Category Archives: Neuroscience

Can Neuroscience Help Humans to Hate Each Other Less? – The Wire

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The recent news of Bajrang Muni Udasin of Sitapur issuing rape threats to Muslim women is one of several such speeches delivered by members of different communities against people they perceive to be others. History is replete with anecdotes in which hate expressed against a particular group subsequently avalanched to violence against them.

Hateful speeches, literature and media reports often paint a picture of other groups in an effort to dehumanise their members. The targeted group, is equated in language with animal or subhuman behaviour. Using terms like termites, rats and bed bugs for a community undermines their agency and paves the way for violence against their people to the extent that it wont provoke the sort of empathy that violence against other groups might. Adolf Hitlers campaign against Jews during World War II is the most well-known example of such a campaign.

As a neurobiologist, I have often wondered if we can locate regions in the brain that contribute to hate towards and dehumanisation of a group of people in a manner that can be measured, and if we can elucidate its mechanism to the extent that we can ameliorate or even eliminate it before it goes overboard.

Gordon Allport, a pioneer of personality psychology and who taught at Harvard University, was the first to publish research on the psychology of hate speech and dehumanisation in his celebrated work The Nature of Prejudice (1954). He argued that prejudice against a group of people can be transmitted through language and proposed that hate speech, which he called antilocution, results in extreme hostility that in turn gives rise to violence.

Also read: The Slow Poison of Hate Speech Harms in Obvious and Insidious Ways

In 2015, Gail and Richard Murrow, of the departments of neurology and neurosurgery, University of North Carolina, argued similarly: that hate speech results in dehumanisation, which in turn leads to unthinking acceptance of atrocities against the target group. Dehumanization automatically reduces the pain empathy that emotionally underpins rights-based attitudes and behavior, they wrote.

Now, a question arises: could the dehumanisation of one group of people have a neurobiological basis? Might some part of the brain be responsible for controlling this behaviour?

In the words of Edmund Glaser, In anatomical terms the brain is a vast assembly of neurons, the cells that are responsible for generating the behaviours that encompass physical movement, sensory perception, human emotions, and human intelligence itself. These neurons are diverse in shape and function. They use chemical compounds called neurotransmitters to communicate with each other. Neurons join each other to form complex neural networks to store, exchange and manipulate information, with different groups of neurons associated with different functions.

In fact, it is an established fact in neuroscience that different functions motor or sensory are associated with particular regions within the brain. In 2006, Lasana Harris and Susan Fiske of the psychology department at Princeton University studied brain activity of humans when encountered with different social groups. They observed the blood-oxygen level dependent signals through MRI scans to understand which particular regions of the brain were associated with dehumanisation. The study found that emotions like pride, envy and pity were controlled by the medial prefrontal cortex (mPFC) in the brain.

When an individual witnessed a person belonging to a certain social group being cast as less human, the mPFC showed a corresponding and relative lack of activation while the amygdala and the insula, two other regions, showed higher activation. These latter regions were found to be associated with disgust. Harris and Fiske wrote, members of some social groups seem to be dehumanized, at least as indicated by the absence of the typical neural signature for social cognition, as well as the exaggerated amygdala and insula reactions (consistent with disgust) and the disgust ratings they elicit.

Glaser whose invention of computer microscopy and subsequent study of brain morphology revolutionised neuroscience in 2009 pointed out that locating the insula or any other region to be the centre of hate in the brain is insufficient. The problem is more complex. He argued that history is full of examples of hatred being spread among people through the use of language: the propagation of hatred, mass hatred, to be truly successful in its violent ends, may require the existence of a hate region existing in specialized variations or mutations in different brains. There must be, he argued, a propagation channel of sorts that allows the brains of multiple people of a social group to synchronise.

In the 1990s, scientists discovered certain neurons in rhesus macaque monkeys that facilitated an automatic mirror neural simulation in one individual of certain motor acts they observed another individual performing. These neurons are called mirror neurons. There has since been a debate over the existence of mirror neurons among humans as well. Several scientists have tried to prove that such a mirror neural mechanism could exist among us and help us express empathy.

