Neuroscience

Articles and news from the latest research reports.

Posts tagged neuroscience

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Mico from Neurowear analyses brainwaves, plays music that fits your mood
The always creative Neurowear company, creator of the overly successful brain-controlled Necomimi cat ears and the wearable tail accessory Shippo, has announced its newest invention, Mico, a system consisting of a pair of headphones, a brainwave sensor and an iOS app, aiming to free users from having to manually select songs ever again.
Mico -short for Music Inspiration from your Subconsciousness- is made up of two parts: the headphones with a sensor and an iPhone application. The headphones read the user’s brain signals and determines whether the person is focused, drowsy or stressed. The device sends this information to the iPhone app which searches for and plays music that matches the user’s mood. As a unique touch, LED signs on the side of the headphones light up, which also lets people know just what kind of state the user is in.
Neurowear recently revealed Zen Tunes, an application that analyses a user’s brainwaves when listening to music and then produces a recommended playlist based on their state of mind. Mico, takes this idea a step further.
According to Neurowear, “Mico frees the user from having to select songs and artists and allows users to encounter new music just by wearing the device. The device detects brainwaves through the sensor on your forehead. Our app then automatically plays music that fits your mood.”
If you like Necomimi, you will probably like Mico just as much. To learn more about the product check out the official Mico website where you can also find a recently posted photo gallery with j-pop star Julie Watai wearing the new device. If you look close enough (search for the indicator signs) you might be even able to tell in what mood Julie was during the photo session.
Release date or price not known at this point but Neurowear will demonstrate the device for the first time at the SXSW Trade Show in Austin, Texas from March 8-13.

Mico from Neurowear analyses brainwaves, plays music that fits your mood

The always creative Neurowear company, creator of the overly successful brain-controlled Necomimi cat ears and the wearable tail accessory Shippo, has announced its newest invention, Mico, a system consisting of a pair of headphones, a brainwave sensor and an iOS app, aiming to free users from having to manually select songs ever again.

Mico -short for Music Inspiration from your Subconsciousness- is made up of two parts: the headphones with a sensor and an iPhone application. The headphones read the user’s brain signals and determines whether the person is focused, drowsy or stressed. The device sends this information to the iPhone app which searches for and plays music that matches the user’s mood. As a unique touch, LED signs on the side of the headphones light up, which also lets people know just what kind of state the user is in.

Neurowear recently revealed Zen Tunes, an application that analyses a user’s brainwaves when listening to music and then produces a recommended playlist based on their state of mind. Mico, takes this idea a step further.

According to Neurowear, “Mico frees the user from having to select songs and artists and allows users to encounter new music just by wearing the device. The device detects brainwaves through the sensor on your forehead. Our app then automatically plays music that fits your mood.”

If you like Necomimi, you will probably like Mico just as much. To learn more about the product check out the official Mico website where you can also find a recently posted photo gallery with j-pop star Julie Watai wearing the new device. If you look close enough (search for the indicator signs) you might be even able to tell in what mood Julie was during the photo session.

Release date or price not known at this point but Neurowear will demonstrate the device for the first time at the SXSW Trade Show in Austin, Texas from March 8-13.

Filed under brain brainwaves Mico Neurowear technology neuroscience science

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Gets stroke patients back on their feet
A robot is now being built to help stroke patients with training, motivation and walking.
In Europe, strokes are the most common cause of physical disability among the elderly. This often result in paralysis of one side of the body, and many patients suffer much reduced physical mobility and are often unable to walk on their own. These are the hard facts the EU project CORBYS has taken seriously. Researchers in six countries are currently developing a robotic system designed to help stroke patients re-train their bodies. The concept is based on helping the patient by constructing a system consisting of powered orthosis to help patient in moving his/her legs and a mobile platform providing patient mobility.
The CORBYS researchers are also working with the cognitive aspects. The aim is to enable the robot to interpret data from the patient and adapt the training programme to his or her capabilities and intention. This will bring rehabilitation robots to the next level.
Back to walking normallyIt is vital to get stroke patients up on their feet as soon as possible. They must have frequent training exercises, and re-learn how to walk so that they can function as good as possible on their own.Why a robot? “Absolutely, because it is difficult to meet these requirements using today’s work-intensive manual method where two therapists assisting the patient by lifting one leg after the other”, says ICT researcher Anders Liverud at SINTEF, which is one of the CORBYS project partners.
Robot-patient learningCORBYS involves the use of physiological data such as heart rate, temperature and muscle activity measurements to provide feedback to the therapist and help control the robot. Do the patient’s legs always go where the patient want? Is the patient getting tired and stressed?
“The walking robot has several settings, and the therapist selects the correct mode based on how far the patient has come in his or her rehabilitation”, says Liverud. “The first step is to attach sensors to the patient’s body and let them walk on a treadmill. A therapist manually corrects the walking pattern and, with the help of the sensors, create a model of the patient’s walking pattern”, he says.
In the next mode, the system adjusts the walking pattern to the defined model. New adjustments are made and are used to improve optimisation of the walking pattern.
“The patient wears an EEG cap which measures brain activity”, says Liverud. “By using these signals combined with input from other physiological and system sensors, the robotic system registers whether the patient wants to stop, change speed or turn, and can adapt immediately”, he says. “The robot continues to correct any walking pattern errors. However, since it also allows the patient the freedom to decide where and how he or she walks, the patient experiences control and keeps motivation to continue with the training”, says Liverud.
Working with EuropeThe European researchers have now completed specification of the system and its components, and construction of the robot is underway.Construction involves a large team. The University of Bremen is heading the project and developing the architecture to integrate all system modules, and German wheelchair, orthosis and robotics experts are constructing the mechanical components, while two UK universities are working with cognitive aspects. Spanish specialists are addressing brain activity measurements and the University of Brussels is looking into robot control. SINTEF is working with the sensors and the final functional integration of the system. In a year’s time construction will be completed and the robot will be tested on stroke patients at rehabilitation institutes in Slovenia and Germany. The CORBYS project has a total budget of EUR 8.7 million.

