Neuroscience

Articles and news from the latest research reports.

Posts tagged science

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Can We Reconcile the Declarative Memory and Spatial Navigation Views on Hippocampal Function?
Some argue that hippocampus supports declarative memory, our capacity to recall facts and events, whereas others view the hippocampus as part of a system dedicated to calculating routes through space, and these two contrasting views are pursued largely independently in current research. Here we offer a perspective on where these views can and cannot be reconciled and update a bridging framework that will improve our understanding of hippocampal function.
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Can We Reconcile the Declarative Memory and Spatial Navigation Views on Hippocampal Function?

Some argue that hippocampus supports declarative memory, our capacity to recall facts and events, whereas others view the hippocampus as part of a system dedicated to calculating routes through space, and these two contrasting views are pursued largely independently in current research. Here we offer a perspective on where these views can and cannot be reconciled and update a bridging framework that will improve our understanding of hippocampal function.

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Filed under hippocampus memory spatial navigation neuroscience science

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Abnormal White Matter Integrity in Chronic Users of Codeine-Containing Cough Syrups: A Tract-Based Spatial Statistics Study

BACKGROUND AND PURPOSE: Codeine-containing cough syrups have become one of the most popular drugs of abuse in young people in the world. Chronic codeine-containing cough syrup abuse is related to impairments in a broad range of cognitive functions. However, the potential brain white matter impairment caused by chronic codeine-containing cough syrup abuse has not been reported previously. Our aim was to investigate abnormalities in the microstructure of brain white matter in chronic users of codeine-containing syrups and to determine whether these WM abnormalities are related to the duration of the use these syrups and clinical impulsivity.
MATERIALS AND METHODS: Thirty chronic codeine-containing syrup users and 30 matched controls were evaluated. Diffusion tensor imaging was performed by using a single-shot spin-echo-planar sequence. Whole-brain voxelwise analysis of fractional anisotropy was performed by using tract-based spatial statistics to localize abnormal WM regions. The Barratt Impulsiveness Scale 11 was surveyed to assess participants’ impulsivity. Volume-of-interest analysis was used to detect changes of diffusivity indices in regions with fractional anisotropy abnormalities. Abnormal fractional anisotropy was extracted and correlated with clinical impulsivity and the duration of codeine-containing syrup use.
RESULTS: Chronic codeine-containing syrup users had significantly lower fractional anisotropy in the inferior fronto-occipital fasciculus of the bilateral temporo-occipital regions, right frontal region, and the right corona radiata WM than controls. There were significant negative correlations among fractional anisotropy values of the right frontal region of the inferior fronto-occipital fasciculus and the right superior corona radiata WM and Barratt Impulsiveness Scale total scores, and between the right frontal region of the inferior fronto-occipital fasciculus and nonplan impulsivity scores in chronic codeine-containing syrup users. There was also a significant negative correlation between fractional anisotropy values of the right frontal region of the inferior fronto-occipital fasciculus and the duration of codeine-containing syrup use in chronic users.
CONCLUSIONS: Chronic codeine-containing syrup abuse may be associated with disruptions in brain WM integrity. These WM microstructural deficits may be linked to higher impulsivity in chronic codeine-containing syrup users.


Full Article

Abnormal White Matter Integrity in Chronic Users of Codeine-Containing Cough Syrups: A Tract-Based Spatial Statistics Study

BACKGROUND AND PURPOSE: Codeine-containing cough syrups have become one of the most popular drugs of abuse in young people in the world. Chronic codeine-containing cough syrup abuse is related to impairments in a broad range of cognitive functions. However, the potential brain white matter impairment caused by chronic codeine-containing cough syrup abuse has not been reported previously. Our aim was to investigate abnormalities in the microstructure of brain white matter in chronic users of codeine-containing syrups and to determine whether these WM abnormalities are related to the duration of the use these syrups and clinical impulsivity.

MATERIALS AND METHODS: Thirty chronic codeine-containing syrup users and 30 matched controls were evaluated. Diffusion tensor imaging was performed by using a single-shot spin-echo-planar sequence. Whole-brain voxelwise analysis of fractional anisotropy was performed by using tract-based spatial statistics to localize abnormal WM regions. The Barratt Impulsiveness Scale 11 was surveyed to assess participants’ impulsivity. Volume-of-interest analysis was used to detect changes of diffusivity indices in regions with fractional anisotropy abnormalities. Abnormal fractional anisotropy was extracted and correlated with clinical impulsivity and the duration of codeine-containing syrup use.

RESULTS: Chronic codeine-containing syrup users had significantly lower fractional anisotropy in the inferior fronto-occipital fasciculus of the bilateral temporo-occipital regions, right frontal region, and the right corona radiata WM than controls. There were significant negative correlations among fractional anisotropy values of the right frontal region of the inferior fronto-occipital fasciculus and the right superior corona radiata WM and Barratt Impulsiveness Scale total scores, and between the right frontal region of the inferior fronto-occipital fasciculus and nonplan impulsivity scores in chronic codeine-containing syrup users. There was also a significant negative correlation between fractional anisotropy values of the right frontal region of the inferior fronto-occipital fasciculus and the duration of codeine-containing syrup use in chronic users.

CONCLUSIONS: Chronic codeine-containing syrup abuse may be associated with disruptions in brain WM integrity. These WM microstructural deficits may be linked to higher impulsivity in chronic codeine-containing syrup users.

Filed under white matter neuroimaging impulsivity codeine cough syrup diffusion tensor imaging neuroscience science

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University spinoff aims to hit the mark precisely with brain-scanning tool

As brain surgeons test new procedures and drugs to treat conditions ranging from psychiatric disorders to brain cancer, accuracy is becoming an ever-greater issue.

image

In treating the brain, the state of the art today starts with images from a magnetic resonance (MR) scanner, usually made a few days before surgery. Then, in the operating room, multiple cameras track instruments as they are inserted through a hole in the skull, creating images that can be superimposed on the original MR scans.

But there is no guarantee that the brain will not shift slightly during the surgery and throw off the best efforts at exact guidance.

