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Summary: People who are more determined, or express more grit have different patterns of cognitive performance, researchers say. However, having more grit does not necessarily translate into having better cognitive performance.

Source: PLOS

A new analysis of the personality trait of grit found that people who showed higher levels of grit also had different patterns of cognitive performancebut not necessarily enhanced cognitive performance.

Nuria Aguerre of the University of Granada, Spain, and colleagues present these findings in the open-access journalPLOS ONE.

A person withgritis someone who displays notable perseverance in pursuit of long-term goals, even in the face of setbacks. Researchers typically measure it with an evaluation tool known as the Grit Scale.

While previous studies have suggested a potential link between grit and certain aspects of cognitive functioning, no studies have directly examined this relationship.

To gain further insight, Aguerre and colleagues had 134 study participants complete questionnaires, including the Grit Scale, to evaluate their personalities according to three traits: grit, impulsiveness, and mindfulness.

The participants also completed four experimental computer-based tasks to measure different facets of cognitive ability, including flexibility, inhibition, the ability to replace irrelevant items in ones working memorywhich holds information temporarilywith newer, relevant items, and the control mode tendency.

Statistical analysis of the questionnaire andexperimental datarevealed that, contrary to the researchers predictions, people with higher grit scores did not necessarily score higher on overall cognitive ability.

However, in line with prior research, grit was statistically linked to the personality traits of low impulsivity and high mindfulness, which are both related toself-regulation.

However, albeit to a lesser statistical extent, participants high in grit did show different patterns ofcognitive performance. The researchers characterized this cognitive profile as showing cautious control: an enhanced ability to pay attention to all available information and remain sensitive to conflicting information in thepresent moment, while relying less on earlier information.

Overall, these findings suggest that different patterns of cognitive abilitynot necessarily greater abilitymay underlie grit. This is in line with other researchers previously proposed ideas.

The researchers describe this study as exploratory and suggest that future research could delve deeper, such as by including a more comprehensive measure of grit and by also considering a cognitive ability known as fluid intelligence.

The authors add: To crown the top of the mountain you do not need very good executive functions. You should be aware of the environment instead.

Author: Press OfficeSource: PLOSContact: Press Office PLOSImage: The image is in the public domain

Original Research: Open access.The relative role of executive control and personality traits in grit by Nuria Aguerre et al. PLOS ONE

Abstract

The relative role of executive control and personality traits in grit

Although grit is predictive of wellbeing, educational achievement, and success in life, it has been conceptualized as largely distinct from cognitive ability.

The present study investigated the link between grit and executive functions since regulation abilities might underlie the expression of grit.

A hundred thirty-four people were administered personality questionnaires (grit, impulsiveness, and mindfulness) and four experimental tasks tapping into Miyakes and Bravers models of executive functioning (including measures of flexibility, inhibition, working memory, and control mode dimensions).

Multivariate analyses showed that two composite scores (trait and executive functioning) were reliably predictive of grit, although it was the trait composite (characterized by low impulsivity and high mindfulness) that explained more variance. Importantly, gritty participants did not demonstrate enhanced executive functioning.

Instead, they exhibited a different pattern of performance that might be reflecting a cautious profile of control, characterized by paying attention to all available information, less reliance on previous contextual cues but sensitive to conflicting information of the current context.

These findings converge with Duckworths idea that high grit people do not necessarily have a greater cognitive capacity. Rather, they use it in a different way.

Neuroscience

Walking Gives the Brain a ‘Step-Up’ in Function for Some – Neuroscience News

June 25, 2022 medical

Summary: For some, cognitive performance on tasks improves while walking via a change in the use of neural resources.

Source: University of Rochester

It has long been thought that when walking is combined with a taskboth suffer. Researchers at the Del Monte Institute for Neuroscience at the University of Rochester found that this is not always the case.

Some young and healthy people improve performance on cognitive tasks while walking by changing the use of neural resources.

However, this does not necessarily mean you should work on a big assignment while walking off that cake from the night before.

There was no predictor of who would fall into which category before we tested them, we initially thought that everyone would respond similarly, said Eleni Patelaki, a biomedical engineering Ph.D. student at the University of Rochester School of Medicine and Dentistry in the Frederick J. and Marion A. Schindler Cognitive Neurophysiology Laboratory and first author of the study out now inCerebral Cortex.

It was surprising that for some of the subjects it was easier for them to do dual-taskingdo more than one taskcompared to single-taskingdoing each task separately. This was interesting and unexpected because most studies in the field show that the more tasks that we have to do concurrently the lower our performance gets.

Improving means changes in the brain

Using the Mobile Brain/Body Imaging system, or MoBI, researchers monitored thebrain activity, kinematics and behavior of 26 healthy 18 to 30-year-olds as they looked at a series of images, either while sitting on a chair or walking on a treadmill. Participants were instructed to click a button each time the image changed. If the same image appeared back-to-back participants were asked to not click.

Performance achieved by each participant in this task while sitting was considered their personal behavioral baseline. When walking was added to performing the same task, investigators found that different behaviors appeared, with some people performing worse than their sitting baselineas expected based on previous studiesbut also with some others improving compared to their sitting baseline.

The electroencephalogram, or EEG, data showed that the 14 participants who improved at the task while walking had a change in frontalbrainfunction which was absent in the 12 participants who did not improve. This brain activity change exhibited by those who improved at the task suggests increased flexibility or efficiency in the brain.