Gets stroke patients back on their feet

A robot is now being built to help stroke patients with training, motivation and walking.

In Europe, strokes are the most common cause of physical disability among the elderly. This often result in paralysis of one side of the body, and many patients suffer much reduced physical mobility and are often unable to walk on their own. These are the hard facts the EU project CORBYS has taken seriously. Researchers in six countries are currently developing a robotic system designed to help stroke patients re-train their bodies. The concept is based on helping the patient by constructing a system consisting of powered orthosis to help patient in moving his/her legs and a mobile platform providing patient mobility.

The CORBYS researchers are also working with the cognitive aspects. The aim is to enable the robot to interpret data from the patient and adapt the training programme to his or her capabilities and intention. This will bring rehabilitation robots to the next level.

Back to walking normally
It is vital to get stroke patients up on their feet as soon as possible. They must have frequent training exercises, and re-learn how to walk so that they can function as good as possible on their own.
Why a robot? “Absolutely, because it is difficult to meet these requirements using today’s work-intensive manual method where two therapists assisting the patient by lifting one leg after the other”, says ICT researcher Anders Liverud at SINTEF, which is one of the CORBYS project partners.

Robot-patient learning
CORBYS involves the use of physiological data such as heart rate, temperature and muscle activity measurements to provide feedback to the therapist and help control the robot. Do the patient’s legs always go where the patient want? Is the patient getting tired and stressed?

“The walking robot has several settings, and the therapist selects the correct mode based on how far the patient has come in his or her rehabilitation”, says Liverud. “The first step is to attach sensors to the patient’s body and let them walk on a treadmill. A therapist manually corrects the walking pattern and, with the help of the sensors, create a model of the patient’s walking pattern”, he says.

In the next mode, the system adjusts the walking pattern to the defined model. New adjustments are made and are used to improve optimisation of the walking pattern.

“The patient wears an EEG cap which measures brain activity”, says Liverud. “By using these signals combined with input from other physiological and system sensors, the robotic system registers whether the patient wants to stop, change speed or turn, and can adapt immediately”, he says. “The robot continues to correct any walking pattern errors. However, since it also allows the patient the freedom to decide where and how he or she walks, the patient experiences control and keeps motivation to continue with the training”, says Liverud.

Working with Europe
The European researchers have now completed specification of the system and its components, and construction of the robot is underway.
Construction involves a large team. The University of Bremen is heading the project and developing the architecture to integrate all system modules, and German wheelchair, orthosis and robotics experts are constructing the mechanical components, while two UK universities are working with cognitive aspects. Spanish specialists are addressing brain activity measurements and the University of Brussels is looking into robot control. SINTEF is working with the sensors and the final functional integration of the system. In a year’s time construction will be completed and the robot will be tested on stroke patients at rehabilitation institutes in Slovenia and Germany. The CORBYS project has a total budget of EUR 8.7 million.

Filed under robots robotics stroke rehabilitation muscle activity brain activity neuroscience science

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Sleep loss precedes Alzheimer’s symptoms
Sleep is disrupted in people who likely have early Alzheimer’s disease but do not yet have the memory loss or other cognitive problems characteristic of full-blown disease, researchers at Washington University School of Medicine in St. Louis report March 11 in JAMA Neurology.
The finding confirms earlier observations by some of the same researchers. Those studies showed a link in mice between sleep loss and brain plaques, a hallmark of Alzheimer’s disease. Early evidence tentatively suggests the connection may work in both directions: Alzheimer’s plaques disrupt sleep, and lack of sleep promotes Alzheimer’s plaques.
“This link may provide us with an easily detectable sign of Alzheimer’s pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat people who have markers of early Alzheimer’s, changes in sleep in response to treatments may serve as an indicator of whether the new treatments are succeeding.”
Sleep problems are common in people who have symptomatic Alzheimer’s disease, but scientists recently have begun to suspect that they also may be an indicator of early disease. The new paper is among the first to connect early Alzheimer’s disease and sleep disruption in humans.
(Image: iStockphoto)

Sleep loss precedes Alzheimer’s symptoms

Sleep is disrupted in people who likely have early Alzheimer’s disease but do not yet have the memory loss or other cognitive problems characteristic of full-blown disease, researchers at Washington University School of Medicine in St. Louis report March 11 in JAMA Neurology.

The finding confirms earlier observations by some of the same researchers. Those studies showed a link in mice between sleep loss and brain plaques, a hallmark of Alzheimer’s disease. Early evidence tentatively suggests the connection may work in both directions: Alzheimer’s plaques disrupt sleep, and lack of sleep promotes Alzheimer’s plaques.

“This link may provide us with an easily detectable sign of Alzheimer’s pathology,” says senior author David M. Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of Washington University’s Department of Neurology. “As we start to treat people who have markers of early Alzheimer’s, changes in sleep in response to treatments may serve as an indicator of whether the new treatments are succeeding.”

Sleep problems are common in people who have symptomatic Alzheimer’s disease, but scientists recently have begun to suspect that they also may be an indicator of early disease. The new paper is among the first to connect early Alzheimer’s disease and sleep disruption in humans.