For 20 years, neurosurgeons have discussed a radical way to achieve real-time accuracy in placement: performing surgery with the brain inside an MR machine, says Walter Block, professor of biomedical engineering at the University of Wisconsin-Madison. “When you open the brain for surgery, the tissue can shift slightly, and that will throw off predictions made in advance.”

To bring the full promise of MR into the operating room, Block has formed a company called InseRT MRI to develop software that allows surgeons to observe the brain in real time on an MR machine during surgery.

Such a system would have a number of applications, he says. Drugs for brain cancer can be delivered over as long as 54 hours. “It would be valuable to see where the drug is going during the first few hours,” Block says. “Drugs move at different rates through gray and white matter, and this ability to recalibrate the treatment plan, based on actual data on where the drug is moving, would allow you to alter the location of the catheter or the flow rate of the medication.”

To get that accuracy advantage, Block does not envision forcing surgeons to learn a new operating environment. “Surgeons have operating room tools and work stations that are familiar to them,” he says. “We are creating a set of tools that make the MR space a comfortable place for the surgeon.”

UW-Madison neurosurgeon Azam Ahmed plans to use the system through test procedures on animal brains and cadavers, Block says. “We are working with Dr. Ahmed to design the workflow so it’s intuitive to him. We are not going to piggyback on top of a large scanner market designed for largely diagnostic purposes, kludging it to make it work for interventional applications.”

The goal is not to develop software that could be spliced into MR manufacturers’ systems, he says, “since every time they alter their software, we would have to change ours.” Instead, Block is borrowing tactics from the smartphone industry. “People write apps that use various phone resources — GPS, the screen, the orientation system. We look at the MR scanner as a set of resources that we can control. An app writer does not have to go to Samsung or Apple and say, ‘We have this idea.’”

Block says his software will interact with the MR machine through a software “portal” being developed by another firm.

One obvious market is the pharmaceutical industry. “Any drug trial in the brain will cost hundreds of millions of dollars,” he says, “and we often see trials being repeated after post-mortem analysis raises questions about the accuracy of drug placement.”

Targeted surgery could also help remove bits of brain tissue to treat severe epilepsy. Marvel Medtech in Cross Plains, Wisconsin, is developing a system that would employ InseRT MRI’s guidance to biopsy breast tumors. The technology also raises the potential for localized psychiatric drug therapy, Block says.

In the brain, the MR-guidance system is already accurate to less than a millimeter, Block says. While conventional stereotactic systems can approach that accuracy “in the best case,” the error can rise to 1.5 or 2 millimeters — a vast distance in an organ as delicate as the human brain, in which damage to healthy tissue must be minimized.

Block says InseRT MRI’s competitive advantage resides in his long experience in medical imaging. “Our value is (faster) time to market. We have come up with ways to circumvent the significant hurdles that now limit image-guided therapy, and we believe we can do this faster than anybody else.”

(Source: news.wisc.edu)

Filed under InseRT MRI MR scans brain imaging neurosurgery neuroscience science

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Learning to play the piano? Sleep on it!

According to researchers at the University of Montreal, the regions of the brain below the cortex play an important role as we train our bodies’ movements and, critically, they interact more effectively after a night of sleep. While researchers knew that sleep helped us the learn sequences of movements (motor learning), it was not known why. “The subcortical regions are important in information consolidation, especially information linked to a motor memory trace. When consolidation level is measured after a period of sleep, the brain network of these areas functions with greater synchrony, that is, we observe that communication between the various regions of this network is better optimized. The opposite is true when there has been no period of sleep,” said Karen Debas, neuropsychologist at the University of Montreal and leader author of the study. A network refers to multiple brain areas that are activated simultaneously.

image

To achieve these results, the researchers, led by Dr. Julien Doyon, Scientific Director of the Functional Neuroimaging Unit of the Institut universitaire de gériatrie de Montréal Research Centre, taught a group of subjects a new sequence of piano-type finger movements on a box. The brains of the subjects were observed using functional magnetic resonance imaging during their performance of the task before and after a period of sleep. Meanwhile, the same test was performed by a control group at the beginning and end of the day, without a period of sleep.

The researchers had already shown that the putamen, a central part of the brain, was more active in subjects who had slept. Furthermore, they had observed improved performance of the task after a night of sleep and not the simple passage of daytime. Using a brain connectivity analysis technique, which identifies brain networks and measures their integration levels, they found that one network emerged from the others—the cortico-striatal network—composed of cortical and subcortical areas, including the putaman and associated cortical regions. “After a night of sleep, we found that this network was more integrated than the others, that is, interaction among these regions was greater when consolidation had occurred. A night of sleep seems to provide active protection of this network, which the passage of daytime does not provide. Moreover, only a night of sleep results in better performance of the task,” Debas said.

These results provide insight into the role of sleep in learning motor skills requiring new movement sequences and reveal, for the first time, greater interaction within the cortico-striatal system after a consolidation phase following sleep. “Our findings open the door to other research opportunities, which could lead us to better understand the mechanisms that take place during sleep and ensure better interaction between key regions of the brain. Indeed, several other studies in my laboratory are examining the role of sleep spindles—brief physiological events during non-rapid eye movement sleep—in the process of motor memory trace consolidation,” Doyon said. “Ultimately, we believe that we will better be able to explain and act on memory difficulties presented by certain clinical populations who have sleeping problems and help patients who are relearning motor sequences in rehabilitation centres,” Debas said.