To thenaked eye, there were no differences in our participants. It wasnt until we started analyzing their behavior and brain activity that we found the surprising difference in the groups neural signature and what makes them handle complex dual-tasking processes differently, Patelaki said.

These findings have the potential to be expanded and translated to populations where we know that flexibility of neural resources gets compromised.

Edward Freedman, Ph.D., associate professor of Neuroscience at the Del Monte Institute led this research that continues to expand how the MoBI is helping neuroscientists discover the mechanisms at work when the brain takes on multiple tasks. His previous work has highlighted the flexibility of a healthy brain, showing the more difficult the task the greater the neurophysiological difference between walking and sitting.

These new findings highlight that the MoBI can show us how the brain responds to walking and how the brain responds to the task, Freedman said.

This gives us a place to start looking in the brains of older adults, especially healthy ones.

Expanding this research toolder adultscould guide scientists to identify a possible marker for super agers or people who have a minimal decline in cognitive functions. This marker would be useful in helping better understand what could be going awry in neurodegenerative diseases.

Author: Press OfficeSource: University of RochesterContact: Press Office University of RochesterImage: The image is in the public domain

Original Research: Open access.Young adults who improve performance during dual-task walking show more flexible reallocation of cognitive resources: a mobile brain-body imaging (MoBI) study by Eleni Patelaki et al. Cerebral Cortex

Abstract

Young adults who improve performance during dual-task walking show more flexible reallocation of cognitive resources: a mobile brain-body imaging (MoBI) study

In young adults, pairing a cognitive task with walking can have different effects on gait and cognitive task performance. In some cases, performance clearly declines whereas in others compensatory mechanisms maintain performance. This study investigates the preliminary finding of behavioral improvement in Go/NoGo response inhibition task performance during walking compared with sitting, which was observed at the piloting stage.

Mobile brain/body imaging (MoBI) was used to record electroencephalographic (EEG) activity, 3-dimensional (3D) gait kinematics and behavioral responses in the cognitive task, during sitting or walking on a treadmill.

In a cohort of 26 young adults, 14 participants improved in measures of cognitive task performance while walking compared with sitting. These participants exhibited walking-related EEG amplitude reductions over frontal scalp regions during key stages of inhibitory control (conflict monitoring, control implementation, and pre-motor stages), accompanied by reduced stride-to-stride variability and faster responses to stimuli compared with those who did not improve. In contrast, 12 participants who did not improve exhibited no EEG amplitude differences across physical condition.

The neural activity changes associated with performance improvement during dual tasking hold promise as cognitive flexibility markers that can potentially help assess cognitive decline in aging and neurodegeneration.

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Neuroscience

People Hurt Other People to Signal Their Own Goodness – Neuroscience News

June 25, 2022 medical

Summary: People who intentionally hurt others because they believe they are morally right or justified, do not respond rationally to material benefits, a new study reports. Researchers say those who punish others to signal their own moral goodness may be more likely to question their claims of moral righteousness when judged negatively by their peers.

Source: UCSD

Findings from a new University of California San Diego Rady School of Management study reveal people often hurt others because in their mind, it is morally right or even obligatory to be violent and as a result, they do not respond rationally to material benefits.

The study has implications for the criminal justice system, suggesting that fines or jail time to penalize bad behavior may not be an effective deterrent as lawmakers hope.

For a majority of offenders, its not worth the trouble to inflict harm purely from a place of cynical greed, said psychologist Tage Rai, an assistant professor of management at the Rady School of Management and author of the study.

For example, as we are seeing with the January 6 hearings, many of the perpetrators of the attack on the Capitol believed the election had been stolen from them and that they were morally in the right to punish the congresspeople who had wronged them.

Many of these people will be materially punished for their actions. Whats unclear is whether that would stop them from doing it again.

Rais findings, published in the journalPsychological Science, are based on multiple experiments with nearly 1,500 study participants. Subjects in an experimental group were paid a monetary bonus to punish others; however, when they were compensated for punishing, it actually made them less likely to do so.

Monetary gains may conflict with their perceived moral justifications, Rai said.

People punish others to signal their own goodness and receiving compensation might make it seem as though theyre driven by greed rather than justice. However, I also find that if your peers tell you youre still a good person even if you take the money, then you no longer have moral qualms about harming others for profit.

Rai added, to prevent criminal acts, lawmakers should leverage social pressure as well.

When people are aware that theyre being judged negatively by their peers, they may find themselves more likely to question their claims of moral righteousness, he said.

Much of Rais research seeks to understand violent behavior and how to prevent it. His previous studies as well as the book he co-authoredVirtuous Violencereveal that most violent criminals have their own notions about what is right and wrong in a given situation.

Knowing that violent offenders often cite their own moral code as the reason why they hurt people, Rai wanted test this theory further by paying people to punish others in a lab experiment.

Across four different experiments in an online economic game, he found providing a monetary bonus for punishing a third party cut participants willingness to do so nearly in half.

The findings suggest people may bemorehesitant to do harm when they stand to profit from it if they anticipate condemnation from their peers, Rai said.

In conclusion, he says understanding what drawspeopleto violence is key to preventing it.

If governments are trying to disincentive criminals, they should also aim to change the moral narratives criminals use to justify their actions, Rai said.

Author: Press OfficeSource: UCSDContact: Press Office UCSDImage: The image is in the public domain

Original Research: Closed access.Material Benefits Crowd Out Moralistic Punishment by Tage S. Rai. Psychological Science

Abstract

Material Benefits Crowd Out Moralistic Punishment

Across four experiments with U.S.-based online participants (N= 1,495 adults), I found that paying people to engage in moralistic punishment reduces their willingness to do so. In an economic game with real stakes, providing a monetary bonus for engaging in third-party punishment of unfair offers nearly cut participants willingness to do so in half.

