.

We know that emotional events occupy a privileged position in our memories — they shape our personalities, represent defeats and achievements, mark milestones in our lives and often drive anxiety and mood disorders.

This study shows that the sleeping brain doesn’t just consolidate all recently encountered information. It appears to select for consolidation only the most emotional part of the experience, and the evidence suggests that REM sleep critically modulates memory for highly arousing emotional information.

(Image: iStock)

Silent stroke can cause Parkinson’s disease

Scientists at The University of Manchester have for the first time identified why a patient who appears outwardly healthy may develop Parkinson’s disease.

Whilst conditions such as a severe stroke have been linked to the disease, for many sufferers the tremors and other symptoms of Parkinson’s disease can appear to come out of the blue. Researchers at the university’s Faculty of Life Sciences have now discovered that a small stroke, also known as a silent stroke, can cause Parkinson’s disease. Their findings have been published in the journal “Brain Behaviour and Immunity”.

Unlike a severe stroke, a silent stroke can show no outward symptoms of having taken place. It happens when a blood vessel in the brain is blocked for only a very short amount of time and often a patient won’t know they have suffered from one. However, it now appears one of the lasting effects of a silent stroke can be the death of dopaminergic neurons in the substantia nigra in the brain, which is an important region for movement coordination.

Dr. Emmanuel Pinteaux led the research: “At the moment we don’t know why dopaminergic neurons start to die in the brain and therefore why people get Parkinson’s disease. There have been suggestions that oxidative stress and aging are responsible. What we wanted to do in our study was to look at what happens in the brain away from the immediate area where a silent stroke has occurred and whether that could lead to damage that might result in Parkinson’s disease.”

The team induced a mild stroke similar to a silent stroke in the striatum area of the brain in mice. They found there was inflammation and brain damage in the striatum following the stroke, which they had expected. What the researchers didn’t expect was the impact on another area of the brain, the substantia nigra. When they analysed the substantia nigra they recorded a rapid loss of Substance P (a key chemical involved in its functions) as well as inflammation.

The team then analysed changes in the brain six days after the mild stroke and found neurodegeneration in the substantia nigra. Dopaminergic neurones had been killed.

Talking about the findings Dr Pinteaux said: “It is well known that inflammation following a stroke can be very damaging to the brain. But what we didn’t fully appreciate was the impact on areas of the brain away from the location of the stroke. Our work identifying that a silent stroke can lead to Parkinson’s disease shows it is more important than ever to ensure stroke patients have swift access to anti-inflammatory medication. These drugs could potentially either delay or stop the on-set of Parkinson’s disease.”

Dr Pinteaux continued: “What our findings also point to is the importance of maintaining a healthy lifestyle. There are already guidelines about exercise and healthy eating to help reduce the risk of having a stroke and our research suggests that a healthy lifestyle can be applied to Parkinson’s disease as well.”

Following the publication of these findings, Dr Pinteaux hopes to set up a clinical investigation on people who have had a silent stroke to assess dopaminergic neuron degeneration. In the meantime he will be working closely will colleagues at The University of Manchester to better understand the mechanisms of inflammation in the substantia nigra. 

Even the Smallest Possible Stroke Can Damage Brain Tissue and Impair Cognitive Function

Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience.

"The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina.

Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy.

These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain.

"It’s controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group.

To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water.

The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can’t feel the far platform, they won’t budge.

"The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain."

When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit.

The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer’s disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage.

"This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer’s disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes."

“We used powerful tools from biological physics, many developed in Kleinfeld’s laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells,” Shih said. “At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier.”

Study Shows Working Memory Is Driven By Prefrontal Cortex And Dopamine

One of the unique features of the human mind is its ability re-prioritize its goals and priorities as situations change and new information arises. This happens when you cancel a planned cruise because you need the money to repair your broke-down car, or when you interrupt your morning jog because your cell phone is ringing in your pocket.

In a new study published in the Proceedings of the National Academy of Sciences (PNAS), researchers from Princeton University say that they have discovered the mechanisms that control how our brains use new information to modify our existing priorities.

The team of researchers at Princeton’s Neuroscience Institute (PNI) used functional magnetic resonance imaging (fMRI) to scan subjects and find out where and how the human brain reprioritizes goals. Unsurprisingly, they found that the shifting of goals takes place in the prefrontal cortex, a region of the brain which is known to be associated with a variety of higher-level behaviors. They also observed that the powerful neurotransmitter dopamine – also known as the “pleasure chemical” – appears to play a critical role in this process.

Using a harmless magnetic pulse, the scientists interrupted activity in the prefrontal cortex of the participants while they were playing games and found they were unable to switch to a different task in the game.

“We have found a fundamental mechanism that contributes to the brain’s ability to concentrate on one task and then flexibly switch to another task,” explained Jonathan Cohen, co-director of PNI and the university’s Robert Bendheim and Lynn Bendheim Thoman Professor in Neuroscience.

“Impairments in this system are central to many critical disorders of cognitive function such as those observed in schizophrenia and obsessive-compulsive disorder.”

Previous research had already demonstrated that when the brain uses new information to modify its goals or behaviors, this information is temporarily filed away into the brain’s working memory, a type of short-term memory storage. Until now, however, scientists have not understood the mechanisms controlling how this information is updated.