(Source: nouvelles.umontreal.ca)

Filed under motor learning sleep putamen memory consolidation functional connectivity neuroscience science

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Influenced by Self-Interest, Humans Less Concerned About Inequity To Others
Strongly influenced by their self-interest, humans do not protest being overcompensated, even when there are no consequences, researchers in Georgia State University’s Brains and Behavior Program have found.
This could imply that humans are less concerned than previously believed about the inequity of others, researchers said. Their findings are published in the journal Brain Connectivity. These findings suggest humans’ sense of unfairness is affected by their self-interest, indicating the interest humans show in others’ outcomes is a recently evolved propensity.
It has long been known that humans show sensitivity when they are at a disadvantage by refusing or protesting outcomes more often when they are offered less money than a social partner. But the research team of physics graduate students Bidhan Lamichhane and Bhim Adhikari and Brains and Behavior faculty Dr. Sarah Brosnan, associate professor of psychology, and Dr. Mukesh Dhamala, associate professor of physics and astronomy, reports that, contrary to expectations, humans do not show any sensitivity when they are overcompensated. They conclude that humans are more interested in their own outcomes than those of others.
“A true sense of fairness means that I get upset if I get paid more than you because I don’t think that’s fair,” Brosnan said. “We thought that people would protest quite a bit in the fixed decision game because it’s a cost-free way to say, ‘This isn’t fair.’ But that’s not what we saw at all. People protested higher offers at roughly the same rate that they refused offers where they got more, indicating that this lack of refusal in advantaged situations may not be because of the cost of refusing. It may just be because people don’t care as much as we thought they did if they’re getting more than someone else.”
The researchers also used functional magnetic resonance imaging (fMRI) to study the underlying brain mechanisms from 18 participants, who played three two-person economic exchange games that involved inequity in their favor and not in their favor. Overcompensated offers triggered a different brain circuit than undercompensated offers and indicate that people may be responding to overcompensation as if it were a reward. This could explain the lack of refusals in this unfair situation, researchers said.
Each game involved three offers for how $100 would be split: fair (amount between $40 to $60), unfair-low (disadvantageous to the subject, amount between $0 to $20) and unfair-overcompensated (advantageous to the subject, amount between $80 to $100). Participants played 30 rounds of each game and earned about two percent of the total amount from the games.
In the first two games, the subject received an offer for how much money they would receive and were then asked whether they wanted to reject or accept it. In the Ultimatum Game, if the responder rejected the offer, neither player received any money, leading to a fair outcome. In the Impunity Game, if the subject rejected the offer, only he or she lost the payoff, meaning the outcome was even more unfair than the offer. The subject got nothing, but the partner still got their proposed amount. In the Fixed Decision Game, the subject could choose to protest or not protest the offers, but this didn’t change the outcome for either player. This allowed subjects to protest offers without an associated cost.
The blood-oxygen level dependent signals of the brain were recorded by an MRI scanner as participants played the games. The results of brain response provided new insights into the functional role of the dorsolateral prefrontal cortex and related networks of brain regions for advantageous inequity and protest.
A network of brain regions consisting of the left caudate, right cingulate and right thalamus had a higher level of activity for overcompensated offers than for fair offers. For protest, a different network, consisting of the right dorsolateral prefrontal cortex, left ventrolateral prefrontal cortex and left substantia nigra, came into play. The researchers also mapped out how the brain activity flow occurred within these networks during decision-making.

Influenced by Self-Interest, Humans Less Concerned About Inequity To Others

Strongly influenced by their self-interest, humans do not protest being overcompensated, even when there are no consequences, researchers in Georgia State University’s Brains and Behavior Program have found.

This could imply that humans are less concerned than previously believed about the inequity of others, researchers said. Their findings are published in the journal Brain Connectivity. These findings suggest humans’ sense of unfairness is affected by their self-interest, indicating the interest humans show in others’ outcomes is a recently evolved propensity.

It has long been known that humans show sensitivity when they are at a disadvantage by refusing or protesting outcomes more often when they are offered less money than a social partner. But the research team of physics graduate students Bidhan Lamichhane and Bhim Adhikari and Brains and Behavior faculty Dr. Sarah Brosnan, associate professor of psychology, and Dr. Mukesh Dhamala, associate professor of physics and astronomy, reports that, contrary to expectations, humans do not show any sensitivity when they are overcompensated. They conclude that humans are more interested in their own outcomes than those of others.

“A true sense of fairness means that I get upset if I get paid more than you because I don’t think that’s fair,” Brosnan said. “We thought that people would protest quite a bit in the fixed decision game because it’s a cost-free way to say, ‘This isn’t fair.’ But that’s not what we saw at all. People protested higher offers at roughly the same rate that they refused offers where they got more, indicating that this lack of refusal in advantaged situations may not be because of the cost of refusing. It may just be because people don’t care as much as we thought they did if they’re getting more than someone else.”

The researchers also used functional magnetic resonance imaging (fMRI) to study the underlying brain mechanisms from 18 participants, who played three two-person economic exchange games that involved inequity in their favor and not in their favor. Overcompensated offers triggered a different brain circuit than undercompensated offers and indicate that people may be responding to overcompensation as if it were a reward. This could explain the lack of refusals in this unfair situation, researchers said.

Each game involved three offers for how $100 would be split: fair (amount between $40 to $60), unfair-low (disadvantageous to the subject, amount between $0 to $20) and unfair-overcompensated (advantageous to the subject, amount between $80 to $100). Participants played 30 rounds of each game and earned about two percent of the total amount from the games.

In the first two games, the subject received an offer for how much money they would receive and were then asked whether they wanted to reject or accept it. In the Ultimatum Game, if the responder rejected the offer, neither player received any money, leading to a fair outcome. In the Impunity Game, if the subject rejected the offer, only he or she lost the payoff, meaning the outcome was even more unfair than the offer. The subject got nothing, but the partner still got their proposed amount. In the Fixed Decision Game, the subject could choose to protest or not protest the offers, but this didn’t change the outcome for either player. This allowed subjects to protest offers without an associated cost.

The blood-oxygen level dependent signals of the brain were recorded by an MRI scanner as participants played the games. The results of brain response provided new insights into the functional role of the dorsolateral prefrontal cortex and related networks of brain regions for advantageous inequity and protest.

A network of brain regions consisting of the left caudate, right cingulate and right thalamus had a higher level of activity for overcompensated offers than for fair offers. For protest, a different network, consisting of the right dorsolateral prefrontal cortex, left ventrolateral prefrontal cortex and left substantia nigra, came into play. The researchers also mapped out how the brain activity flow occurred within these networks during decision-making.