(Image: iStockphoto)

Filed under sleep sleep loss alzheimer's disease dementia memory loss neuroscience psychology science

103 notes

Sleep Discovery Could Lead to Therapies That Improve Memory
A team of sleep researchers led by UC Riverside psychologist Sara C. Mednick has confirmed the mechanism that enables the brain to consolidate memory and found that a commonly prescribed sleep aid enhances the process. Those discoveries could lead to new sleep therapies that will improve memory for aging adults and those with dementia, Alzheimer’s and schizophrenia.
The groundbreaking research appears in a paper, “The Critical Role of Sleep Spindles in Hippocampal-Dependent Memory: A Pharmacology Study,” published in the Journal of Neuroscience.
Earlier research found a correlation between sleep spindles — bursts of brain activity that last for a second or less during a specific stage of sleep — and consolidation of memories that depend on the hippocampus. The hippocampus, part of the cerebral cortex, is important in the consolidation of information from short-term to long-term memory, and spatial navigation. The hippocampus is one of the first regions of the brain damaged by Alzheimer’s disease.
Mednick and her research team demonstrated, for the first time, the critical role that sleep spindles play in consolidating memory in the hippocampus, and they showed that pharmaceuticals could significantly improve that process, far more than sleep alone.
In addition to Mednick the research team includes: Elizabeth A. McDevitt, UC San Diego; James K. Walsh, VA San Diego Healthcare System, La Jolla, Calif; Erin Wamsley, St. Luke’s Hospital, St. Louis, Mo.; Martin Paulus, Stanford University; Jennifer C. Kanady, Harvard Medical School; and Sean P.A. Drummond, UC Berkeley.
“We found that a very common sleep drug can be used to increase verbal memory,” said Mednick, the lead author of the paper that outlines results of two studies conducted over five years with a $651,999 research grant from the National Institutes of Health. “This is the first study to show you can manipulate sleep to improve memory. It suggests sleep drugs could be a powerful tool to tailor sleep to particular memory disorders.”
(Image credit)

Sleep Discovery Could Lead to Therapies That Improve Memory

A team of sleep researchers led by UC Riverside psychologist Sara C. Mednick has confirmed the mechanism that enables the brain to consolidate memory and found that a commonly prescribed sleep aid enhances the process. Those discoveries could lead to new sleep therapies that will improve memory for aging adults and those with dementia, Alzheimer’s and schizophrenia.

The groundbreaking research appears in a paper, “The Critical Role of Sleep Spindles in Hippocampal-Dependent Memory: A Pharmacology Study,” published in the Journal of Neuroscience.

Earlier research found a correlation between sleep spindles — bursts of brain activity that last for a second or less during a specific stage of sleep — and consolidation of memories that depend on the hippocampus. The hippocampus, part of the cerebral cortex, is important in the consolidation of information from short-term to long-term memory, and spatial navigation. The hippocampus is one of the first regions of the brain damaged by Alzheimer’s disease.

Mednick and her research team demonstrated, for the first time, the critical role that sleep spindles play in consolidating memory in the hippocampus, and they showed that pharmaceuticals could significantly improve that process, far more than sleep alone.

In addition to Mednick the research team includes: Elizabeth A. McDevitt, UC San Diego; James K. Walsh, VA San Diego Healthcare System, La Jolla, Calif; Erin Wamsley, St. Luke’s Hospital, St. Louis, Mo.; Martin Paulus, Stanford University; Jennifer C. Kanady, Harvard Medical School; and Sean P.A. Drummond, UC Berkeley.

“We found that a very common sleep drug can be used to increase verbal memory,” said Mednick, the lead author of the paper that outlines results of two studies conducted over five years with a $651,999 research grant from the National Institutes of Health. “This is the first study to show you can manipulate sleep to improve memory. It suggests sleep drugs could be a powerful tool to tailor sleep to particular memory disorders.”

(Image credit)

Filed under memory alzheimer's disease brain activity memory consolidation sleep neuroscience science

177 notes

Suzanne Dickson: Brain mechanisms of food reward
Studying what makes us want to eat, could help devise approaches to prevent obesity, which is becoming widespread in Europe.
Suzanne Dickson is a Professor of physiology and neuroendocrinology at the Institute of Neuroscience and Physiology, based at the Sahlgrenska Academy at the University of Gothenburg, Sweden. She tells youris.com about her involvement in the EU funded NeuroFAST project. Her focus is on the impact of appetite-regulating gut hormones on parts of the brain that influence food preference and food reward.
This research is also driven by the huge unmet need of treating the growing group of obese patients.
What is the focus of your work relating to food and the brain?We work on food reward, which involves neurobiological circuits linked to the addiction process. We decided to work on this because increasing evidence linked excessive over-eating to brain pathways involved in reward, including pathways known to be targets for addictive drugs.  Over-eating can be influenced by genetic predisposition traits, psychiatric diseases, cues from the environment that trigger expectation of a food reward. Other factors include socio-economic pressures, stressful lifestyle including stress in the workplace or home.
What is the nature of food reward?Our specific focus is on the property of the reward value. If animals find food rewarding, they will display altered behaviours that indicate that the reward value of the food is changed. Members of our team are working with sugars, fats and combinations of the above. We have also been working in clinical projects with foods of similar taste but with altered caloric value. By targeting brain mechanisms involved in food reward, we hope to reveal new mechanisms that will help develop new treatment strategies for obesity.
We have studied an area of the brain called ventral tegmental area (VTA) is a key node in the brain’s reward pathway. It is the home of the dopamine cells that are activated by rewards, including food rewards. Its role is very complex. Many believe that these cells are involved in food searching behaviours or food motivation, for example. However, they also can be activated simply by cues associated with foods akin to deciding to consume a chocolate bar by the sight of one at the cashier in a supermarket and novelty of the reward stimulus appears to play a role.
Did you identify the difference between the brain’s pleasure center and hunger center?The pleasure centres are involved in food intake that is linked to its reward value. Whether we are hungry or fed, by raising the reward value of food the reward system encourages us to eat more, especially rewarding food. This system has been critical during the evolution process to ensure survival from famine. In our modern environment that generates obesity, food reward is no longer our friend as it encourages us to over-indulge in sweet and fatty food, even when we are not hungry.
By contrast, the hunger pathways can be considered more primitive. They detect and respond to nutrient deficit. If we enter negative energy balance, homeostatic pathways become activated informing higher feeding networks to initiate feeding behaviours.
What strategies have studied to try and find ways to limit over-eating?We have recently learned from the field of bariatric—weight loss—surgery that it is possible to change reward behaviour towards food. This involves unknown mechanisms that are likely linked to the brain’s food reward system. We focus particularly on a hormone called ghrelin whose secretion is altered after bariatric surgery. We hope to reveal new information that is of clinical and therapeutic relevance for future drug strategies for this disease area.
So far, in the laboratory, we have learned a lot about the basic brain mechanisms controlling food reward and the role played by gut hormones in regulating these. We therefore know a lot more about mechanisms—namely about the brain systems and circuits underpinning over-eating—especially for calorie dense foods.
(Image credit: Zorrilla Laboratory, The Scripps Research Institute)

