Neuroscience

Articles and news from the latest research reports.

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Smoking and hyperactivity (ADHD) share common genetic risk factor
A variation of a particular gene may link the behaviours typical of childhood attention hyperactivity disorder, or ADHD for short, and those associated with smoking, suggests research published online in the Archives of Disease in Childhood (1, 2)
Childhood ADHD and subsequent smoking in adulthood frequently go hand in hand, say the authors, with people who have been diagnosed with ADHD more likely to start smoking early and to smoke twice as much as those without the condition.
The researchers focused on five variations in DNA sequences (single nucleotide polymorphisms or SNPs) in different genes that are strongly associated with different aspects of smoking behaviour, such as the number of cigarettes smoked every day, and taking up and quitting smoking.

Smoking and hyperactivity (ADHD) share common genetic risk factor

A variation of a particular gene may link the behaviours typical of childhood attention hyperactivity disorder, or ADHD for short, and those associated with smoking, suggests research published online in the Archives of Disease in Childhood (1, 2)

Childhood ADHD and subsequent smoking in adulthood frequently go hand in hand, say the authors, with people who have been diagnosed with ADHD more likely to start smoking early and to smoke twice as much as those without the condition.

The researchers focused on five variations in DNA sequences (single nucleotide polymorphisms or SNPs) in different genes that are strongly associated with different aspects of smoking behaviour, such as the number of cigarettes smoked every day, and taking up and quitting smoking.

Filed under ADHD smoking DNA genetics behavior performance neuroscience psychology science

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More Than Good Vibes: Researchers Propose the Science Behind Mindfulness
Achieving mindfulness through meditation has helped people maintain a healthy mind by quelling negative emotions and thoughts, such as desire, anger and anxiety, and encouraging more positive dispositions such as compassion, empathy and forgiveness. Those who have reaped the benefits of mindfulness know that it works. But how exactly does it work?
Researchers at Brigham and Women’s Hospital (BWH) have proposed a new model that shifts how we think about mindfulness. Rather than describing mindfulness as a single dimension of cognition, the researchers demonstrate that mindfulness actually involves a broad framework of complex mechanisms in the brain.
In essence, they have laid out the science behind mindfulness.
This new model of mindfulness is published in the October 25, 2012 issue of Frontiers in Human Neuroscience. The model was recently presented to His Holiness The Dalai Lama in a private meeting, entitled “Mind and Life XXIV: Latest Findings in Contemplative Neuroscience.”

More Than Good Vibes: Researchers Propose the Science Behind Mindfulness

Achieving mindfulness through meditation has helped people maintain a healthy mind by quelling negative emotions and thoughts, such as desire, anger and anxiety, and encouraging more positive dispositions such as compassion, empathy and forgiveness. Those who have reaped the benefits of mindfulness know that it works. But how exactly does it work?

Researchers at Brigham and Women’s Hospital (BWH) have proposed a new model that shifts how we think about mindfulness. Rather than describing mindfulness as a single dimension of cognition, the researchers demonstrate that mindfulness actually involves a broad framework of complex mechanisms in the brain.

In essence, they have laid out the science behind mindfulness.

This new model of mindfulness is published in the October 25, 2012 issue of Frontiers in Human Neuroscience. The model was recently presented to His Holiness The Dalai Lama in a private meeting, entitled “Mind and Life XXIV: Latest Findings in Contemplative Neuroscience.”

Filed under mindfulness cognition meditation brain neuroscience psychology science