Filed under decision making self-interest unfairness neuroimaging prefrontal cortex psychology neuroscience science

243 notes

Scientists Discover Area of Brain Responsible for Exercise Motivation
Scientists at Seattle Children’s Research Institute have discovered an area of the brain that could control a person’s motivation to exercise and participate in other rewarding activities – potentially leading to improved treatments for depression.
Dr. Eric Turner, a principal investigator in Seattle Children’s Research Institute’s Center for Integrative Brain Research, together with lead author Dr. Yun-Wei (Toni) Hsu, have discovered that a tiny region of the brain – the dorsal medial habenula – controls the desire to exercise in mice. The structure of the habenula is similar in humans and rodents and these basic functions in mood regulation and motivation are likely to be the same across species.  
Exercise is one of the most effective non-pharmacological therapies for depression. Determining that such a specific area of the brain may be responsible for motivation to exercise could help researchers develop more targeted, effective treatments for depression. 
“Changes in physical activity and the inability to enjoy rewarding or pleasurable experiences are two hallmarks of major depression,” Turner said. “But the brain pathways responsible for exercise motivation have not been well understood. Now, we can seek ways to manipulate activity within this specific area of the brain without impacting the rest of the brain’s activity.” 
Dr. Turner’s study, titled “Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement,” was published today by the Journal of Neuroscience and funded by the National Institute of Mental Health and National Institute on Drug Abuse. The study used mouse models that were genetically engineered to block signals from the dorsal medial habenula. In the first part of the study, Dr. Turner’s team collaborated with Dr. Horacio de la Iglesia, a professor in University of Washington’s Department of Biology, to show that compared to typical mice, who love to run in their exercise wheels, the genetically engineered mice were lethargic and ran far less. Turner’s genetically engineered mice also lost their preference for sweetened drinking water. 
“Without a functioning dorsal medial habenula, the mice became couch potatoes,” Turner said. “They were physically capable of running but appeared unmotivated to do it.” 
In a second group of mice, Dr. Turner’s team activated the dorsal medial habenula using optogenetics – a precise laser technology developed in collaboration with the Allen Institute for Brain Science. The mice could “choose” to activate this area of the brain by turning one of two response wheels with their paws. The mice strongly preferred turning the wheel that stimulated the dorsal medial habenula, demonstrating that this area of the brain is tied to rewarding behavior.  
Past studies have attributed many different functions to the habenula, but technology was not advanced enough to determine roles of the various subsections of this area of the brain, including the dorsal medial habenula. 
“Traditional methods of stimulation could not isolate this part of the brain,” Turner said. “But cutting-edge technology at Seattle Children’s Research Institute makes discoveries like this possible.” 
As a professor in the University of Washington Department of Psychiatry and Behavioral Sciences, Dr. Turner treats depression and hopes this research will make a difference in the lives of future patients. 
“Working in mental health can be frustrating,” Turner said. “We have not made a lot of progress in developing new treatments. I hope the more we can learn about how the brain functions the more we can help people with all kinds of mental illness.”

Scientists Discover Area of Brain Responsible for Exercise Motivation

Scientists at Seattle Children’s Research Institute have discovered an area of the brain that could control a person’s motivation to exercise and participate in other rewarding activities – potentially leading to improved treatments for depression.

Dr. Eric Turner, a principal investigator in Seattle Children’s Research Institute’s Center for Integrative Brain Research, together with lead author Dr. Yun-Wei (Toni) Hsu, have discovered that a tiny region of the brain – the dorsal medial habenula – controls the desire to exercise in mice. The structure of the habenula is similar in humans and rodents and these basic functions in mood regulation and motivation are likely to be the same across species.  

Exercise is one of the most effective non-pharmacological therapies for depression. Determining that such a specific area of the brain may be responsible for motivation to exercise could help researchers develop more targeted, effective treatments for depression. 

“Changes in physical activity and the inability to enjoy rewarding or pleasurable experiences are two hallmarks of major depression,” Turner said. “But the brain pathways responsible for exercise motivation have not been well understood. Now, we can seek ways to manipulate activity within this specific area of the brain without impacting the rest of the brain’s activity.” 

Dr. Turner’s study, titled “Role of the Dorsal Medial Habenula in the Regulation of Voluntary Activity, Motor Function, Hedonic State, and Primary Reinforcement,” was published today by the Journal of Neuroscience and funded by the National Institute of Mental Health and National Institute on Drug Abuse. The study used mouse models that were genetically engineered to block signals from the dorsal medial habenula. In the first part of the study, Dr. Turner’s team collaborated with Dr. Horacio de la Iglesia, a professor in University of Washington’s Department of Biology, to show that compared to typical mice, who love to run in their exercise wheels, the genetically engineered mice were lethargic and ran far less. Turner’s genetically engineered mice also lost their preference for sweetened drinking water. 

“Without a functioning dorsal medial habenula, the mice became couch potatoes,” Turner said. “They were physically capable of running but appeared unmotivated to do it.” 

In a second group of mice, Dr. Turner’s team activated the dorsal medial habenula using optogenetics – a precise laser technology developed in collaboration with the Allen Institute for Brain Science. The mice could “choose” to activate this area of the brain by turning one of two response wheels with their paws. The mice strongly preferred turning the wheel that stimulated the dorsal medial habenula, demonstrating that this area of the brain is tied to rewarding behavior.  

Past studies have attributed many different functions to the habenula, but technology was not advanced enough to determine roles of the various subsections of this area of the brain, including the dorsal medial habenula. 

“Traditional methods of stimulation could not isolate this part of the brain,” Turner said. “But cutting-edge technology at Seattle Children’s Research Institute makes discoveries like this possible.” 

As a professor in the University of Washington Department of Psychiatry and Behavioral Sciences, Dr. Turner treats depression and hopes this research will make a difference in the lives of future patients. 