In 2015, Murrow and Murrow proposed that neural simulation mechanisms, whether in the form of mirror neurons or other neural mechanisms, do exist in the human brain, and that such neural simulation is the source of the pain empathy theorized to motivate prosocial and helping behavior. They further argued that this human mirror neural system responds only to actions performed by other members of the same species, i.e. humans.

So if a group is dehumanised, our brains may not be able to empathise with its members.

As war, war crimes, extremism and terrorism demand our attention, neuroscientists around the world must start devoting more of their time and resources to understand the neurobiological basis of hate better, with support from governments and other stakeholders. Glaser himself had an optimistic vision in mind:

if the hate center(s) is (are) inhibited, as by some yet-unknown medication targeting hate neurons, hate would be suppressed or removed, and the brain and the person would continue hate-free until the drug is discontinued. One might also suggest that there are other centers in the brain that connect to the hate center and are capable of reducing or inhibiting its activity. By modifying the activity of these centers, therefore, one could also increase or decrease the level of hatred.

This may seem like science fiction today, but theres no reason it cant be reality in sufficient time.

Mahino Fatima is a neurobiologist, former assistant professor (ad hoc) at Miranda House, Delhi University, and DST-SERB-NPDF, ICMR-Research Associate, School of Life Sciences, Jawaharlal Nehru University, New Delhi.

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Can Neuroscience Help Humans to Hate Each Other Less? - The Wire

New Discoveries About the Origin of the Brains Immune System – Neuroscience News

Summary: New findings reveal phagocytes do not fully mature until after birth, contradicting previous assumptions that they mature during embryonic development.

Source: University of Freiberg

What gets into the brain and what doesnt is strictly regulated. Researchers at the Faculty of Medicine at the University of Freiburg have now studied phagocytes that coat the blood vessels in the brain and reinforce the blood-brain barrier.

As the scientists from the Institute of Neuropathology at the Medical CenterUniversity of Freiburg together with an international research team have shown, these cells only mature fully after birth according to a defined step-by-step developmental program.

Until now, it had been assumed that this process was completed during embryonic development.

Their studies, which were published in the journalNatureon April 20, 2022, were initially carried out on genetically modified mouse lines and were confirmed on human samples. They are expected to provide important insights into the development and treatment of diseases of the brain.

We were able to show that theimmune cellswe studied migrate from the cerebral membrane to theblood vesselsin the brain shortly before birth and mature there. This process is probably not completed until weeks after birth and could partly explain why the brain is so vulnerable at the beginning of life, says Prof. Dr. Marco Prinz, Medical Director of the Institute of Neuropathology at the Medical CenterUniversity of Freiburg and head of the Collaborative Research Center/Transregio 167NeuroMac and member of the Cluster of Excellence CIBSS -Centre for Integrative Biological Signalling Studies at the University of Freiburg.

The late timing of the maturation of the phagocytes, also called macrophages, was very surprising to us, since theprecursor cellsare already present in the brain long before, says Prinz.

In addition, the scientists were able to show for the first time that the vessels, as structure-giving cells of the brain, send important signals for normal development of the brains macrophages.

Theblood-brain barrieris formed by cells on the blood vessels of the brain. They control which substances can enter the brain and which cannot. This protects the brain from harmful substances and pathogens. The blood-brain barrier is particularly permeable in the case of infectious diseases, certain brain tumors and oxygen deficiency.

Significance for Alzheimers, multiple sclerosis and more

In addition to the blood-brain barrier, the immune cells we studied control what can reach thebrain cellsfrom the blood, they eat pathogens and prevent excessive inflammation. They are also involved in the development of cancer, Alzheimers disease and multiple sclerosis. Our findings could be important for a better understanding of these diseases and future therapies, Prinz adds.

Color-coded cells and gene analyses

For their study, the researchers led by the two first authors Dr. Takahiro Masuda from Kyushu University, Japan, and Dr. Lukas Amann from the Faculty of Medicine at the University of Freiburg used several newly established mouse lines.

With these, different types of brain macrophages and theirprogenitor cellscould be specifically labeled for the first time and later found in the different brain regions using high-resolution microscopy. In addition, they examined the gene activity of individual cells and thus determined their degree of maturity.