100 notes


The endocannabinoid system in normal and pathological brain ageing
The role of endocannabinoids as inhibitory retrograde transmitters is now widely known and intensively studied. However, endocannabinoids also influence neuronal activity by exerting neuroprotective effects and regulating glial responses. This review centres around this less-studied area, focusing on the cellular and molecular mechanisms underlying the protective effect of the cannabinoid system in brain ageing. The progression of ageing is largely determined by the balance between detrimental, pro-ageing, largely stochastic processes, and the activity of the homeostatic defence system. Experimental evidence suggests that the cannabinoid system is part of the latter system. Cannabinoids as regulators of mitochondrial activity, as anti-oxidants and as modulators of clearance processes protect neurons on the molecular level. On the cellular level, the cannabinoid system regulates the expression of brain-derived neurotrophic factor and neurogenesis. Neuroinflammatory processes contributing to the progression of normal brain ageing and to the pathogenesis of neurodegenerative diseases are suppressed by cannabinoids, suggesting that they may also influence the ageing process on the system level. In good agreement with the hypothesized beneficial role of cannabinoid system activity against brain ageing, it was shown that animals lacking CB1 receptors show early onset of learning deficits associated with age-related histological and molecular changes. In preclinical models of neurodegenerative disorders, cannabinoids show beneficial effects, but the clinical evidence regarding their efficacy as therapeutic tools is either inconclusive or still missing.

The endocannabinoid system in normal and pathological brain ageing

The role of endocannabinoids as inhibitory retrograde transmitters is now widely known and intensively studied. However, endocannabinoids also influence neuronal activity by exerting neuroprotective effects and regulating glial responses. This review centres around this less-studied area, focusing on the cellular and molecular mechanisms underlying the protective effect of the cannabinoid system in brain ageing. The progression of ageing is largely determined by the balance between detrimental, pro-ageing, largely stochastic processes, and the activity of the homeostatic defence system. Experimental evidence suggests that the cannabinoid system is part of the latter system. Cannabinoids as regulators of mitochondrial activity, as anti-oxidants and as modulators of clearance processes protect neurons on the molecular level. On the cellular level, the cannabinoid system regulates the expression of brain-derived neurotrophic factor and neurogenesis. Neuroinflammatory processes contributing to the progression of normal brain ageing and to the pathogenesis of neurodegenerative diseases are suppressed by cannabinoids, suggesting that they may also influence the ageing process on the system level. In good agreement with the hypothesized beneficial role of cannabinoid system activity against brain ageing, it was shown that animals lacking CB1 receptors show early onset of learning deficits associated with age-related histological and molecular changes. In preclinical models of neurodegenerative disorders, cannabinoids show beneficial effects, but the clinical evidence regarding their efficacy as therapeutic tools is either inconclusive or still missing.

Filed under brain aging cannabis endocannabinoids neurodegenerative diseases neuroscience science

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The Brain An Electric Cure for the Mind

Why does shock therapy beat back depression? New experiments show how such a blunt 
treatment can have such positive effects.

Ian Reid, a psychiatrist at the Royal Cornhill Hospital in the Scottish city of Aberdeen, has treated people with severe depression for 25 years. “It’s a very nasty illness, depression,” he says. “I have worked with people who have cancer and depression, and more than one of them has said, ‘If I had to choose one of those two diseases, I’d go for the cancer.’ ”

When patients come to Royal Cornhill with major depression, they’re first treated with psychotherapy and antidepressants. Only about 40 percent respond to their first medication. Sometimes a different one will do the trick, but in Reid’s experience, about 10 to 20 percent of depressed people respond to no drug at all. In those cases, Reid regularly shifts to a third option. It’s officially called electroconvulsive therapy, or ECT—better known by its unofficial name, shock therapy.

Reid is an expert on ECT, and over the years he has received plenty of grief for it. “There are people on the Internet who describe me as a Nazi, as a barbarian,” he says. “And there’s one person who suggested I should get ECT so I know what I’m doing.”

Reid is not surprised by the reactions. For many people, the sum of their knowledge about ECT comes from the 1975 movie One Flew Over the Cuckoo’s Nest. Jack Nicholson plays Randle McMurphy, a criminal hoping to escape hard labor by spending his term in a mental institution. But McMurphy gets more than he bargained for, including a harrowing session of ECT. The hospital staff straps him down, puts a piece of rubber in his mouth so he won’t bite off his own tongue, and delivers a blast of electricity to his temples. He writhes in agony and then slumps back, his body limp.

That scene bears no resemblance to what Reid does for his patients. For one thing, he gives them anesthesia and muscle relaxants so they don’t experience any flailing. But most crucially, ECT works. “You can watch someone going from being unresponsive and soiling themselves to being completely transformed,” Reid says.