“Working in mental health can be frustrating,” Turner said. “We have not made a lot of progress in developing new treatments. I hope the more we can learn about how the brain functions the more we can help people with all kinds of mental illness.”

Filed under motivation habenula exercise depression optogenetics neuroscience science

79 notes

Difficulty assessing effort drives motivation deficits in schizophrenia

Individuals with schizophrenia often have trouble engaging in daily tasks or setting goals for themselves, and a new study from San Francisco State University suggests the reason might be their difficulty in assessing the amount of effort required to complete tasks.

The research, detailed in an article published this week in the Journal of Abnormal Psychology, can assist health professionals in countering motivation deficits among patients with schizophrenia and help those patients function normally by breaking up larger, complex tasks into smaller, easier-to-grasp ones.

"This is one of the first studies to carefully and systematically look at the daily activities of people with schizophrenia — what those people are doing, what goals are they setting for themselves," said David Gard, an associate professor of psychology at SF State who has spent years researching motivation and emotion. "We knew that people with schizophrenia were not engaging in a lot of goal-directed behavior. We just didn’t know why."

In 2011, Gard received a grant from the National Institute of Mental Health to study the reasons behind this difficulty in goal setting. An earlier article detailing other research from this study, published in May in the journal Schizophrenia Research, showed that when people with schizophrenia do set goals for themselves, they set them for the same reasons as persons without: to connect with others. But motivation deficits are still common among these individuals, and his latest study set out to pinpoint the reason.

Through a series of cognitive assessments and random phone calls, Gard and his colleagues at SF State and the University of California, San Francisco collected data from 47 people with and 41 people without schizophrenia. Participants were called four times a day, randomly throughout the day, for a week and asked about their current mood, as well as what they were doing; how much enjoyment they were getting out of it; and what their goals for the rest of the day were. The results were coded by variables such as how much pleasure they were getting out of their daily activities and how much effort was involved, then compared that with the results from the cognitive assessments.

Gard and his fellow researchers found that, while people with schizophrenia engage in low-impact, pleasurable goals — such as watching TV or eating food for enjoyment — as much as others, they have greater difficulty with more complex undertakings or goals requiring more effort.

"There’s something breaking down in the process around assessing high-effort, high-reward goals," Gard said. "When the reward is high and the effort is high, that’s when people with schizophrenia struggle to hold in mind and go after the thing that they want for themselves."

The findings indicate that health-care providers who want to help individuals with schizophrenia set goals for themselves should break larger tasks into smaller, simpler ones with small rewards. For example, instead of guiding a patient specifically toward the larger goal of getting in physical shape, a provider could instead encourage them to gradually walk a little bit more every day.

"That’s something we would do for everyone else, but it might have been avoided in patients with schizophrenia because we thought they weren’t experiencing as much pleasure from their activities as they actually are," Gard added. "We can help them to identify things that are pleasurable and reward them toward larger goals."

(Source: news.sfsu.edu)

Filed under schizophrenia motivation goal-directed behavior psychology neuroscience science

192 notes

ADHD children make poor decisions due to less differentiated learning processes
Which shirt do we put on in the morning? Do we drive to work or take the train? From which takeaway joint do we want to buy lunch? We make hundreds of different decisions every day. Even if these often only have a minimal impact, it is extremely important for our long-term personal development to make decisions that are as optimal as possible. People with ADHD often find this difficult, however. They are known to make impulsive decisions, often choosing options which bring a prompt but smaller reward instead of making a choice that yields a greater reward later on down the line. Researchers from the University Clinics for Child and Adolescent Psychiatry, University of Zurich, now reveal that different decision-making processes are responsible for such suboptimal choices and that these take place in the middle of the frontal lobe.
Mathematical models help to understand the decision-making processes
In the study, the decision-making processes in 40 young people with and without ADHD were examined. Lying in a functional magnetic resonance imaging scanner to record the brain activity, the participants played a game where they had to learn which of two images carried more frequent rewards. In order to understand the impaired mechanisms of participants with ADHD better, learning algorithms which originally stemmed from the field of artificial intelligence were used to evaluate the data. These mathematical models help to understand the precise learning and decision-making mechanisms better. “We were able to demonstrate that young people with ADHD do not inherently have difficulties in learning new information; instead, they evidently use less differentiated learning patterns, which is presumably why sub-optimal decisions are often made”, says first author Tobias Hauser.
Multimodal imaging affords glimpses inside the brain
In order to study the brain processes that triggered these impairments, the authors used multimodal imaging methods, where the participants were examined using a combined measurement of functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) to record the electrical activity and the blood flow in the brain. It became apparent that participants with ADHD exhibit an altered functioning in the medial prefrontal cortex – a region in the middle of the frontal lobe. This part of the brain is heavily involved in decision-making processes, especially if you have to choose between several options, and in learning from errors. Although a change in activity in this region was already discovered in other contexts for ADHD, the Zurich researchers were now also able to pinpoint the precise moment of this impairment, which already occurred less than half a second after a feedback, i.e. at a very early stage.
Psychologist Tobias Hauser, who is now researching at the Wellcome Trust Centre for Neuroimaging, University College London, is convinced that the results fundamentally improve our understanding of the mechanisms of impaired decision-making behavior in people with ADHD. The next step will be to study the brain messenger substances. “If our findings are confirmed, they will provide key clues as to how we might be able to design therapeutic interventions in future,” explains Hauser.
Literature: 
Tobias U. Hauser, Reto Iannaccone, Juliane Ball, Christoph Mathys, Daniel Brandeis, Susanne Walitza & Silvia Brem: Role of Medial Prefrontal Cortex in Impaired Decision Making in Juvenile Attention-Deficit/Hyperactivity Disorder, in: JAMA Psychiatry

ADHD children make poor decisions due to less differentiated learning processes

Which shirt do we put on in the morning? Do we drive to work or take the train? From which takeaway joint do we want to buy lunch? We make hundreds of different decisions every day. Even if these often only have a minimal impact, it is extremely important for our long-term personal development to make decisions that are as optimal as possible. People with ADHD often find this difficult, however. They are known to make impulsive decisions, often choosing options which bring a prompt but smaller reward instead of making a choice that yields a greater reward later on down the line. Researchers from the University Clinics for Child and Adolescent Psychiatry, University of Zurich, now reveal that different decision-making processes are responsible for such suboptimal choices and that these take place in the middle of the frontal lobe.