We were also able to confirm the data on human brains. This gives us a much deeper understanding of the timing and molecular mechanisms in the development of the cells. This knowledge can now be used to explore new and more specific therapeutic approaches forbraindiseases, says biologist Dr. Lukas Amann, who works at the Institute of Neuropathology at the Medica CenterUniversity of Freiburg.

Author: Press OfficeSource: University of FreibergContact: Press Office University of FreibergImage: The image is credited to University of Freiburg / Dr. Lukas Amann

Original Research: Closed access.Specification of CNS macrophage subsets occurs postnatally in defined niches by Lukas Amann et al. Nature

Abstract

Specification of CNS macrophage subsets occurs postnatally in defined niches

All tissue-resident macrophages of the central nervous system (CNS)including parenchymal microglia, as well as CNS-associated macrophages (CAMs) such as meningeal and perivascular macrophagesare part of the CNS endogenous innate immune system that acts as the first line of defence during infections or trauma.

It has been suggested that microglia and all subsets of CAMs are derived from prenatal cellular sources in the yolk sac that were defined as early erythromyeloid progenitors.

However, the precise ontogenetic relationships, the underlying transcriptional programs and the molecular signals that drive the development of distinct CAM subsets in situ are poorly understood.

Here we show, using fate-mapping systems, single-cell profiling and cell-specific mutants, that only meningeal macrophages and microglia share a common prenatal progenitor.

By contrast, perivascular macrophages originate from perinatal meningeal macrophages only after birth in an integrin-dependent manner. The establishment of perivascular macrophages critically requires the presence of arterial vascular smooth muscle cells.

Together, our data reveal a precisely timed process in distinct anatomical niches for the establishment of macrophagesubsetsin the CNS.

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New Discoveries About the Origin of the Brains Immune System - Neuroscience News

Feeling Sensations, Including Ones Connected to Sadness, May Be Key to Depression Recovery – Neuroscience News

Summary: Suppressing or blocking out physical sensations related to emotions such as sadness can hinder recovery from depression symptoms and may cause a relapse into depression.

Source: University of Toronto

The physical sensations that accompany sadness can feel as undesirable as they are intensea constriction of the chest, watery eyes and a raw throat, to name a few.

But Norman Farb, an associate professor of psychology at the University of Toronto Mississauga, and Zindel Segal, a distinguished professor of psychology inmood disordersat U of T Scarborough, have discovered that keeping sensation alive in the face of stress is critical for well-being, particularly for those who have recovered from depression.

In the largest neuroimaging study to date of psychotherapy for preventing relapse and recurrence in depression, the researchers linked past depression with a greater tendency to shut downsensory processingwhen faced with an emotional stressor.

They also found that blocking out sensation is related to a greater risk of depressive relapse.

We dont like feeling bad things, (but) we dont really think about the implications of balancing our short-term relief with our long-term health, says Farb.

Our research explains why working to keep feeling is so important. It lays the groundwork for seeing thatemotional stressactually robs us of sensationand to undo stress, one must counter this inhibitory effect.

The study, published recently in the journalNeuroImage: Clinical, was co-authored by Farb and Segal, along with Ph.D. student Philip Desormeau, in the psychological clinical science graduate department at U of T Scarborough, and Cornell University Professor Adam Anderson.

The study included 166 participants who had recovered from depression but were vulnerable to a future episode. They were divided into two groups. Over an eight-week period, one group underwentcognitive therapywith a well-being focus, while the other group underwent mindfulness-based cognitive therapy.

Between cognitive therapy sessions, 85 participants also had theirbrain activitymeasured through a fMRI scan while watching four consecutive clips from TV shows that wouldnt normally produce an emotional trigger as a baselinefor example, a lifestyle-related show on HGTVas well as clips from an emotionally charged movie such as 1983s Terms of Endearment.

For the following two years, researchers followed up with participants every two months.

Farb says he and colleagues discovered something fascinating while studying the brain scans of those who relapsed: they had more of a tendency to shut down.

When exposed to the emotionally charged video clips, the parts of their brain that control sensations shut down more often than those who had not relapsed. Researchers also found that those who reported higher feelings of sadness during the movie clips werent necessarily more likely to suffer a relapse.

What actually determined their depression levels was how much that sadness was accompanied by a sensory shutdown, Farb says.