In judgments of hypothetical transgressions, participants viewed punishers who accepted payment as having worse character and rated the punishers punitive actions as less morally acceptable. Willingness to engage in punishment was restored if participants were offered large enough payments or were told that punishment accompanied by payment still signals moral virtue.

Data were consistent with a signal-corruption mechanism whereby payment interferes with the prosocial signal that moralistic punishment provides about a punishers motives.

These findings have implications for the cultural evolution of punishment and suggest that understanding perpetrators sociomoral incentives is essential to implementing conflict-reduction policies.

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Discovery of Gene Involved in Chronic Pain Creates New Treatment Target – Neuroscience News

June 25, 2022 medical

Summary: The absence of the NCX3 gene amplifies pain signals within the spinal cord, a new mouse study reveals. Increasing levels of NCX3 in the spinal cord helped reduce symptoms associated with chronic pain.

Source: University of Oxford

Oxford researchers have discovered a gene that regulates pain sensitization by amplifying pain signals within the spinal cord, helping them to understand an important mechanism underlying chronic pain in humans and providing a new treatment target.

Chronic pain is a common issue affecting millions of people worldwide, but why some people are more prone to it and what factors lead tochronic painare not fully understood.

It is well known that repeated stimulation, such as with a sharp pin prick, can lead to a heightened sensitivity to pain. This process is called pain wind-up and contributes to clinical pain disorders.

In a two-part study, researchers from Oxfords Nuffield Department of Clinical Neurosciences first comparedgenetic variationin samples from more than 1,000 participants from Colombia, to look for clues as to whether there were any genetic variants more common in people who experienced greater pain wind-up. They noted a significant difference in variants of one specific gene (the protein Sodium Calcium exchanger type-3, NCX3).

The researchers then undertook a series of experiments in mice, to understand how NCX3 regulates pain wind-up and whether it may be a treatment target. NCX3 was expressed in the mousespinal cordneurons that process and transmitpain signalsto the brain.

NCX3 was needed by these neurons to export the excess calcium that builds up following activity. In the absence of NCX3 the spinal cord neurons showed more activity in response to injury signals from the periphery and pain wind-up was increased.

Conversely, increasing the levels of NCX3 within the spinal cord could reduce pain in the mouse.

David Bennett, professor of neurology and neurobiology of the Nuffield Department of Clinical Neuroscience, said: This is the first time that we have been able to study pain in humans and then to directly demonstrate the mechanism behind it in mice, which provides us with a really broad understanding of the factors involved and how we can begin developing new treatments for it.

Professor Bennett added: Chronic pain is a global problem, and can be immensely debilitating. We carried out the study in Colombia because of the mixed ancestry of the population there, including Native Indian, African and European populations, which gave us a broad range of genetic diversity to look at. This makes these findings so exciting because of their potential international applications.

The findings imply that any drugs which can increase activity of NCX3 would be predicted to reducepainsensitization in humans.

Author: Press OfficeSource: University of OxfordContact: Press Office University of OxfordImage: The image is in the public domain

Original Research: Open access.Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms by Teodora Trendafilova et al. Neuron

Abstract

Sodium-calcium exchanger-3 regulates pain wind-up: From human psychophysics to spinal mechanisms

Repeated application of noxious stimuli leads to a progressively increased pain perception; this temporal summation is enhanced in and predictive of clinical pain disorders. Its electrophysiological correlate is wind-up, in which dorsal horn spinal neurons increase their response to repeated nociceptor stimulation.

To understand the genetic basis of temporal summation, we undertook a GWAS of wind-up in healthy human volunteers and found significant association withSLC8A3encoding sodium-calcium exchanger type 3 (NCX3).NCX3was expressed in mouse dorsal horn neurons, and mice lackingNCX3showed normal, acute pain but hypersensitivity to the second phase of the formalin test and chronic constriction injury.

Dorsal horn neurons lackingNCX3showed increased intracellular calcium following repetitive stimulation, slowed calcium clearance, and increased wind-up. Moreover, virally mediated enhanced spinal expression ofNCX3reduced central sensitization.

Our study highlights Ca2+efflux as a pathway underlying temporal summation and persistent pain, which may be amenable to therapeutic targeting.

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Silence for Thought: Special Interneuron Networks in the Human Brain – Neuroscience News

June 25, 2022 medical

Summary: Human cortical networks have evolved a novel neural network that relies on abundant connections between inhibitory interneurons.

Source: Max Planck Institute

The analysis of the human brain is a central goal of neuroscience. However, for methodological reasons, research has largely focused on model organisms, in particular the mouse.

Now, neuroscientists gained novel insights on human neural circuitry using tissue obtained from neurosurgical interventions. Three-dimensional electron microscope data revealed a novel expanded network of interneurons in humans compared to mouse.

The discovery of this prominent network component in the human cortex encourages further detailed analysis of its function in health and disease.

At first glance, brains of mouse and human are surprisingly similar: the nerve cells that form our brains have very similar shapes and properties, the molecular mechanisms of electrical excitation are highly conserved, and many biophysical phenomena found in other species seem to also apply to human brains.

So, is it primarily the fact that our brains are 1,000-fold larger, house 1000-fold more nerve cells that allows us to play chess and write childrens books, which mice arguably cannot do?, asks Moritz Helmstaedter, director at the Max Planck Institute for Brain Research (Frankfurt) who led the new study published on June 23 in the journalScience.