In Scotland, a country of 5 million, 400 people receive the treatment each year. And for about 75 percent of them, it brings relief. “ECT outperforms psychotherapeutic treatments and antidepressant drugs,” Reid notes. Yet its effectiveness is a mystery. “It doesn’t sound intuitive at all,” he admits. “Making someone have a seizure, giving them an electric shock, and making something as complex as depression better just seems crazy.”

Read more …

Filed under brain depression electroconvulsive therapy shock therapy neuroscience psychology science

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How the brain controls our habits
Habits are behaviors wired so deeply in our brains that we perform them automatically. This allows you to follow the same route to work every day without thinking about it, liberating your brain to ponder other things, such as what to make for dinner.
However, the brain’s executive command center does not completely relinquish control of habitual behavior. A new study from MIT neuroscientists has found that a small region of the brain’s prefrontal cortex, where most thought and planning occurs, is responsible for moment-by-moment control of which habits are switched on at a given time.
“We’ve always thought — and I still do — that the value of a habit is you don’t have to think about it. It frees up your brain to do other things,” says Institute Professor Ann Graybiel, a member of the McGovern Institute for Brain Research at MIT. “However, it doesn’t free up all of it. There’s some piece of your cortex that’s still devoted to that control.”
The new study offers hope for those trying to kick bad habits, says Graybiel, senior author of the new study, which appears this week in the Proceedings of the National Academy of Sciences. It shows that though habits may be deeply ingrained, the brain’s planning centers can shut them off. It also raises the possibility of intervening in that brain region to treat people who suffer from disorders involving overly habitual behavior, such as obsessive-compulsive disorder.

How the brain controls our habits

Habits are behaviors wired so deeply in our brains that we perform them automatically. This allows you to follow the same route to work every day without thinking about it, liberating your brain to ponder other things, such as what to make for dinner.

However, the brain’s executive command center does not completely relinquish control of habitual behavior. A new study from MIT neuroscientists has found that a small region of the brain’s prefrontal cortex, where most thought and planning occurs, is responsible for moment-by-moment control of which habits are switched on at a given time.

“We’ve always thought — and I still do — that the value of a habit is you don’t have to think about it. It frees up your brain to do other things,” says Institute Professor Ann Graybiel, a member of the McGovern Institute for Brain Research at MIT. “However, it doesn’t free up all of it. There’s some piece of your cortex that’s still devoted to that control.”

The new study offers hope for those trying to kick bad habits, says Graybiel, senior author of the new study, which appears this week in the Proceedings of the National Academy of Sciences. It shows that though habits may be deeply ingrained, the brain’s planning centers can shut them off. It also raises the possibility of intervening in that brain region to treat people who suffer from disorders involving overly habitual behavior, such as obsessive-compulsive disorder.

Filed under brain habits behavior OCD optogenetics neuroscience psychology science

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Stay-at-home transcription factor saves axons
The old saw that local actions can have global consequences holds true for neurons, too. Selvaraj et al. show that a transcription factor remains in the axon to help prevent neurodegeneration.
In neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), neurons usually die in stages, with axons deteriorating first and the cells themselves perishing later. Axon degeneration may represent a turning point for patients, after which so much neuronal damage has accumulated that treatments won’t work. Researchers have tested several proteins for their ability to save axons. One of these molecules, ciliary neurotrophic factor (CNTF), rescues axons in rodents and extends their lives. But it caused severe side effects in patients during clinical trials. “Acting on the same pathway but farther downstream could be an ideal way to improve the situation for motor neuron disease” and possibly for other neurodegenerative diseases, says senior author Michael Sendtner.
To discover how CNTF works, Selvaraj et al. studied pmn mutant mice that mimic ALS. The researchers found that CNTF not only prevented the shrinkage of the rodents’ motor neurons, it also reduced the number of swellings along the axon that are markers of degeneration. Another sign that CNTF was beneficial was the movement of mitochondria, which continually shuttle back and forth along the axons of healthy motor neurons. In axons from pmn mice, stalled mitochondria were prevalent, but treatment with CNTF accelerated the organelles to normal speeds.