He adds that when our brains shut outsensory informationduring anegative mood, we are left with only our thoughts to make sense of what is happening. Often, these thoughts fail to provide a wider view of what is going onand blocking out bodily sensations locks people into an echo chamber of their negative views.

Our thoughts are there to nail things down so you can hold onto them over time, and thats fine as long as they keep getting updatedbut the thing that updates it is new sensations, Farb explains.

The researchers say their findings help explain why negative everyday life situationssuch as getting criticized at a work meeting or butting heads with your spousecould cause a relapse in somebody who has recovered from depression.

Segal says such seemingly minor events can trigger deeper feelings of inadequacy and worthlessness in those with a history of depression.

This negative mood gets tied up with thoughts about themselves and can be easily perpetuated over time, and the person can feel worse, Segal says, adding that such thoughts often produce bodily sensations.

If the person suppresses these bodily sensations, their thoughts will compound into more and more depressive reactions.

Farb adds that the study could help clinical researchers create new assessments around sensory inhibition as a risk marker for depression. It could also contribute to developing targeted therapies that help people recovering fromdepressionbecome better at noticing their sensations throughout the day, which, in turn, could help them counter negative moods that can shut down sensation and lock in depressive thinking.

We dont have to wait until the person starts to really spiral, where it takes a lot of resources and time and effort to pull them out, Farb says.

You can start to notice if the person is starting to fit the profile of someone whos getting really sensory-avoidant. We can address it then, before the person stops showing up to work or taking care of their kids.

Author: Kristy StraussSource: University of TorontoContact: Kristy Strauss University of TorontoImage: The image is in the public domain

Original Research: Open access.Static and treatment-responsive brain biomarkers of depression relapse vulnerability following prophylactic psychotherapy: Evidence from a randomized control trial by Norman A.S. Farb et al. NeuroImage: Clinical

Abstract

Static and treatment-responsive brain biomarkers of depression relapse vulnerability following prophylactic psychotherapy: Evidence from a randomized control trial

Neural reactivity to dysphoric mood induction indexes the tendency for distress to promote cognitive reactivity and sensory avoidance. Linking these responses to illness prognosis following recovery from Major Depressive Disorder informs our understanding of depression vulnerability and provides engagement targets for prophylactic interventions.

A prospective fMRI neuroimaging design investigated the relationship between dysphoric reactivity and relapse following prophylactic intervention. Remitted depressed outpatients (N=85) were randomized to 8weeks of Cognitive Therapy with a Well-Being focus or Mindfulness Based Cognitive Therapy. Participants were assessed before and after therapy and followed for 2years to assess relapse status. Neural reactivity common to both assessment points identified static biomarkers of relapse, whereas reactivity change identified dynamic biomarkers.

Dysphoric mood induction evoked prefrontal activation and sensory deactivation. Controlling for past episodes, concurrent symptoms and medication status, somatosensory deactivation was associated with depression recurrence in a static pattern that was unaffected by prophylactic treatment, HR 0.04, 95% CI [0.01, 0.14],p<.001. Treatment-related prophylaxis was linked to reduced activation of the left lateral prefrontal cortex (LPFC), HR 3.73, 95% CI [1.33, 10.46],p=.013. Contralaterally, the right LPFC showed dysphoria-evoked inhibitory connectivity with the right somatosensory biomarker

These findings support a two-factor model of depression relapse vulnerability, in which: enduring patterns of dysphoria-evoked sensory deactivation contribute to episode return, but vulnerability may be mitigated by targeting prefrontal regions responsive to clinical intervention. Emotion regulation during illness remission may be enhanced by reducing prefrontal cognitive processes in favor of sensory representation and integration.

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Feeling Sensations, Including Ones Connected to Sadness, May Be Key to Depression Recovery - Neuroscience News

The Brain Employs an Alarm System to Suppress Intrusive Thoughts – Neuroscience News

Summary: The anterior cingulate cortex generates a reactive alarm, increasing its activity to signal to the dorsolateral prefrontal cortex to stop intrusive thoughts and memories.

Source: SfN

Forget what you saw: a brain region detects when you are about to think of an unwanted memory and alerts other regions to suppress it, according to research recently published inJournal of Neuroscience.