By analyzing the neuronal networks in mice, monkeys and humans and mapping their complete structure in biopsies of brain tissue, so called connectomes, Helmstaedter and his team have discovered that human cortical networks have evolved a novel neuronal network type that is essentially absent in mice. This neuronal network relies on abundant connections between inhibitory interneurons.

Using biopsies from neurosurgical interventions, performed by neurosurgeon Hanno-Sebastian Meyer and his team at TU Munich, the researchers applied 3-dimensional electron microscopy to map about a million synapses in human brain samples.

Their data revealed, in humans, an unexpected bias of interneurons (enriched in humans) connecting with each other, while the innervation (synaptic connections) to principal neurons largely remained similar.

This suggests to us an almost ten-fold expansion of an interneuron-to-interneuron network, says Sahil Loomba, one of the studies lead authors.

Interneurons make about a fourth to a third of cortical nerve cells that behave in a very peculiar way: they are highly active, however, not to activate other neurons, rather to silence them. Just like kindergarten caretakers, or guards in the museum: their very laborious and highly energy consuming activity is to keep others peaceful, quiet, explains Helmstaedter.

Now imagine a room full of museum guards, all mutually silencing each other. This is what the human brain has developed!

But what could this mean? Theoretical work has suggested that such networks of silencers can prolong the time over which recent events can be kept in the neuronal network: expand the working memory.

In fact, it is highly plausible that longer working memory will help you deal with more complex tasks, expand your ability for reasoning, says Helmstaedter.

The new discovery suggests a first clear network innovation in humans that deserves intense further study.

He adds: It could also be a site of pathological change, and must be studied in the context of neuropsychiatric disorders. And last but not least: none of todays main AI methods uses such interneuron-to-interneuron networks.

Author: Irina EpsteinSource: Max Planck InstituteContact: Irina Epstein Max Planck InstituteImage: The image is credited to Loomba, Helmstaedter, MPI for Brain Research; Loomba et al., Science

Original Research: Closed access.Connectomic comparison of mouse and human cortex by Moritz Helmstaedter et al. Science

Abstract

Connectomic comparison of mouse and human cortex

The human cerebral cortex houses 1,000 times more neurons than the cerebral cortex of a mouse, but the possible differences in synaptic circuits between these species are still poorly understood.

We used 3-dimensional electron microscopy of mouse, macaque and human cortical samples to study their cell type composition and synaptic circuit architecture.

The 2.5-fold increase in interneurons in humans compared to mouse was compensated by a change in axonal connection probabilities and therefore did not yield a commensurate increase in inhibitory-vs-excitatory synaptic input balance on human pyramidal cells.

Rather, increased inhibition created an expanded interneuron-to-interneuron network, driven by an expansion of interneuron-targeting interneuron types and an increase in their synaptic selectivity for interneuron innervation.

These constitute key neuronal network alterations in human cortex.

Neuroscience

How the Brain Interprets Motion While in Motion – Neuroscience News

June 25, 2022 medical

Summary: Researchers have discovered a novel neural mechanism involved in casual inference that helps the brain detect objects in motion while we are moving.

Source: University of Rochester

Imagine youre sitting on a train. You look out the window and see another train on an adjacent track that appears to be moving. But, has your train stopped while the other train is moving, or are you moving while the other train is stopped?

The same sensory experienceviewing a traincan yield two very different perceptions, leading you to feel either a sensation of yourself in motion or a sensation of being stationary while an object moves around you.

Human brains are constantly faced with such ambiguous sensory inputs. In order to resolve the ambiguity and correctly perceive the world, our brains employ a process known as causal inference.

Causal inference is a key to learning, reasoning, and decision making, but researchers currently know little about the neurons involved in the process.

In a new paper published in the journaleLife, researchers at the University of Rochester, including Greg DeAngelis, the George Eastman Professor of Brain and Cognitive Sciences, and his colleagues at Sungkyunkwan University and New York University, describe a novel neural mechanism involved in causal inference that helps thebraindetect object motion during self-motion.

The research offers new insights into how the brain interpretssensory informationand may have applications in designing artificial intelligence devices and developing treatments and therapies to treatbrain disorders.

While much has been learned previously about how the brain processesvisual motion, most laboratory studies of neurons have ignored the complexities introduced by self-motion, DeAngelis says. Under natural conditions, identifying how objects move in the world is much more challenging for the brain.

Now imagine a still, crouching lion waiting to spot prey; it is easy for the lion to spot a moving gazelle. Just like the still lion, when an observer is stationary, it is easy for her to detect when objects move in the world, because motion in the world directly maps to motion on the retina.

However, when the observer is also moving, her eyes are taking in motion everywhere on her retina as she moves relative to objects in the scene.

This causes a complex pattern of motion that makes it more difficult for the brain to detect when an object is moving in the world and when it is stationary; in this case, the brain has to distinguish between image motion that results from the observer herself versus image motion of other objects around the self.

The researchers discovered a type of neuron in the brain that has a particular combination of response properties, which makes the neuron well-suited to contribute to the task of distinguishing between self-motion and the motion of other objects.

Although the brain probably uses multiple tricks to solve this problem, this new mechanism has the advantage that it can be performed in parallel at each local region of the visual field, and thus may be faster to implement than more global processes, DeAngelis says. This mechanism might also be applicable to autonomous vehicles, which also need to rapidly detect moving objects.