Stay-at-home transcription factor saves axons

The old saw that local actions can have global consequences holds true for neurons, too. Selvaraj et al. show that a transcription factor remains in the axon to help prevent neurodegeneration.

In neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS), neurons usually die in stages, with axons deteriorating first and the cells themselves perishing later. Axon degeneration may represent a turning point for patients, after which so much neuronal damage has accumulated that treatments won’t work. Researchers have tested several proteins for their ability to save axons. One of these molecules, ciliary neurotrophic factor (CNTF), rescues axons in rodents and extends their lives. But it caused severe side effects in patients during clinical trials. “Acting on the same pathway but farther downstream could be an ideal way to improve the situation for motor neuron disease” and possibly for other neurodegenerative diseases, says senior author Michael Sendtner.

To discover how CNTF works, Selvaraj et al. studied pmn mutant mice that mimic ALS. The researchers found that CNTF not only prevented the shrinkage of the rodents’ motor neurons, it also reduced the number of swellings along the axon that are markers of degeneration. Another sign that CNTF was beneficial was the movement of mitochondria, which continually shuttle back and forth along the axons of healthy motor neurons. In axons from pmn mice, stalled mitochondria were prevalent, but treatment with CNTF accelerated the organelles to normal speeds.

Filed under axons motor neuron disease nerve cells neurodegenerative disorders mutations neuroscience science

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Sport Makes Middle-Aged People Smarter
High-intensity interval training makes middle-aged people not only healthier but smarter, showed a Montreal Heart Institute (MHI) study led by Dr. Anil Nigam of the MHI and University of Montreal, in collaboration with the Montreal Geriatric University Institute.
“We worked with six adults who all followed a four-month program of twice weekly interval training on stationary bicycles and twice weekly resistance training. Cognitive function, VO2max and brain oxygenation during exercise testing revealed that the participants’ cognitive functions had greatly improved thanks to the exercise,” Dr. Nigam said. VO2max is the maximum capacity of an individual’s body to transport and use oxygen during exercise. It impacts on the body’s ability to oxygenate the brain and is related to cognitive function.
“Our participants underwent a battery of cognitive, biological and physiological tests before the program began in order to determine their cognitive functions, body composition, cardiovascular risk, brain oxygenation during exercise and maximal aerobic capacity,” Dr. Nigam explained.
“After the program was finished, we discovered that their waist circumference and particularly their trunk fat mass had decreased. We also found that their VO2max, insulin sensitivity had increased significantly, in tandem with their score on the cognitive tests and the oxygenation signals in the brain during exercise,” Dr Nigam said. Insulin sensitivity is the ability of sugar to enter body tissue (mainly liver and muscle.)

Sport Makes Middle-Aged People Smarter

High-intensity interval training makes middle-aged people not only healthier but smarter, showed a Montreal Heart Institute (MHI) study led by Dr. Anil Nigam of the MHI and University of Montreal, in collaboration with the Montreal Geriatric University Institute.

“We worked with six adults who all followed a four-month program of twice weekly interval training on stationary bicycles and twice weekly resistance training. Cognitive function, VO2max and brain oxygenation during exercise testing revealed that the participants’ cognitive functions had greatly improved thanks to the exercise,” Dr. Nigam said. VO2max is the maximum capacity of an individual’s body to transport and use oxygen during exercise. It impacts on the body’s ability to oxygenate the brain and is related to cognitive function.

“Our participants underwent a battery of cognitive, biological and physiological tests before the program began in order to determine their cognitive functions, body composition, cardiovascular risk, brain oxygenation during exercise and maximal aerobic capacity,” Dr. Nigam explained.

“After the program was finished, we discovered that their waist circumference and particularly their trunk fat mass had decreased. We also found that their VO2max, insulin sensitivity had increased significantly, in tandem with their score on the cognitive tests and the oxygenation signals in the brain during exercise,” Dr Nigam said. Insulin sensitivity is the ability of sugar to enter body tissue (mainly liver and muscle.)