Suzanne Dickson: Brain mechanisms of food reward

Studying what makes us want to eat, could help devise approaches to prevent obesity, which is becoming widespread in Europe.

Suzanne Dickson is a Professor of physiology and neuroendocrinology at the Institute of Neuroscience and Physiology, based at the Sahlgrenska Academy at the University of Gothenburg, Sweden. She tells youris.com about her involvement in the EU funded NeuroFAST project. Her focus is on the impact of appetite-regulating gut hormones on parts of the brain that influence food preference and food reward.

This research is also driven by the huge unmet need of treating the growing group of obese patients.

What is the focus of your work relating to food and the brain?
We work on food reward, which involves neurobiological circuits linked to the addiction process. We decided to work on this because increasing evidence linked excessive over-eating to brain pathways involved in reward, including pathways known to be targets for addictive drugs.  Over-eating can be influenced by genetic predisposition traits, psychiatric diseases, cues from the environment that trigger expectation of a food reward. Other factors include socio-economic pressures, stressful lifestyle including stress in the workplace or home.

What is the nature of food reward?
Our specific focus is on the property of the reward value. If animals find food rewarding, they will display altered behaviours that indicate that the reward value of the food is changed. Members of our team are working with sugars, fats and combinations of the above. We have also been working in clinical projects with foods of similar taste but with altered caloric value. By targeting brain mechanisms involved in food reward, we hope to reveal new mechanisms that will help develop new treatment strategies for obesity.

We have studied an area of the brain called ventral tegmental area (VTA) is a key node in the brain’s reward pathway. It is the home of the dopamine cells that are activated by rewards, including food rewards. Its role is very complex. Many believe that these cells are involved in food searching behaviours or food motivation, for example. However, they also can be activated simply by cues associated with foods akin to deciding to consume a chocolate bar by the sight of one at the cashier in a supermarket and novelty of the reward stimulus appears to play a role.

Did you identify the difference between the brain’s pleasure center and hunger center?
The pleasure centres are involved in food intake that is linked to its reward value. Whether we are hungry or fed, by raising the reward value of food the reward system encourages us to eat more, especially rewarding food. This system has been critical during the evolution process to ensure survival from famine. In our modern environment that generates obesity, food reward is no longer our friend as it encourages us to over-indulge in sweet and fatty food, even when we are not hungry.

By contrast, the hunger pathways can be considered more primitive. They detect and respond to nutrient deficit. If we enter negative energy balance, homeostatic pathways become activated informing higher feeding networks to initiate feeding behaviours.

What strategies have studied to try and find ways to limit over-eating?
We have recently learned from the field of bariatric—weight loss—surgery that it is possible to change reward behaviour towards food. This involves unknown mechanisms that are likely linked to the brain’s food reward system. We focus particularly on a hormone called ghrelin whose secretion is altered after bariatric surgery. We hope to reveal new information that is of clinical and therapeutic relevance for future drug strategies for this disease area.

So far, in the laboratory, we have learned a lot about the basic brain mechanisms controlling food reward and the role played by gut hormones in regulating these. We therefore know a lot more about mechanisms—namely about the brain systems and circuits underpinning over-eating—especially for calorie dense foods.

(Image credit: Zorrilla Laboratory, The Scripps Research Institute)

Filed under obesity food reward addiction ventral tegmental area reward system neuroscience science