Unraveling a complicated circuit of neurons

Causal inference involves a complicated circuit of neurons and other sensory mechanisms that are not widely understood, DeAngelis says, because sensory perception works so well most of the time, so we take for granted how difficult of a computational problem it is.

In actuality, sensory signals are noisy and incomplete. Additionally, there are many possible events that could happen in the world that would produce similar patterns of sensory input.

Consider a spot of light that moves across theretinaof the eye. The same visual input could be the result of a variety of situations: it could be caused by an object that moves in the world while the viewer remains stationary, such as a person standing still at a window and observing a moving ambulance with a flashing light; it could be caused by a moving observer viewing a stationary object, such as a runner noticing a lamppost from a distance; or it could be caused by many different combinations of object motion, self-motion, and depth.

The brain has a difficult problem to solve: it must infer what most likely caused the specific pattern of sensory signals that it received. It can then draw conclusions about the situation and plan appropriate actions in response.

Building on these latest results and using data science, lab experiments, computer models, and cognitive theory, DeAngelis, Haefner, and their colleagues will continue working to pinpoint single neurons and groups ofneuronsthat are involved in the process.

Their goal is to identify how the brain generates a consistent view of reality through interactions between the parts of the brain that process sensory stimuli and the parts of the brain that make decisions and plan actions.

Developing therapies and artificial intelligence

Recognizing how the brain uses causal inference to separate self-motion from object motion may help in designing artificial intelligence and autopilot devices.

Understanding how the brain infers self-motion andobject motionmight provide inspiration for improving existing algorithms for autopilot devices on planes and self-driving cars, Haefner says. For example, a planes circuitry must take into account the planes self-motionin the air while also avoiding other moving planes appearing around it.

The research may additionally have important applications in developing treatments and therapies for neural disorders such as autism and schizophrenia, conditions in which casual inference is thought to be impaired.

While the project is basic science focused on understanding the fundamental mechanisms of causal inference, this knowledge should eventually be applicable to the treatment of these disorders, DeAngelis says.

Author: Lindsey ValichSource: University of RochesterContact: Lindsey Valich University of RochesterImage: The image is in the public domain

Original Research: Open access.A neural mechanism for detecting object motion during self-motion by HyungGoo R Kim et al. eLife

Abstract

A neural mechanism for detecting object motion during self-motion

Detection of objects that move in a scene is a fundamental computation performed by the visual system. This computation is greatly complicated by observer motion, which causes most objects to move across the retinal image.

How the visual system detects scene-relative object motion during self-motion is poorly understood.

Human behavioral studies suggest that the visual system may identify local conflicts between motion parallax and binocular disparity cues to depth and may use these signals to detect moving objects.

We describe a novel mechanism for performing this computation based on neurons in macaque middle temporal (MT) area with incongruent depth tuning for binocular disparity and motion parallax cues.

Neurons with incongruent tuning respond selectively to scene-relative object motion, and their responses are predictive of perceptual decisions when animals are trained to detect a moving object during self-motion.

This finding establishes a novel functional role for neurons with incongruent tuning for multiple depth cues.

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How the Brain Interprets Motion While in Motion - Neuroscience News

Neuroscience

Smoking Increases the Risk of Depression and Schizophrenia – Neuroscience News

June 25, 2022 medical

Summary: New research finds smoking significantly increases the risk of a person developing schizophrenia or depression.

Source: University of Bristol

Smoking increases the risk of developing schizophrenia by between 53% and 127% and of developing depression by 54% to 132%, a report by academics from the University of Bristol published today has shown.

More research is needed to identify why this is the case, and more evidence is needed for other mental health conditions such as anxiety or bipolar disorder.

The evidence presented today at the Royal College of Psychiatrists International Congress has been shared with the government, which is currently developing a new Tobacco Control Plan for publication later this year.

The Congress will also be given new data on the numbers of smokers withmental healthconditions. Rates ofsmokingare much higher among people with mentalhealthconditions than those without, and among Englands 6 million smokers there are an estimated:

These analyses are timely as the government is currently considering recommendations by the Khan Review for the forthcoming Tobacco Control Plan to deliver its Smokefree 2030 ambition.

The independent review by Javed Khan was commissioned by the Secretary of State to help the government to identify the most impactful interventions to reduce the uptake of smoking, and support people to stop smoking, for good. One of Khans 15 recommendations was that action is needed to tackle the issue of smoking and mental health.

One of the authors of the new report Professor Marcus Munafo Professor of Biological Psychology at the University of Bristol, said: There is no longer any doubt that smoking is bad for mental health and this needs to be a priority in the forthcoming Tobacco Control Plan.

Those working with people with mental health conditions need to understand and address the vicious cycle of bidirectional effects, whereby having symptoms of mental illness causes individuals to smoke more and to be more likely to become addicted.

At the same time, smoking also increases the risk of subsequent mental illness and exacerbates mental health symptoms. Lower rates of smoking will improve overall levels of good mental health as well asphysical health.

Alongside the report a joint publication by Action on Smoking and Health (ASH) and the Royal College of Psychiatrists Public Mental Health Implementation Centre sets out how a public mental health approach to smoking can be taken to address smoking and reduce poor mental health.

The NHS has pledged to put support in place for smokers on mental health wards and those accessing support in the community, but this is largely confined to those with severe mental illness.

Dr. Adrian James, president of the Royal College of Psychiatrists said: Smoking addiction is not a trivial matter; it causes serious harm to both body and mind. Smokers with mental health conditions can quit with the right support from healthcare professionals. Its our duty as psychiatrists to offer them the help they need to succeed.