Filed under brain body cognition aging health neuroscience psychology science

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Neurotransmitters Linked to Mating Behavior Are Shared by Mammals and Worms
When it comes to sex, animals of all shapes and sizes tend to behave in predictable ways. There may be a chemical reason for that. New research from Rockefeller University has shown that chemicals in the brain — neuropeptides known as vasopressin and oxytocin — play a role in coordinating mating and reproductive behavior in animals ranging from humans to fish to invertebrates.
"Our research shows that molecules similar to vasopressin and oxytocin have an ancient and evolutionarily conserved role in controlling a critical social behavior, mating," says Cori Bargmann, Torsten N. Wiesel Professor and head of the Lulu and Anthony Wang Laboratory of Neural Circuits and Behavior. "This work suggests that these molecules encode the same kind of information in the brains of very different animals."
Bargmann, whose laboratory studies the relationship between genes, neural circuits and behavior in the C. elegans roundworm, says vasopressin and oxytocin have been implicated in a variety of reproductive and social behaviors in humans and other mammals, including pair bonding, maternal bonding and aggressive and affiliative behaviors. Mice that lack oxytocin may develop social amnesia, and humans who sniff oxytocin through an inhaler change their cooperative behavior in computer games, behaving as though they “trust” other players more.

Neurotransmitters Linked to Mating Behavior Are Shared by Mammals and Worms

When it comes to sex, animals of all shapes and sizes tend to behave in predictable ways. There may be a chemical reason for that. New research from Rockefeller University has shown that chemicals in the brain — neuropeptides known as vasopressin and oxytocin — play a role in coordinating mating and reproductive behavior in animals ranging from humans to fish to invertebrates.

"Our research shows that molecules similar to vasopressin and oxytocin have an ancient and evolutionarily conserved role in controlling a critical social behavior, mating," says Cori Bargmann, Torsten N. Wiesel Professor and head of the Lulu and Anthony Wang Laboratory of Neural Circuits and Behavior. "This work suggests that these molecules encode the same kind of information in the brains of very different animals."

Bargmann, whose laboratory studies the relationship between genes, neural circuits and behavior in the C. elegans roundworm, says vasopressin and oxytocin have been implicated in a variety of reproductive and social behaviors in humans and other mammals, including pair bonding, maternal bonding and aggressive and affiliative behaviors. Mice that lack oxytocin may develop social amnesia, and humans who sniff oxytocin through an inhaler change their cooperative behavior in computer games, behaving as though they “trust” other players more.

Filed under C. elegans mating neurotransmitters neuropeptides neuroscience psychology science

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Eye Movements and the Search for Biomarkers for Schizophrenia

There is a long history of research on impaired eye movements associated with schizophrenia. Using a series of simple viewing tests, researchers of a new paper in Biological Psychiatry explored the ability of these eye movement tests to distinguish people with and without the diagnosis of schizophrenia.

Using their complete dataset, they were able to develop a model that could discriminate all schizophrenia cases from healthy control subjects with an impressive 98.3% accuracy.

Drs. Philip Benson and David St. Clair, lead authors on the paper, agreed that their findings were remarkable: “It has been known for over a hundred years that individuals with psychotic illnesses have a variety of eye movement abnormalities, but until our study, using a novel battery of tests, no one thought the abnormalities were sensitive enough to be used as potential clinical diagnostic biomarkers.”

Their battery of tests included smooth pursuit, free-viewing, and gaze fixation tasks. In smooth pursuit, people with schizophrenia have well-documented deficits in the ability to track slow-moving objects smoothly with their eyes. Their eye movements tend to fall behind the moving object and then catch-up with the moving object using a rapid eye movement, called a saccade.. A picture is displayed in the free-viewing test, and where most individuals follow a typical pattern with their gaze as they scan the picture, those with schizophrenia follow an abnormal pattern. In a fixation task, the instruction is to keep a steady gaze on a single unmoving target, which tends to be difficult for individuals with schizophrenia.

As expected, the researchers found that the performance of individuals with schizophrenia was abnormal compared to the healthy volunteer group on each of the eye tests. At right is an example of the differences, with the eye tracking of a schizophrenia case in red and a healthy control in blue.

The researchers then used several methods to model the data. The accuracy of each of the created algorithms was then tested by using eye test data from another group of cases and controls. Combining all the data, one of the models achieved 98.3% accuracy.