Mathematical models help to understand the decision-making processes

In the study, the decision-making processes in 40 young people with and without ADHD were examined. Lying in a functional magnetic resonance imaging scanner to record the brain activity, the participants played a game where they had to learn which of two images carried more frequent rewards. In order to understand the impaired mechanisms of participants with ADHD better, learning algorithms which originally stemmed from the field of artificial intelligence were used to evaluate the data. These mathematical models help to understand the precise learning and decision-making mechanisms better. “We were able to demonstrate that young people with ADHD do not inherently have difficulties in learning new information; instead, they evidently use less differentiated learning patterns, which is presumably why sub-optimal decisions are often made”, says first author Tobias Hauser.

Multimodal imaging affords glimpses inside the brain

In order to study the brain processes that triggered these impairments, the authors used multimodal imaging methods, where the participants were examined using a combined measurement of functional magnetic resonance imaging (fMRI) and electroencephalography (EEG) to record the electrical activity and the blood flow in the brain. It became apparent that participants with ADHD exhibit an altered functioning in the medial prefrontal cortex – a region in the middle of the frontal lobe. This part of the brain is heavily involved in decision-making processes, especially if you have to choose between several options, and in learning from errors. Although a change in activity in this region was already discovered in other contexts for ADHD, the Zurich researchers were now also able to pinpoint the precise moment of this impairment, which already occurred less than half a second after a feedback, i.e. at a very early stage.

Psychologist Tobias Hauser, who is now researching at the Wellcome Trust Centre for Neuroimaging, University College London, is convinced that the results fundamentally improve our understanding of the mechanisms of impaired decision-making behavior in people with ADHD. The next step will be to study the brain messenger substances. “If our findings are confirmed, they will provide key clues as to how we might be able to design therapeutic interventions in future,” explains Hauser.

Literature:

Tobias U. Hauser, Reto Iannaccone, Juliane Ball, Christoph Mathys, Daniel Brandeis, Susanne Walitza & Silvia Brem: Role of Medial Prefrontal Cortex in Impaired Decision Making in Juvenile Attention-Deficit/Hyperactivity Disorder, in: JAMA Psychiatry

Filed under ADHD decision making prefrontal cortex neuroimaging brain activity psychology neuroscience science

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(Image caption: In a study of brains from children with autism, neurons in brains from autistic patients did not undergo normal pruning during childhood and adolescence. The images show representative neurons from unaffected brains (left) and brains from autistic patients (right); the spines on the neurons indicate the location of synapses. Credit: Guomei Tang, PhD and Mark S. Sonders, PhD/Columbia University Medical Center)
Children with Autism Have Extra Synapses in Brain
Children and adolescents with autism have a surplus of synapses in the brain, and this excess is due to a slowdown in a normal brain “pruning” process during development, according to a study by neuroscientists at Columbia University Medical Center (CUMC). Because synapses are the points where neurons connect and communicate with each other, the excessive synapses may have profound effects on how the brain functions. The study was published in the August 21 online issue of the journal Neuron.
A drug that restores normal synaptic pruning can improve autistic-like behaviors in mice, the researchers found, even when the drug is given after the behaviors have appeared.
“This is an important finding that could lead to a novel and much-needed therapeutic strategy for autism,” said Jeffrey Lieberman, MD, Lawrence C. Kolb Professor and Chair of Psychiatry at CUMC and director of New York State Psychiatric Institute, who was not involved in the study.
Although the drug, rapamycin, has side effects that may preclude its use in people with autism, “the fact that we can see changes in behavior suggests that autism may still be treatable after a child is diagnosed, if we can find a better drug,” said the study’s senior investigator, David Sulzer, PhD, professor of neurobiology in the Departments of Psychiatry, Neurology, and Pharmacology at CUMC.
During normal brain development, a burst of synapse formation occurs in infancy, particularly in the cortex, a region involved in autistic behaviors; pruning eliminates about half of these cortical synapses by late adolescence. Synapses are known to be affected by many genes linked to autism, and some researchers have hypothesized that people with autism may have more synapses.
To test this hypothesis, co-author Guomei Tang, PhD, assistant professor of neurology at CUMC, examined brains from children with autism who had died from other causes. Thirteen brains came from children ages two to 9, and thirteen brains came from children ages 13 to 20. Twenty-two brains from children without autism were also examined for comparison.
Dr. Tang measured synapse density in a small section of tissue in each brain by counting the number of tiny spines that branch from these cortical neurons; each spine connects with another neuron via a synapse.
By late childhood, she found, spine density had dropped by about half in the control brains, but by only 16 percent in the brains from autism patients.
“It’s the first time that anyone has looked for, and seen, a lack of pruning during development of children with autism,” Dr. Sulzer said, “although lower numbers of synapses in some brain areas have been detected in brains from older patients and in mice with autistic-like behaviors.”
Clues to what caused the pruning defect were also found in the patients’ brains; the autistic children’s brain cells were filled with old and damaged parts and were very deficient in a degradation pathway known as “autophagy.” Cells use autophagy (a term from the Greek for self-eating) to degrade their own components.
Using mouse models of autism, the researchers traced the pruning defect to a protein called mTOR. When mTOR is overactive, they found, brain cells lose much of their “self-eating” ability. And without this ability, the brains of the mice were pruned poorly and contained excess synapses. “While people usually think of learning as requiring formation of new synapses, “Dr. Sulzer says, “the removal of inappropriate synapses may be just as important.”
The researchers could restore normal autophagy and synaptic pruning—and reverse autistic-like behaviors in the mice—by administering rapamycin, a drug that inhibits mTOR. The drug was effective even when administered to the mice after they developed the behaviors, suggesting that such an approach may be used to treat patients even after the disorder has been diagnosed.
Because large amounts of overactive mTOR were also found in almost all of the brains of the autism patients, the same processes may occur in children with autism.
“What’s remarkable about the findings,” said Dr. Sulzer, “is that hundreds of genes have been linked to autism, but almost all of our human subjects had overactive mTOR and decreased autophagy, and all appear to have a lack of normal synaptic pruning. This says that many, perhaps the majority, of genes may converge onto this mTOR/autophagy pathway, the same way that many tributaries all lead into the Mississippi River. Overactive mTOR and reduced autophagy, by blocking normal synaptic pruning that may underlie learning appropriate behavior, may be a unifying feature of autism.”
Alan Packer, PhD, senior scientist at the Simons Foundation, which funded the research, said the study is an important step forward in understanding what’s happening in the brains of people with autism.
“The current view is that autism is heterogeneous, with potentially hundreds of genes that can contribute. That’s a very wide spectrum, so the goal now is to understand how those hundreds of genes cluster together into a smaller number of pathways; that will give us better clues to potential treatments,” he said.
“The mTOR pathway certainly looks like one of these pathways. It is possible that screening for mTOR and autophagic activity will provide a means to diagnose some features of autism, and normalizing these pathways might help to treat synaptic dysfunction and treat the disease.”