Joanne Hart, former smoker who has recovered from depression said: Stopping smoking changed my life for the better, both physically and mentally. It is shocking to learn that smoking could have been one of the reasons for my depression. As a smoker I knew I was damaging my health but when times were tough it was easy to think that it was helping mentallyeveryone should know the opposite is true.

Deborah Arnott, chief executive, ASH, said: The Khan Review is called Making Smoking Obsoletethis cannot be achieved if we ignore the more than a million smokers with mental health conditions. While the NHS has started to roll out support to quit for those withsevere mental illnessthere is little provision for those with commonmental health conditionslike depression and anxietya plan is needed.

Author: Press OfficeSource: University of BristolContact: Press Office University of BristolImage: The image is in the public domain

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‘Travel Therapy’: Could a Vacation Help Mental Health and Well-Being? – Neuroscience News

June 25, 2022 medical

Summary: Vacations may not just be an opportunity for recreation, they may also provide mental and overall health benefits.

Source: Edith Cowen University

Many of us will have likely heard of music therapy and art therapy but what about travel therapy?

A new cross-disciplinarypaperfrom Edith Cowan University (ECU) proposes we change the way we view tourism, seeing it not just as a recreational experience but as an industry that can provide real health benefits.

The collaboration between ECUs Centre for Precision Health and School of Business and Law found many aspects of going on holiday could have a positive impact on those with mental health issues or conditions.

Lead researcherDr Jun Wensaid the diverse team of tourism, public health and marketing experts investigated how tourism could benefit those living with dementia.

Medical experts can recommend dementia treatments such as music therapy, exercise, cognitive stimulation, reminiscence therapy, sensory stimulation and adaptations to a patients mealtimes and environment, Dr Wen said.

These are all also often found when on holidays.

This research is among the first to conceptually discuss how these tourism experiences could potentially work as dementiainterventions.

Holiday fun or treatment?

Dr Wen said the varied nature of tourism meant there were many opportunities to incorporate treatments for conditions such as dementia.

For example, being in new environments and having new experiences could provide cognitive and sensory stimulation.

Exercise has been linked to mental wellbeing and travelling often involves enhanced physical activity, such as more walking, Dr Wen said.

Mealtimes are often different on holiday: theyre usually more social affairs with multiple people and family-style meals have been found to positively influence dementia patients eating behaviour.

And then theres the basics like fresh air and sunshine increasing vitamin D and serotonin levels.

Everything that comes together to represent a holistic tourism experience, makes it easy to see how patients with dementia may benefit from tourism as an intervention.

A shift in thinking

Dr Wen said COVID-19s impact on travel in recent years had raised questions about tourisms value beyond lifestyle and economic factors.

Tourism has been found to boost physical and psychological wellbeing, he said.

So, after COVID, its a good time to identify tourisms place in public health and not just for healthy tourists, but vulnerable groups.

Dr Wen said he hoped a new line of collaborative research could begin to examine how tourism can enhance the lives of people with various conditions.

Were trying to do something new in bridging tourism and health science, he said.

There will have to be more empirical research and evidence to see if tourism can become one of the medical interventions for different diseases like dementia or depression.

So, tourism is not just about traveling and having fun; we need to rethink the role tourism plays in modern society.

Author: Sam JeremicSource: Edith Cowen UniversityContact: Sam Jeremic Edith Cowen UniversityImage: The image is in the public domain

Original Research: Closed access.Tourism as a dementia treatment based on positive psychology by Jun Wen et al. Tourism Management

Abstract

Tourism as a dementia treatment based on positive psychology

No research in tourism or medicine has addressed the potential relationship between travel and the medical treatment ofdementia. Given tourisms increasingly important role in society, a cross-disciplinary team of tourism and dementia experts provide insight into the potential benefits of tourism for individuals with dementia.

This conceptual effort critically reviews the tourism and dementia literature and addresses pertinent knowledge gaps. Tourism is presented as a possible way to improve dementia patients well-being as an adjunct to non-pharmacological interventions.

Accordingly, a conceptual framework is proposed to highlight the nexus between tourism experiences and dementia interventions.

Future interdisciplinary research directions are also described.

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'Travel Therapy': Could a Vacation Help Mental Health and Well-Being? - Neuroscience News

Neuroscience

How Different Cell Types in the Brain Work Together to Suppress Nausea – Neuroscience News

June 25, 2022 medical

Summary: Disabling activity in an area of the brain stem called the area postrema reduces nausea, while activating this area promotes vomiting, a new study reveals. The findings could lead to the development of new therapies to curb nausea.

Source: Harvard

Nausea is a bit of a catchall sensation for the human body: the unpleasant sick feeling can hit us as a result of everything from pregnancy or a migraine to eating spoiled food or undergoing chemotherapy.

Yet despite its ubiquity, scientists still dont understand precisely hownauseaworks on a mechanistic level.

Now, a team of researchers led bycell biologistsat Harvard Medical School is making strides in deepening our understanding of thebrainpathways that control nausea.

In a study conducted in mice and published June 14 inCell Reports, the scientists described a mechanism by which inhibitory neurons in a specific brain region suppress the activity of nausea-causing excitatory neurons to tamp down nausea.

The work illuminates the basic biology of nausea. If affirmed in further studies in animals and humans, it could inform the development of better anti-nausea medications.