177 notes

You’re such a jerk 
If that headline makes you feel bad, an expert says it’s because we’re genetically wired to take offense.
Insults are painful because we have certain social needs. We seek to be among other people, and once among them, we seek to form relationships with them and to improve our position on the social hierarchy. They are also painful because we have a need to project our self-image and to have other people not only accept this image, but support it. If we didn’t have these needs, being insulted wouldn’t feel bad. Furthermore, although different people experience different amounts of pain on being insulted, almost everyone will experience some pain. Indeed, we would search long and hard to find a person who is never pained by insults—or who himself never feels the need to insult others.
These observations raise a question: why do we have the social needs we do? According to evolutionary psychologists, our social needs—and, more generally, our psychological propensities—are the result of nature rather than nurture. More precisely, they are a consequence of our evolutionary past. The views of evolutionary psychologists are of interest in this, a study of insults, for the simple reason that they allow us to gain a deeper understanding of why it is painful when others insult us and why we go out of our way to cause others pain by insulting them.
We humans find some things to be pleasant and other things to be unpleasant. We find it pleasant, for example, to eat sweet, fattening foods or to have sex, and we find it unpleasant to be thirsty, swallow bitter substances, or get burned. Notice that we don’t choose for these things to be pleasant or unpleasant. It is true that we can, if we are strong-willed, voluntarily do things that are unpleasant, such as put our finger in a candle flame. We can also refuse to do things that are pleasant: we might, for example, forgo opportunities to have sex. But this doesn’t alter the basic biological fact that getting burned is painful and having sex is pleasurable. Whether or not an activity is pleasant is determined, after all, by our wiring, and we do not have it in our power—not yet, at any rate—to alter this wiring.
Why are we wired to be able to experience pleasure and pain? Why aren’t we wired to be immune to pain while retaining our ability to experience pleasure? And given that we possess the ability to experience both pleasure and pain, why do we find a particular activity to be pleasant rather than painful? Why, for example, do we find it pleasant to have sex but unpleasant to get burned? Why not the other way around? I have given the long answer to these questions elsewhere. For our present purposes—namely, to explain why we have the social needs we do—the short answer will suffice.
We have the ability to experience pleasure and pain because our evolutionary ancestors who had this ability were more likely to survive and reproduce than those who didn’t. Creatures with this ability could, after all, be rewarded (with pleasurable feelings) for engaging in certain activities and punished (with unpleasant feelings) for engaging in others. More precisely, they could be rewarded for doing things (such as having sex) that would increase their chances of surviving and reproducing, and be punished for doing things (such as burning themselves) that would lessen their chances.
This makes it sound as if a designer was responsible for our wiring, but evolutionary psychologists would reject this notion. Evolution, they would remind us, has no designer and no goal. To the contrary, species evolve because some of their members, thanks to the genetic luck-of-the-draw, have a makeup that increases their chances of surviving and reproducing. As a result, they (probably) have more descendants than genetically less fortunate members of their species. And because they spread their genes more effectively, they have a disproportionate influence on the genetic makeup of future members of their species.
Evolutionary psychologists would go on to remind us that if our evolutionary ancestors had found themselves in a different environment, we would be wired differently and as a result would find different things to be pleasant and unpleasant. Suppose that getting burned, rather than being detrimental to our evolutionary ancestors, had somehow increased their chances of surviving and reproducing. Under these circumstances, those individuals who were wired so that it felt good to get burned would have been more effective at spreading their genes than those who were wired so that it felt bad. And as a result we, their descendants, would also be wired so that it felt good to get burned.
Evolutionary psychologists would also remind us that the evolutionary process is imperfect. For one thing, although the wiring we inherited from our ancestors might have allowed them to flourish on the savannahs of Africa, it isn’t optimal for the rather different environment in which we today find ourselves. Our ancestors who had a penchant for consuming sweet, fattening foods, for example, were less likely to starve than those who didn’t. The problem is that we who have inherited that penchant live in an environment in which sweet, fattening foods are abundant. In this environment, being wired so that it is pleasant to consume, say, ice cream, increases our chance of getting heart disease and other illnesses, and thereby arguably lessens our chance of surviving.

You’re such a jerk

If that headline makes you feel bad, an expert says it’s because we’re genetically wired to take offense.

Insults are painful because we have certain social needs. We seek to be among other people, and once among them, we seek to form relationships with them and to improve our position on the social hierarchy. They are also painful because we have a need to project our self-image and to have other people not only accept this image, but support it. If we didn’t have these needs, being insulted wouldn’t feel bad. Furthermore, although different people experience different amounts of pain on being insulted, almost everyone will experience some pain. Indeed, we would search long and hard to find a person who is never pained by insults—or who himself never feels the need to insult others.

These observations raise a question: why do we have the social needs we do? According to evolutionary psychologists, our social needs—and, more generally, our psychological propensities—are the result of nature rather than nurture. More precisely, they are a consequence of our evolutionary past. The views of evolutionary psychologists are of interest in this, a study of insults, for the simple reason that they allow us to gain a deeper understanding of why it is painful when others insult us and why we go out of our way to cause others pain by insulting them.

We humans find some things to be pleasant and other things to be unpleasant. We find it pleasant, for example, to eat sweet, fattening foods or to have sex, and we find it unpleasant to be thirsty, swallow bitter substances, or get burned. Notice that we don’t choose for these things to be pleasant or unpleasant. It is true that we can, if we are strong-willed, voluntarily do things that are unpleasant, such as put our finger in a candle flame. We can also refuse to do things that are pleasant: we might, for example, forgo opportunities to have sex. But this doesn’t alter the basic biological fact that getting burned is painful and having sex is pleasurable. Whether or not an activity is pleasant is determined, after all, by our wiring, and we do not have it in our power—not yet, at any rate—to alter this wiring.

Why are we wired to be able to experience pleasure and pain? Why aren’t we wired to be immune to pain while retaining our ability to experience pleasure? And given that we possess the ability to experience both pleasure and pain, why do we find a particular activity to be pleasant rather than painful? Why, for example, do we find it pleasant to have sex but unpleasant to get burned? Why not the other way around? I have given the long answer to these questions elsewhere. For our present purposes—namely, to explain why we have the social needs we do—the short answer will suffice.

We have the ability to experience pleasure and pain because our evolutionary ancestors who had this ability were more likely to survive and reproduce than those who didn’t. Creatures with this ability could, after all, be rewarded (with pleasurable feelings) for engaging in certain activities and punished (with unpleasant feelings) for engaging in others. More precisely, they could be rewarded for doing things (such as having sex) that would increase their chances of surviving and reproducing, and be punished for doing things (such as burning themselves) that would lessen their chances.

This makes it sound as if a designer was responsible for our wiring, but evolutionary psychologists would reject this notion. Evolution, they would remind us, has no designer and no goal. To the contrary, species evolve because some of their members, thanks to the genetic luck-of-the-draw, have a makeup that increases their chances of surviving and reproducing. As a result, they (probably) have more descendants than genetically less fortunate members of their species. And because they spread their genes more effectively, they have a disproportionate influence on the genetic makeup of future members of their species.

Evolutionary psychologists would go on to remind us that if our evolutionary ancestors had found themselves in a different environment, we would be wired differently and as a result would find different things to be pleasant and unpleasant. Suppose that getting burned, rather than being detrimental to our evolutionary ancestors, had somehow increased their chances of surviving and reproducing. Under these circumstances, those individuals who were wired so that it felt good to get burned would have been more effective at spreading their genes than those who were wired so that it felt bad. And as a result we, their descendants, would also be wired so that it felt good to get burned.