"It is encouraging to see the high sensitivity of this model for the diagnosis of schizophrenia. It will be interesting to see the extent to which this approach enables clinical investigators to distinguish people with schizophrenia from individuals with other psychiatric disorders," commented Dr. John Krystal, Editor of Biological Psychiatry.

Benson and St Clair have already started that work, stating, “We now have exciting unpublished data showing that patterns of eye movement abnormalities are specific to different psychiatric subgroups, another key requirement for diagnostic biomarkers. The next thing we want to know is when the abnormalities are first detectable and can they be used as disease markers for early intervention studies in major mental illness?”

"We are also keen to explore how best our findings can be developed for use in routine clinical practice," they added. Typical neuropsychological assessments are time-consuming, expensive, and require highly trained individuals to administer. In comparison, these eye tests are simple, cheap, and take only minutes to conduct. This means that a predictive model with such precision could potentially be incorporated in clinics and hospitals to aid physicians by augmenting traditional symptom-based diagnostic criteria.

(Source: alphagalileo.org)

Filed under brain eye movements mental illness schizophrenia biomarkers neuroscience psychology science

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New study sheds light on how and when vision evolved

Opsins, the light-sensitive proteins key to vision, may have evolved earlier and undergone fewer genetic changes than previously believed, according to a new study from the National University of Ireland Maynooth and the University of Bristol published in Proceedings of the National Academy of Sciences (PNAS) .

The study, which used computer modelling to provide a detailed picture of how and when opsins evolved, sheds light on the origin of sight in animals, including humans. The evolutionary origins of vision remain hotly debated, partly due to inconsistent reports of phylogenetic relationships among the earliest opsin-possessing animals.
Dr Davide Pisani of Bristol’s School of Earth Sciences and colleagues at NUI Maynooth performed a computational analysis to test every hypothesis of opsin evolution proposed to date. The analysis incorporated all available genomic information from all relevant animal lineages, including a newly sequenced group of sponges (Oscarella carmela) and the Cnidarians, a group of animals thought to have possessed the world’s earliest eyes.
Using this information, the researchers developed a timeline with an opsin ancestor common to all groups appearing some 700 million years ago. This opsin was considered ‘blind’ yet underwent key genetic changes over the span of 11 million years that conveyed the ability to detect light.
Dr Pisani said: “The great relevance of our study is that we traced the earliest origin of vision and we found that it originated only once in animals. This is an astonishing discovery because it implies that our study uncovered, in consequence, how and when vision evolved in humans.”

(Image credit: Roland Bircher)

New study sheds light on how and when vision evolved

Opsins, the light-sensitive proteins key to vision, may have evolved earlier and undergone fewer genetic changes than previously believed, according to a new study from the National University of Ireland Maynooth and the University of Bristol published in Proceedings of the National Academy of Sciences (PNAS) .

The study, which used computer modelling to provide a detailed picture of how and when opsins evolved, sheds light on the origin of sight in animals, including humans. The evolutionary origins of vision remain hotly debated, partly due to inconsistent reports of phylogenetic relationships among the earliest opsin-possessing animals.

Dr Davide Pisani of Bristol’s School of Earth Sciences and colleagues at NUI Maynooth performed a computational analysis to test every hypothesis of opsin evolution proposed to date. The analysis incorporated all available genomic information from all relevant animal lineages, including a newly sequenced group of sponges (Oscarella carmela) and the Cnidarians, a group of animals thought to have possessed the world’s earliest eyes.

Using this information, the researchers developed a timeline with an opsin ancestor common to all groups appearing some 700 million years ago. This opsin was considered ‘blind’ yet underwent key genetic changes over the span of 11 million years that conveyed the ability to detect light.

Dr Pisani said: “The great relevance of our study is that we traced the earliest origin of vision and we found that it originated only once in animals. This is an astonishing discovery because it implies that our study uncovered, in consequence, how and when vision evolved in humans.”

(Image credit: Roland Bircher)

Filed under evolution opsins vision cuttlefish phylogeny neuroscience psychology science

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