Mediating malaise

Nausea evolved to help us survive by prompting vomiting when we ingest toxins or contract an infection. However, nausea can become a major problem when it occurs in other contextsfor example, during pregnancy or as a side effect of treatments for cancer or diabetes. If untreated, uncontrolled vomiting can lead to electrolyte imbalances and, in rare cases, life-threatening dehydration.

Current medications for nausea associated with these conditions arent all that effective, in large part because scientists dont have a detailed understanding of how the brain produces the sensation.

We cannot really develop better treatment strategies until we know the mechanism of nausea, said lead author Chuchu Zhang, a research fellow in cell biology at HMS.

Zhang and senior author Stephen Liberles, professor of cell biology in the Blavatnik Institute at HMS, are studying a region of the brain stem called the area postrema that appears to be involved in nausea.

Earlier research found that stimulating this brain region induces vomiting, while disabling it reduces nausea, but how it plays a role in nausea was not known, so we thought this would be a good place to start, Zhang said.

In a2020 studyinNeuron, Zhang and Liberles identified excitatory neurons in the area postrema that cause nausea, along with their associated receptors. Specifically, theycharacterized neurons that express the receptor for GLP1, a protein linked toblood sugarand appetite control. This receptor, they noted, is a common target for diabetes drugs, for which nausea is a major side effect.

When neurons with GLP1 receptors were turned on, mice showed signs of nausea, and when the neurons were turned off, the nausea behaviors stopped. The team also mapped these nausea-inducing neurons, located outside theblood-brain barrier, which allows them to easily detect toxins in the blood.

Understanding what receptors are expressed in the area postrema tells us what kinds of pathways may be involved in nausea signaling, Zhang said.

One traditional approach to intervene in nausea is to block those signaling pathways using pharmacological inhibitors, Liberles added.

However, the researchers wondered if there could be another way to reduce nauseaone that focuses instead on inhibitory neurons that suppress excitatory neurons in the area postrema.

An alternative path

In the new study, the researchers explored the structure and function of inhibitory neurons in the area postrema. Mapping these neurons revealed that they form a dense network that connects with nearby excitatory neurons. When the researchers activated these inhibitory neurons, the mice stopped nausea behaviors that are typically caused by excitatory neurons.

Delving deeper, the team identified three types of inhibitory neurons in the area postrema. One of these types expresses a receptor for GIP, a small protein released by the digestive system after eating, stimulating the release of insulin to control blood sugar.

We were curious whether this population of inhibitory neurons marked by the receptor for GIP could be manipulated to suppress nausea behavior, and how that mechanism works, Zhang said.

When the researchers used GIP to activate these inhibitory neurons, inhibitory currents prompted by the chemical messenger GABA flowed to nearby excitatory neurons, reducing their activity. On a behavioral level, giving mice GIP to activate these inhibitory neurons eliminated nausea behaviors. On the flip side, when the inhibitory neurons were destroyed, mice continued to show signs of nausea, even after receiving GIP.

Because mice dont vomit, Zhang noted, the study relied on observing the presence of behaviors suggestive of nausea, such as avoiding toxic substances. Given that the same brain pathways exist in humans, the researchers say the mechanism is likely conserved.

By identifying inhibitory neurons that suppress nausea in a pharmacologically accessible brain region, we can simply engage these neurons to counteract nausea responses, Liberles explained.

The brain stem inhibitory neurons in the area postrema are potentially a great clinical target for anti-nausea drug development, Zhang added. Its definitely a new strategy for developing anti-nausea treatments.

GIP is already being studied as a potential treatment for nausea, Zhang said. In fact, preliminary research has shown that giving GIP or activating GIP receptors can reduce nausea in animals that do vomit, including ferrets, dogs, and shrews. Scientists are currently working on incorporating GIP into diabetes treatments that target GLP1 receptors, with the goal of decreasing nausea as a side effect.

Zhang and Liberles plan to continue exploring the basic biology of nausea, including how these inhibitory neurons in the brain are naturally activated, and what other brain regions are involved in controlling their activity.

The team also wants to investigate additional receptors expressed byinhibitory neurons, and the various signaling factors that engage them.

Because there are different ways to trigger nausea, there are probably different receptors and signaling factors involved that could be used as drug targets to suppress nausea. Zhang said.

We want to know more about the various nausea mechanisms so that we can develop even better treatment strategies that are tailored to specific conditions.

Author: Catherine CarusoSource: HarvardContact: Catherine Caruso HarvardImage: The image is credited to Chuchu Zhang

Original Research: Open access.A brainstem circuit for nausea suppression by Chuchu Zhang et al. Cell Reports

Abstract

A brainstem circuit for nausea suppression

Nausea is a discomforting sensation of gut malaise that remains a major clinical challenge. Several visceral poisons induce nausea through the area postrema, a sensory circumventricular organ that detects bloodborne factors.

Here, we use genetic approaches based on an area postrema cell atlas to reveal inhibitory neurons that counteract nausea-associated poison responses.

The gut hormone glucose insulinotropic peptide (GIP) activates area postrema inhibitory neurons that project locally and elicit inhibitory currents in nausea-promoting excitatory neurons through -aminobutyric acid (GABA) receptors.

Moreover, GIP blocks behavioral responses to poisons in wild-type mice, with protection eliminated by targeted area postrema neuron ablation.

These findings provide insights into the basic organization of nausea-associated brainstem circuits and reveal that area postrema inhibitory neurons are an effective pharmacological target for nausea intervention.