Evolutionary psychologists would also remind us that the evolutionary process is imperfect. For one thing, although the wiring we inherited from our ancestors might have allowed them to flourish on the savannahs of Africa, it isn’t optimal for the rather different environment in which we today find ourselves. Our ancestors who had a penchant for consuming sweet, fattening foods, for example, were less likely to starve than those who didn’t. The problem is that we who have inherited that penchant live in an environment in which sweet, fattening foods are abundant. In this environment, being wired so that it is pleasant to consume, say, ice cream, increases our chance of getting heart disease and other illnesses, and thereby arguably lessens our chance of surviving.

Filed under insults social rejection self image self promotion evolution genetics psychology neuroscience emotions science

225 notes

The Hidden Costs of Cognitive Enhancement
Gentle electrical zaps to the brain can accelerate learning and boost performance on a wide range of mental tasks, scientists have reported in recent years. But a new study suggests there may be a hidden price: Gains in one aspect of cognition may come with deficits in another.
Researchers who study transcranial electrical stimulation, which uses electrodes placed on the scalp, see it as a potentially promising way to enhance cognition in neurological patients, struggling students, and perhaps even ordinary people. Scientists have used it to speed up rehab in people whose speech or movement has been affected by a stroke, and DARPA has studied it as a way to accelerate learning in intelligence analysts or soldiers on the lookout for bad guys and bombs.
Until now, the papers coming out of this field have reported one good-news finding after another.
“This is the first paper to my knowledge to show a cost associated with the gains in cognitive function,” said neuropsychologist Rex Jung of the University of New Mexico, who was not associated with the study. “It’s a really nice demonstration.”
Cognitive neuroscientist Roi Cohen Kadosh of the University of Oxford, who led the study, has been investigating brain stimulation to boost mathematical abilities. He has applied for a patent on a brain stimulator he hopes could help math-challenged students get a better grip on the basics, or even help the mathematically inclined perform even better.
Cohen Kadosh and his colleague Teresa Iuculano investigated 19 volunteers as they learned a new numerical system by trial and error. The new system was based on arbitrary symbols: A cylinder represented the number five, for example, and a triangle represented the number nine. In several training sessions the volunteers viewed pairs of symbols on a computer screen and pressed a key to indicate which one represented a bigger quantity. At first they had to guess, but they eventually learned which symbols corresponded with which numbers.
All of the volunteers wore electrodes on their scalp during these training session. Some received mild electrical stimulation that targeted the posterior parietal cortex, an area implicated in previous studies of numerical cognition. Others received stimulation of the dorsolateral prefrontal cortex, an area involved in a wide range of functions, including learning and memory. A third group received sham stimulation that caused a slight tingling of the skin but no change in brain activity.
Those who had the parietal area involved in numerical cognition stimulated learned the new number system more quickly than those who got sham stimulation, the researchers report in the Journal of Neuroscience. But at the end of the weeklong study their reaction times were slower when they had to put their newfound knowledge to use to solve a new task that they hadn’t seen during the training sessions. ”They had trouble accessing what they’d learned,” Cohen Kadosh said.
The volunteers who had the prefrontal area involved in learning and memory stimulated showed the opposite pattern. They were slower than the control group to learn the new numerical system, but they performed faster on the new test at the end of the experiment. The bottom line, says Cohen Kadosh, is that stimulating either brain region had both benefits and drawbacks. ”Just like with drugs, there seem to be side effects,” he said.
Going forward, Cohen Kadosh says, more work is needed on how to maximize the benefits and minimize the costs of electrical brain stimulation. He thinks the approach has promise, but only when it’s used strategically, by picking the right brain regions to target and stimulating them while a person is training on the skill they want to improve. ”I think it’s going to be useless unless you pair it with some type of cognitive training,” he said.
But that’s not stopping some people from giving it a try on their own. Although it should be obvious that DIY brain stimulation is a bad idea, both Jung and Cohen Kadosh say there seems to be growing interest in the general public in using it for cognitive enhancement.
“There are some do it yourself websites I’ve stumbled across that are pretty frightening,” Jung said. “People are definitely tinkering around with this in their garage.”
The new study suggests one way that could backfire. And that’s not all, said Jung. ”You can burn yourself if nothing else.”

The Hidden Costs of Cognitive Enhancement

Gentle electrical zaps to the brain can accelerate learning and boost performance on a wide range of mental tasks, scientists have reported in recent years. But a new study suggests there may be a hidden price: Gains in one aspect of cognition may come with deficits in another.

Researchers who study transcranial electrical stimulation, which uses electrodes placed on the scalp, see it as a potentially promising way to enhance cognition in neurological patients, struggling students, and perhaps even ordinary people. Scientists have used it to speed up rehab in people whose speech or movement has been affected by a stroke, and DARPA has studied it as a way to accelerate learning in intelligence analysts or soldiers on the lookout for bad guys and bombs.

Until now, the papers coming out of this field have reported one good-news finding after another.

“This is the first paper to my knowledge to show a cost associated with the gains in cognitive function,” said neuropsychologist Rex Jung of the University of New Mexico, who was not associated with the study. “It’s a really nice demonstration.”

Cognitive neuroscientist Roi Cohen Kadosh of the University of Oxford, who led the study, has been investigating brain stimulation to boost mathematical abilities. He has applied for a patent on a brain stimulator he hopes could help math-challenged students get a better grip on the basics, or even help the mathematically inclined perform even better.