Crespo Garca et al. measured participants brain activity with both EEG and fMRI while they completed a memory task.

The participants memorized sets of words (i.e., gate and train) and were asked to either recall a cue words pair (see gate, think about train) or only focus on the cue word (see gate, only think about gate).

During proactive memory suppression, activity increased in the anterior cingulate cortex (ACC), a brain region involved in cognitive control, within the first 500 milliseconds of the task.

The ACC relayed information to the dorsolateral prefrontal cortex (DLPFC), which then inhibited activity in the hippocampus, a key region for memory recall.

The activity levels in the ACC and DLPFC remained low for the rest of the trial, a sign of success the memory was stopped early enough so no more suppression was needed.

If the memory was not suppressed in time, the ACC generated a reactive alarm, increasing its activity to signal to the DLPFC to stop the intrusion.

Author: Calli McMurraySource: SfNContact: Calli McMurray SfNImage: The image is credited to Crespo Garca et al

Original Research: Closed access.Anterior Cingulate Cortex Signals the Need to Control Intrusive Thoughts During Motivated Forgetting by Crespo Garca et al. Journal of Neuroscience

Abstract

Anterior Cingulate Cortex Signals the Need to Control Intrusive Thoughts During Motivated Forgetting

How do people limit awareness of unwanted memories? When such memories intrude, a control process engages the right DLPFC (rDLPFC) to inhibit hippocampal activity and stop retrieval. It remains unknown how the need for control is detected, and whether control operates proactively to prevent unwelcome memories from being retrieved, or responds reactively, to counteract intrusions.

We hypothesized that dorsal ACC (dACC) detects the emergence of an unwanted trace in awareness and transmits the need for inhibitory control to rDLPFC. During a memory suppression task, we measured in humans (both sexes) trial-by-trial variations in dACCs theta power and N2 amplitude, two EEG markers thought to reflect the need for control.

With simultaneous EEG-fMRI recordings, we tracked interactions between dACC, rDLPFC and hippocampus during suppression.

We found a clear role of dACC in detecting the need for memory control and upregulating prefrontal inhibition. Importantly, we identified distinct early (350-400 ms) and late (500-700 ms) dACC contributions, suggesting both proactive control prior to recollection, and reactive control in response to intrusions.

Stronger early activity was associated with reduced hippocampal activity and diminished BOLD signal in dACC and rDLPFC, suggesting that pre-empting retrieval reduced overall control demands.

In the later window, dACC activity was larger and effective connectivity analyses revealed robust communication from dACC to rDLPFC and from rDLPFC to hippocampus, tied to successful forgetting.

Together, our findings support a model in which dACC detects the emergence of unwanted content, triggering top-down inhibitory control, and in which rDLPFC countermands intruding thoughts that penetrate awareness.

Significance Statement:

Preventing unwanted memories from coming to mind is an adaptive ability of humans. This ability relies on inhibitory control processes in the prefrontal cortex to modulate hippocampal retrieval processes.

How and when reminders to unwelcome memories come to trigger prefrontal control mechanisms remains unknown. Here we acquired neuroimaging data with both high spatial and temporal resolution as participants suppressed specific memories.

We found that the anterior cingulate cortex detects the need for memory control, responding both proactively to early warning signals about unwelcome content and reactively to intrusive thoughts themselves.

When unwanted traces emerge in awareness, anterior cingulate communicates with prefrontal cortex and triggers top-down inhibitory control over the hippocampus through specific neural oscillatory networks.

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The Brain Employs an Alarm System to Suppress Intrusive Thoughts - Neuroscience News

When Severe Infection Causes Long-Term Mood Disorders – Neuroscience News

Summary: The activation of a neural circuit comprising of the central nucleus of the amygdala and the bed nucleus of the stria terminalis in the first hours following sepsis infection induced anxiety behaviors in mice two weeks after the infection cleared. The behaviors mimicked the PTSD symptoms patients experience following sepsis infection.

Source: Intitute Pastuer

The brain is able to detect and regulate localized or systemic inflammation by using two communication pathways. The first, humoral, makes use of specific brain structures that enable circulating inflammatory mediators to enter the brain. The second, neural, involves nerves whose sensory afferents transmit the inflammatory signal detected at local level.