(Image caption: In a study of brains from children with autism, neurons in brains from autistic patients did not undergo normal pruning during childhood and adolescence. The images show representative neurons from unaffected brains (left) and brains from autistic patients (right); the spines on the neurons indicate the location of synapses. Credit: Guomei Tang, PhD and Mark S. Sonders, PhD/Columbia University Medical Center)

Children with Autism Have Extra Synapses in Brain

Children and adolescents with autism have a surplus of synapses in the brain, and this excess is due to a slowdown in a normal brain “pruning” process during development, according to a study by neuroscientists at Columbia University Medical Center (CUMC). Because synapses are the points where neurons connect and communicate with each other, the excessive synapses may have profound effects on how the brain functions. The study was published in the August 21 online issue of the journal Neuron.

A drug that restores normal synaptic pruning can improve autistic-like behaviors in mice, the researchers found, even when the drug is given after the behaviors have appeared.

“This is an important finding that could lead to a novel and much-needed therapeutic strategy for autism,” said Jeffrey Lieberman, MD, Lawrence C. Kolb Professor and Chair of Psychiatry at CUMC and director of New York State Psychiatric Institute, who was not involved in the study.

Although the drug, rapamycin, has side effects that may preclude its use in people with autism, “the fact that we can see changes in behavior suggests that autism may still be treatable after a child is diagnosed, if we can find a better drug,” said the study’s senior investigator, David Sulzer, PhD, professor of neurobiology in the Departments of Psychiatry, Neurology, and Pharmacology at CUMC.

During normal brain development, a burst of synapse formation occurs in infancy, particularly in the cortex, a region involved in autistic behaviors; pruning eliminates about half of these cortical synapses by late adolescence. Synapses are known to be affected by many genes linked to autism, and some researchers have hypothesized that people with autism may have more synapses.

To test this hypothesis, co-author Guomei Tang, PhD, assistant professor of neurology at CUMC, examined brains from children with autism who had died from other causes. Thirteen brains came from children ages two to 9, and thirteen brains came from children ages 13 to 20. Twenty-two brains from children without autism were also examined for comparison.

Dr. Tang measured synapse density in a small section of tissue in each brain by counting the number of tiny spines that branch from these cortical neurons; each spine connects with another neuron via a synapse.

By late childhood, she found, spine density had dropped by about half in the control brains, but by only 16 percent in the brains from autism patients.

“It’s the first time that anyone has looked for, and seen, a lack of pruning during development of children with autism,” Dr. Sulzer said, “although lower numbers of synapses in some brain areas have been detected in brains from older patients and in mice with autistic-like behaviors.”

Clues to what caused the pruning defect were also found in the patients’ brains; the autistic children’s brain cells were filled with old and damaged parts and were very deficient in a degradation pathway known as “autophagy.” Cells use autophagy (a term from the Greek for self-eating) to degrade their own components.

Using mouse models of autism, the researchers traced the pruning defect to a protein called mTOR. When mTOR is overactive, they found, brain cells lose much of their “self-eating” ability. And without this ability, the brains of the mice were pruned poorly and contained excess synapses. “While people usually think of learning as requiring formation of new synapses, “Dr. Sulzer says, “the removal of inappropriate synapses may be just as important.”

The researchers could restore normal autophagy and synaptic pruning—and reverse autistic-like behaviors in the mice—by administering rapamycin, a drug that inhibits mTOR. The drug was effective even when administered to the mice after they developed the behaviors, suggesting that such an approach may be used to treat patients even after the disorder has been diagnosed.

Because large amounts of overactive mTOR were also found in almost all of the brains of the autism patients, the same processes may occur in children with autism.

“What’s remarkable about the findings,” said Dr. Sulzer, “is that hundreds of genes have been linked to autism, but almost all of our human subjects had overactive mTOR and decreased autophagy, and all appear to have a lack of normal synaptic pruning. This says that many, perhaps the majority, of genes may converge onto this mTOR/autophagy pathway, the same way that many tributaries all lead into the Mississippi River. Overactive mTOR and reduced autophagy, by blocking normal synaptic pruning that may underlie learning appropriate behavior, may be a unifying feature of autism.”

Alan Packer, PhD, senior scientist at the Simons Foundation, which funded the research, said the study is an important step forward in understanding what’s happening in the brains of people with autism.

“The current view is that autism is heterogeneous, with potentially hundreds of genes that can contribute. That’s a very wide spectrum, so the goal now is to understand how those hundreds of genes cluster together into a smaller number of pathways; that will give us better clues to potential treatments,” he said.

“The mTOR pathway certainly looks like one of these pathways. It is possible that screening for mTOR and autophagic activity will provide a means to diagnose some features of autism, and normalizing these pathways might help to treat synaptic dysfunction and treat the disease.”