Cohen Kadosh and his colleague Teresa Iuculano investigated 19 volunteers as they learned a new numerical system by trial and error. The new system was based on arbitrary symbols: A cylinder represented the number five, for example, and a triangle represented the number nine. In several training sessions the volunteers viewed pairs of symbols on a computer screen and pressed a key to indicate which one represented a bigger quantity. At first they had to guess, but they eventually learned which symbols corresponded with which numbers.

All of the volunteers wore electrodes on their scalp during these training session. Some received mild electrical stimulation that targeted the posterior parietal cortex, an area implicated in previous studies of numerical cognition. Others received stimulation of the dorsolateral prefrontal cortex, an area involved in a wide range of functions, including learning and memory. A third group received sham stimulation that caused a slight tingling of the skin but no change in brain activity.

Those who had the parietal area involved in numerical cognition stimulated learned the new number system more quickly than those who got sham stimulation, the researchers report in the Journal of Neuroscience. But at the end of the weeklong study their reaction times were slower when they had to put their newfound knowledge to use to solve a new task that they hadn’t seen during the training sessions. ”They had trouble accessing what they’d learned,” Cohen Kadosh said.

The volunteers who had the prefrontal area involved in learning and memory stimulated showed the opposite pattern. They were slower than the control group to learn the new numerical system, but they performed faster on the new test at the end of the experiment. The bottom line, says Cohen Kadosh, is that stimulating either brain region had both benefits and drawbacks. ”Just like with drugs, there seem to be side effects,” he said.

Going forward, Cohen Kadosh says, more work is needed on how to maximize the benefits and minimize the costs of electrical brain stimulation. He thinks the approach has promise, but only when it’s used strategically, by picking the right brain regions to target and stimulating them while a person is training on the skill they want to improve. ”I think it’s going to be useless unless you pair it with some type of cognitive training,” he said.

But that’s not stopping some people from giving it a try on their own. Although it should be obvious that DIY brain stimulation is a bad idea, both Jung and Cohen Kadosh say there seems to be growing interest in the general public in using it for cognitive enhancement.

“There are some do it yourself websites I’ve stumbled across that are pretty frightening,” Jung said. “People are definitely tinkering around with this in their garage.”

The new study suggests one way that could backfire. And that’s not all, said Jung. ”You can burn yourself if nothing else.”

Filed under transcranial electrical stimulation cognition cognitive function brain stimulation parietal cortex learning neuroscience science

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Mutated Gene Causes Nerve Cell Death

The British astrophysicist Stephen Hawking is likely to be the world’s most famous person living with amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig’s disease. ALS is a progressive disease affecting motor neurons, nerve cells that control muscle function, and nearly always leads to death. Researchers at the Institute of Molecular Biotechnology of the Austrian Academy of Sciences (IMBA) in Vienna have now identified a completely new mechanism in the onset of motor neuron diseases. Their findings could be the basis for future treatments for these presently incurable diseases.

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A new principle on motor neuron death
The IMBA scientists, working with an international team of researchers under the leadership of Josef Penninger and Javier Martinez, discovered a completely new fundamental mechanism that triggers the death of motor neurons. Motor neurons are nerve cells responsible for stimulating muscles. The loss of these motor neurons in mice with a genetic mutation in a gene named CLP11 leads to severe and progressive muscular paralysis and, in some cases, to death.
"We’ve been working on resolving the function of the CLP1 gene in a living organism for a long time. To do that, we developed model mice in which the function of CLP1 was genetically inactivated. To our utter surprise we discovered that deactivating CLP1 increases the sensitivity of cell die when exposed to oxidative stress2. That leads to enhanced activity of the p53 protein3 and then to the permanent destruction of motor neurons," says Toshikatsu Hanada, a postdoctoral researcher working in the lab of Josef Penninger and first author of the study along with Stefan Weitzer.

Stephen Hawking - a most renowned patient
Motor neuron diseases (MNDs), such as amyotrophic lateral sclerosis (ALS) and spinal muscular atrophy (SMA), are chronic disorders of the neuromuscular system. These diseases are caused by damage in the motor nerve cells in the brain and spinal cord, and the nerves can no longer stimulate motion in the muscles. The primary symptoms are muscular weakness, muscular dystrophy, and problems swallowing or speaking. Stephen Hawking was diagnosed with ALS 50 years ago. But not all ALS patients live so long with the disease: so far there are no treatments for ALS. Nearly all ALS patients die of paralysis of respiratory muscles within a few years.

Completely new disease mechanism
Javier Martinez, an IMBA team leader and co-author of the study, is a specialist in the field of ribonucleic acid (RNA) research. His research group had discovered the CLP1 gene in an earlier study, published in Nature in 2007. Until now, the exact essential function of CLP1 in RNA biology was unclear. “By deactivating CLP1, we have discovered a previously unknown new species of RNA,” says Javier Martinez about the scientific relevance of the work. “The accumulation of this RNA is a consequence of increased oxidative stress in the cell. We see this as one of the triggers for the loss of motor neurons that occurs in ALS and other neuromuscular diseases. Thus our findings describe a completely new mechanism of motor neuron diseases.”

Seminal findings
Josef Penninger, scientific director at the IMBA and last-author of the study, is excited about the researchers’ findings: “This surprising discovery of a role of CLP1 in the onset of motor neuron diseases is an entirely new principle in how RNA talks to oxidative stress. Nearly all genetic mutations found in ALS patients affect either RNA metabolism or oxidative stress, suggesting a possibly unifying principle for these diseases. Our work may have revealed the ‘missing link’ in how these two biological systems communicate and trigger incurable diseases like ALS.”

Stefan Weitzer sees tremendous potential for these findings: “We’ve discovered a new mechanism that leads to the death of motor neurons. If this holds true for other neuronal disease, our results could be one day used to drive the development of treatments for previously incurable diseases. In our work we also describe how the p53 protein regulates the loss of motor neurons. Removing p53 saves mice with CLP1 mutations from certain death.” If scientists are successful in applying these findings to people, the researchers may have discovered a treatment approach to cure ALS and similar diseases. The authors, however, caution that more studies will be needed to translate their findings to human medicine.