The vagus nerve therefore uses identified receptors to detect a digestive or lung inflammation. Specific brain structures and networks perceive and integrate these humoral and neural messages and orchestrate a regulatory response involving neuroendocrine, neurovegetative and behavioral elements. These corrective interventions are controlled respectively by the hypothalamus and the hypophysis the autonomic nervous system and the limbic system.

Neuroendocrine activation is characterized by the release of cortisol, the main stress hormone. The autonomic response involves the combined activation of the sympathetic and vagal systems, with the latter believed to induce a local anti-inflammatory response.

Behavioral changes affect mood, attention, sleep and appetite.

The aim of the overall response is to control inflammation so as to preserve bodily integrity, or homeostasis. But in some circumstances, it can be ill adapted and can lead to immunological and/or psychological disorders.

A severe infection known as sepsis is the most common condition capable of inducing this defense strategy against inflammatory stress. Sepsis is the leading cause of death worldwide and represents a major public health challenge.

What makes the situation worse is that sepsis is also associated with chronic psychological disorders such as anxiety, depression and post-traumatic stress disorder.

These conditions significantly increase suicide risk and have a lasting impact on the personal, social and professional lives of patients.

No preventive treatments have so far been demonstrated to be effective, probably because of a lack of understanding of the pathophysiology of these disorders, especially the neural networks implicated in their onset, explains Professor Tarek Sharshar, Head of the Sainte-Anne Neurology Department.

In an experimental study published in the journalBrain, a team of scientists from the Institut Pasteur (Perception and Memory laboratory) and clinicians from the Paris Psychiatry and Neurosciences University Hospital Group (GHU) (Neurological Resuscitation Department) used pharmacogenetic techniques to identify a dedicated neural circuit comprising the central nucleus of the amygdala and the bed nucleus of the stria terminalis.

The activation of this circuit in the first few hours of sepsis induces anxious behavior two weeks after the infection has cleared. This behavior observed in mice mimics the post-traumatic stress disorder observed in patients recovering from sepsis.

This discovery paves the way for new therapeutic strategies for sepsis: we observed that administering an agent capable of preventing the hyperactivation of this circuit reduces the risks of developing anxiety disorders, explains Professor Pierre-Marie Lledo, Institut Pasteur and CNRS. This effect is thought to be partly linked with reduced activation of the vagal afferent integration center.

This study is of particular interest because it identifies both a dedicated circuit for post-sepsis anxiety and a potential pharmacological treatment. The latter will soon be tested in a multicenter randomized therapeutic trial. By revealing the link between neuroinflammation and psychiatric disorders, this research resonates with the current context of the COVID-19 pandemic and long COVID.

Author: Burlet-Parendel AnneSource: Institut PasteurContact: Burlet-Parendel Anne Institut PasteurImage: The image is credited to Institut Pasteur/Mariana Alonso and Pierre-Marie Lledo

Original Research: Open access.Silencing of amygdala circuits during sepsis prevents the development of anxiety-related behaviors by Tarek Sharshar et al. Brain

Abstract

Silencing of amygdala circuits during sepsis prevents the development of anxiety-related behaviors

Sepsis is a life-threatening condition induced by a deregulated host response to severe infection. Post-sepsis syndrome includes long-term psychiatric disorders, such as persistent anxiety and post-traumatic stress disorder, whose neurobiological mechanisms remain unknown.

Using a reference mouse model of sepsis, we showed that mice that recovered from sepsis further developed anxiety-related behaviours associated with an exaggerated fear memory.

In the brain, sepsis induced an acute pathological activation of a specific neuronal population of the central nucleus of the amygdala, which projects to the ventral bed nucleus of the stria terminalis.

Using viral-genetic circuit tracing andin vivocalcium imaging, we observed that sepsis induced persistent changes in the connectivity matrix and in the responsiveness of these central amygdala neurons projecting to the ventral bed nucleus of the stria terminalis.

The transient and targeted silencing of this subpopulation only during the acute phase of sepsis with a viral pharmacogenetic approach, or with the anti-epileptic and neuroprotective drug levetiracetam, prevented the subsequent development of anxiety-related behaviours.