Filed under synapses autophagy mTOR autism ASD brain development neuroscience science

147 notes

Breastfeeding linked to lower risk of postnatal depression
A new study of over 10,000 mothers has shown that women who breastfed their babies were at significantly lower risk of postnatal depression than those who did not.
A new study of over 10,000 mothers has shown that women who breastfed their babies were at significantly lower risk of postnatal depression than those who did not.
The study, by researchers in the UK and Spain, and published today in the journal Maternal and Child Health, shows that mothers who planned to breastfeed and who actually went on to breastfeed were around 50% less likely to become depressed than mothers who had not planned to, and who did not, breastfeed. Mothers who planned to breastfeed, but who did not go on to breastfeed, were over twice as likely to become depressed as mothers who had not planned to, and who did not, breastfeed.
The relationship between breastfeeding and depression was most pronounced when babies were 8 weeks old, but much smaller when babies were 8 months or older.
The research, funded by the Economic and Social Research Council, used data drawn from the Avon Longitudinal Survey of Parents and Children (ALSPAC), a study of 13,998 births in the Bristol area in the early 1990s. Maternal depression was measured using the Edinburgh Postnatal Depression Scale when babies were 8 weeks, and 8, 21 and 33 months old. Depression was also assessed at two points during pregnancy, enabling the researchers to take into account mothers’ pre-existing mental health conditions.
This is one of the largest studies of its kind; as well as being one of the few studies taking into account mothers’ previous mental health, it also controls for socioeconomic factors such as income and relationship status, and for other potential confounders such as how babies were delivered, and whether they were premature.
“Breastfeeding has well-established benefits to babies, in terms of their physical health and cognitive development; our study shows that it also benefits the mental health of mothers,” says Dr Maria Iacovou, from the University of Cambridge’s Department of Sociology and a Bye Fellow at Fitzwilliam College.
“In fact, the effects on mothers’ mental health that we report in this study are also likely to have an impact on babies, since maternal depression has previously been shown to have negative effects on many aspects of children’s development.”
Dr Iacovou believes that health authorities should not only be encouraging women to breastfeed, but should also provide a level of support that will help mothers who want to breastfeed succeed.
“Lots of mothers and babies take to breastfeeding pretty easily. But for many others, it doesn’t come naturally at all; for these mothers, having someone with the training, the skills, and perhaps most importantly the time to help them get it right, can make all the difference,” she adds.
“However good the level of support that’s provided, there will be some mothers who wanted to breastfeed and who don’t manage to. It’s clear that these mothers need a great deal of understanding and support; there is currently hardly any skilled specialist help for these mothers, and this is something else that health providers should be thinking about.”
Around one in 12 women in the sample experienced depressive symptoms during pregnancy, while one in eight experienced depression at one or more of the four measurement points after giving birth.
According to figures from the UK’s Department of Health, almost three-quarters of mothers initiated breastfeeding in 2012/13; by the time of the 6-8 week check, only 47% of babies were being breastfed. This is one of the lowest rates of breastfeeding in Europe.

Breastfeeding linked to lower risk of postnatal depression

A new study of over 10,000 mothers has shown that women who breastfed their babies were at significantly lower risk of postnatal depression than those who did not.

A new study of over 10,000 mothers has shown that women who breastfed their babies were at significantly lower risk of postnatal depression than those who did not.

The study, by researchers in the UK and Spain, and published today in the journal Maternal and Child Health, shows that mothers who planned to breastfeed and who actually went on to breastfeed were around 50% less likely to become depressed than mothers who had not planned to, and who did not, breastfeed. Mothers who planned to breastfeed, but who did not go on to breastfeed, were over twice as likely to become depressed as mothers who had not planned to, and who did not, breastfeed.

The relationship between breastfeeding and depression was most pronounced when babies were 8 weeks old, but much smaller when babies were 8 months or older.

The research, funded by the Economic and Social Research Council, used data drawn from the Avon Longitudinal Survey of Parents and Children (ALSPAC), a study of 13,998 births in the Bristol area in the early 1990s. Maternal depression was measured using the Edinburgh Postnatal Depression Scale when babies were 8 weeks, and 8, 21 and 33 months old. Depression was also assessed at two points during pregnancy, enabling the researchers to take into account mothers’ pre-existing mental health conditions.

This is one of the largest studies of its kind; as well as being one of the few studies taking into account mothers’ previous mental health, it also controls for socioeconomic factors such as income and relationship status, and for other potential confounders such as how babies were delivered, and whether they were premature.

“Breastfeeding has well-established benefits to babies, in terms of their physical health and cognitive development; our study shows that it also benefits the mental health of mothers,” says Dr Maria Iacovou, from the University of Cambridge’s Department of Sociology and a Bye Fellow at Fitzwilliam College.

“In fact, the effects on mothers’ mental health that we report in this study are also likely to have an impact on babies, since maternal depression has previously been shown to have negative effects on many aspects of children’s development.”

Dr Iacovou believes that health authorities should not only be encouraging women to breastfeed, but should also provide a level of support that will help mothers who want to breastfeed succeed.

“Lots of mothers and babies take to breastfeeding pretty easily. But for many others, it doesn’t come naturally at all; for these mothers, having someone with the training, the skills, and perhaps most importantly the time to help them get it right, can make all the difference,” she adds.

“However good the level of support that’s provided, there will be some mothers who wanted to breastfeed and who don’t manage to. It’s clear that these mothers need a great deal of understanding and support; there is currently hardly any skilled specialist help for these mothers, and this is something else that health providers should be thinking about.”

Around one in 12 women in the sample experienced depressive symptoms during pregnancy, while one in eight experienced depression at one or more of the four measurement points after giving birth.

According to figures from the UK’s Department of Health, almost three-quarters of mothers initiated breastfeeding in 2012/13; by the time of the 6-8 week check, only 47% of babies were being breastfed. This is one of the lowest rates of breastfeeding in Europe.

Filed under breastfeeding postpartum depression maternal depression neuroscience science

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