This study was performed in collaboration with research groups from the Medical Universities of Vienna and Innsbruck, the University Medical Center at Hamburg-Eppendorf in Germany, the Harvard Medical School, the Harvard Stem Cell Institute, the Boston Children’s and Massachusetts General Hospitals, the Keio University School of Medicine in Tokyo, Oita University in Japan, and the Weizmann Institute of Science in Rehovot in Israel.

Their work, “CLP1 links tRNA metabolism to progressive motor-neuron loss”, was published on March 10, 2013 in “Nature”, an internationally renowned journal.

(Source: imba.oeaw.ac.at)

Filed under Lou Gehrig's disease ALS cell death motor neurons muscular paralysis genetics neuroscience science

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Affecting Perception

When most of us admire a piece of art, it triggers a cascade of complex neural activity; a wash of emotion and meaning that fills our brains and prompts deep thought. But does that happen for people with neurological conditions, too?

Forthcoming Oxford-based exhibition Affecting Perception seeks to explore that very question, through a combination of art, seminars and school workshops. Organised by Martha Crawford, Cosima Gretton and Rachel Stratton, who together form the AXNS collective, the aim is to understand how artists and their work are affected by neurological conditions.

The team is working with the University’s Department of Experimental Psychology and artists who suffer from conditions ranging from dementia to brain damage, in order to help the public understand how art and neuroscience are intertwined. “We’re trying to engage the community with the kind of learning usually kept in the University,” explains Martha Crawford.

Helping them achieve that are Prof. Glyn Humphreys and Prof. Charles Spence, both from the University’s Department of Experimental Psychology. Individually, they’ll be leading seminars during the exhibition which explore the overlap between academia and art. “There’s a coarse level of understanding of neuropsychology outside of academia, which means people are sometimes scared of neurological conditions,” explains Professor Glyn Humphreys. “I think anything we can do to raise awareness has to be a good thing.”

During the course of the four-week exhibition, Prof. Humprheys will talk about visual agnosia: a condition where patients can’t associate visual stimulus with meaning. It’s a rare condition, but it’s of interest to artists and scientists alike. Separating meaning and aesthetic is a trick used by artists to explore the two more thoughtfully; Humphreys’ patients still have little choice but to face the world that way.

Elsewhere, Prof. Spence will talk about subtle forms of synesthesia, called cross-modal correspondences, which affect us all. Synesthesia is that odd condition where stimulating one sense leads to automatic experiences in a second; cross-modal correspondences are more subtle, like the way red stars make many of us think of bitter flavours. Plenty of famous creatives have used the phenomenon to great effect — and during his talk, Spence will explain how it can help amplify our enjoyment of art.

There’s no denying that these are weighty subject indeed. But by understanding them just a little better we can achieve a better grasp on the neurological conditions that many suffer — and break down the stigma attached to them, too.

Affecting Perception runs from 4th-31st March 2013 at venues across Oxford. Admission is free. For more information, visit http://axnscollective.org.

Filed under art visual perception neurological disorders neurodegenerative diseases neuroscience science

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Right-Handed Males, Left-Handed Females?
This is true for sugar gliders (Petaurus breviceps) and grey short-tailed opossums (Monodelphis domestica), say biologists from Saint Petersburg State University, Russia.
Their study, published in the open access journal BMC Evolutionary Biology, shows that handedness in marsupials is dependent on gender.
This preference of one hand over another has developed despite the absence of a corpus callosum, the part of the brain, which in placental mammals allows one half of the brain to communicate with the other.
Many animals show a distinct preference for using one hand (paw, hoof) over another. This is often related to posture – an animal is more likely to show manual laterality if it is upright, related to the difficulty of the task, more complex tasks show a handed preference, or even with age. As an example of all three: crawling human babies show less hand preference than toddlers.
Some species also show a distinct sex effect in handedness but among non-marsupial mammals this tendency is for left-handed males and right-handed females.
In contrast, the team from Russia shows that male quadruped marsupials, such as who walk on all fours, tend to be right-handed while the females are left-handed, especially as tasks became more difficult.
“Marsupials do not have a corpus callosum – which connects the two halves of the mammalian brain together. Reversed sex related handedness is an indication of how the marsupial brain has developed different ways of the two halves of the brain communicating in the absence of the corpus callosum,” explains senior author Dr Yegor Malashichev.

Right-Handed Males, Left-Handed Females?

This is true for sugar gliders (Petaurus breviceps) and grey short-tailed opossums (Monodelphis domestica), say biologists from Saint Petersburg State University, Russia.

Their study, published in the open access journal BMC Evolutionary Biology, shows that handedness in marsupials is dependent on gender.

This preference of one hand over another has developed despite the absence of a corpus callosum, the part of the brain, which in placental mammals allows one half of the brain to communicate with the other.

Many animals show a distinct preference for using one hand (paw, hoof) over another. This is often related to posture – an animal is more likely to show manual laterality if it is upright, related to the difficulty of the task, more complex tasks show a handed preference, or even with age. As an example of all three: crawling human babies show less hand preference than toddlers.

Some species also show a distinct sex effect in handedness but among non-marsupial mammals this tendency is for left-handed males and right-handed females.

In contrast, the team from Russia shows that male quadruped marsupials, such as who walk on all fours, tend to be right-handed while the females are left-handed, especially as tasks became more difficult.

“Marsupials do not have a corpus callosum – which connects the two halves of the mammalian brain together. Reversed sex related handedness is an indication of how the marsupial brain has developed different ways of the two halves of the brain communicating in the absence of the corpus callosum,” explains senior author Dr Yegor Malashichev.

Filed under animals marsupials handedness hand preference corpus callosum neuroscience science

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