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How Different Cell Types in the Brain Work Together to Suppress Nausea - Neuroscience News

Neuroscience

Helping the Brain to Heal the Gut – Neuroscience News

June 25, 2022 medical

Summary: Researchers say using psychological interventions like CBT may help to alleviate anxiety and other symptoms associated with IBS.

Source: University of Pennsylvania

On its surface, thesubredditfor irritable bowel syndrome (IBS) is a den of tongue-in-cheek humor; its logo reimagines the classic Reddit alien gripping its gut in discomfort, scatological memes abound, and the most active members sit on the porcelain throne.

Beyond the joking veneer, however, the online community shares stories of how the disorder has tinged almost every aspect of members lives with shame and discomfort. In some cases, the resulting anxiety, depression, and avoidance can be debilitating, disabling, or even life-threatening.

Spend 10 minutes on the IBS subreddit, and there will be at least one person who is suicidal, posting to that list saying, I cant take this anymore. This has destroyed my life,' says Melissa Hunt, aclinical psychologistin Penns Department of Psychology.

This is part of why Hunt has spent almost two decades studying and treating IBS, and why she just published the second edition of her book Reclaim Your Life from IBS, which offers a proven treatment plan for those suffering with the disorder.

A year after the first edition went out of print, Hunt was finding copies selling on eBay for hundreds of dollars. In response to the demand, she wanted to provide an update that included more tools to aid in treatment as well as a review of the most recent advances in the field.

Gut-brain connection

One of the most important advances is a deepened understanding of the mechanism of IBS, which is now characterized as a disorder of the gut-brain interaction, says Hunt. Signals from the gut that might go unnoticed in individuals without IBS instead get transmitted to and interpreted by the brain as pain or the urgent need for a bowel movement. This can lead to anxiety, and the intestine, which is lined with stress hormone receptors, responds by cramping and spasming.

And then youre off to the races with this positive feedback loop of increasing hypervigilance by the brain and then hypersensitivity in the gut, says Hunt.

Symptomatically, IBS manifests as abdominal pain and either constipation, diarrhea, or alternating bouts of both, and by some estimates as many as 15% of the population struggles with some form of the disorder.

For those who are more prone to diarrhea, the anxiety around explaining frequent trips to the restroom or being too far away from a convenient restroom can lead them to avoid social situations and may ultimately manifest as agoraphobia.

People get incredibly paranoid: I cant go to a restaurant because Ill have an attack. I dont want to have to leave the table and be away from everybody, and what if the bathroom is occupied? It would be a disaster, so I should just stay home,' says Hunt. Your life gets really small really quickly.

The world-shrinking nature of the condition, paired with frequent physical discomfort, can lead to desperation. Many take extreme measures, usually in the form of dietary restrictions or multiple medications, in an attempt to reduce their symptoms.

However, even the effectiveness and side effects of many clinically prescribed interventions, such as laxatives or antibiotic treatments, can vary. For example, one diet that often works well to treat IBS symptoms, called low-FODMAP, is so restrictive that adherence is virtually impossible unless patients can prepare every meal themselves, says Hunt. Counterintuitively, this diet can harm intestinal health by starving important gut bacteria, she says.

What these treatments all share is their focus on the gut side of the gut-brain interaction. Instead, Hunt focuses on the brain. She usescognitive behavioral therapyto help patients reduce their anxiety and hypervigilance around gut sensations and encourages them to slowly expose themselves to food and situations that they associate with their individual IBS symptoms.

She also teaches them to stop catastrophizing, falling into the mental trap that the worst outcome is bound to happen. This approach actually leads to reductions in visceral hypersensitivity, allowing people to alleviate symptoms while eating whatever they want.

If half of whats going on in IBS is the way the brain is interpreting those signals, then therapy that helps you reinterpret those signals in a different way is going to help, says Hunt.

Thats why talking about it is going to change their urgent diarrhea, which is initially hard for some patients to believe.

Making treatment accessible

When Hunt initially tested andpublisheda study of a low-intensity CBT treatment with limited but active therapist involvement, she was surprised by its efficacy in reducing symptoms and improving quality of life, she says. Several peers encouraged her to pursue larger studies and publish more on the subject.

Although more studies might look more prestigious, Hunt says she felt she could reach more patients and treatment providers with a self-help book. So, she wrote the first edition, which she tested with arandomized controlled trial, the gold standard for studying a treatments effectiveness.

As in the first study, participating patients saw consistent improvements in their quality of life and IBS symptoms.

In the second edition, she explores advances in treatment made in the past decade. She added a chapter on diet, which explores recent research on restrictive diets and the ways healthy eating habits might help alleviate symptoms.

She also dives into the benefits of exercise and nonjudgmental ways for people to help motivate themselves in that arena.

Hunt says she hopes the new edition will be useful to both patients and clinicians, including gastroenterologists, and therapists.

Throughout the book, she offers more clinical anecdotes so that readers might find a case that resonates, and she ends with two mock patient stories, to show how someone might work through the text with and without a therapist.

Ultimately, Hunt says the book will give people like those on the IBS subreddit access to affordable, scientifically proven help.

The real goal of treatment for IBS is to get people their lives back, not necessarily to make the symptoms go away forever, says Hunt.

You may have GI discomfort from time to timeeveryone doesbut you can still live a very rich, meaningful life.

Author: Luis Melecio-ZambranoSource: University of PennsylvaniaContact: Luis Melecio-Zambrano University of PennsylvaniaImage: The image is in the public domain

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Helping the Brain to Heal the Gut - Neuroscience News