Specific inhibition of brain anxiety and fear circuits during the sepsis acute phase constitutes a preventive approach to preclude the post-infection psychiatric outcomes.

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When Severe Infection Causes Long-Term Mood Disorders - Neuroscience News

An analysis of neuroscience and psychiatry papers published from 2009 and 2019 outlines opportunities for increasing discovery of sex differences -…

Our survey of 3193 papers across six journals in neuroscience and psychiatry revealed some insights into the inclusion, use, and analyses of both sexes in research in the sample years, 2009 and 2019 (Fig.6). Most papers in our sample had studies that used both males and females in 2019, a 30% increase from 2009, irrespective of discipline. On the face of it, this is a positive indication of greater knowledge and awareness on the importance of sex and gender as variables in research. However, we found the majority of papers we sampled in 2019, did not use what we consider an optimal design or analysis for the discovery of possible sex differences. This is concerning, as scientific discovery will lose out on valuable information if researchers are neglecting to embrace the power of studying potential sex differences. Specifically, we determined that out of the total number of papers sampled that reported studies using both males and females, 16.5% reported using an optimal design for discovery of sex differences. Most of the sampled papers that used both sexes (75%) either did not specify sample size, used unequal proportions of the sexes, or used the sexes inconsistently within the studies in the paper and furthermore, 58% of these papers did not include an analysis by sex. Only 6% of the total number of papers reporting studies using both sexes included sex as a discovery variable, and this value was consistent across years and disciplines.

Optimal design refers to relatively based sample size and use of males and females consistently across the experiments whereas optimal analyses refers to the use of sex as a discovery variable. Although the percentage of studies in the sample of neuroscience and psychiatry papers analysed has increased the use of optimal design and analyses has not changed as much and remain at low levels. There are nine times the percentage of male-only compared to female-only studies.

Furthermore, the percentage of papers reporting studies using optimal designs or analyses for discovery of sex differences has not meaningfully shifted between 2009 and 2019 across either discipline, despite the number of recent initiatives such as SABV, SGBA and SAGER14,16,31. It is possible that these percentages will increase with time as these mandates are relatively recent. These findings should serve as a reminder to researchers, funders and publishers, that if we are to harness the wealth of knowledge from studying the sexes, more needs to be done to improve the appropriate application of sex in reporting and analyses for discovery.

As noted, there has been an increase in the reporting of both sexes in both psychiatry and neuroscience papers in our sample to almost 70% in 2019 from 20% in 2009. The neuroscience sample showed a 50% increase in reporting the use of both sexes over the years whereas the increase between 2019 and 2009 was only 10% in the psychiatry sample. This difference between the disciplines is likely driven by the majority of papers in the psychiatry sample using humans as participants, which may be a direct result of an earlier (2001) NIH mandate to include males and females in clinical research. The majority of neuroscience and psychiatry papers in our sample reported studies that used both sexes in 2019, which is encouraging. Our finding of a 50% increase in the 2019 neuroscience sample compared to 2009 sample is higher than previous work22,23, indicating an upward trend over the years sampled. For example, past research sampling neuroscience papers reporting the use of both sexes has found an almost 20% increase between 2010201425 and a 34% increase across the same time points assessed here22. In addition, the 68% of papers reporting studies that included males and females in 2019 in our study is higher than the 52% of neuroscience papers reporting the use of both sexes in 201723, againlikely reflecting an upward trend across years. The large progress made in neuroscience across the 10 years was also noted by Woitowich22 who reported an increase to 63% in 2019 using a sampling of 20 articles from 4 journals, two of which overlapped with ours (Journal of Neuroscience and Nature Neuroscience). In the present work we sampled from 3 journals in neuroscience, similar to Meitzen and colleagues23,27 who sampled neuroscience papers in 6 journals, 3 of which overlapped with the journals we chose (Nature Neuroscience, Neuron, Journal of Neuroscience). Thus, collectively, multiple studies, using different journals and methods of sampling, consistently indicate that there is an increasing trend in papers that include males and females in their work.

Although the use of both males and females in research has been steadily increasing to include a majority of studies, research highlighting or mentioning sex differences is scarce. Why might this be? We examined whether papers were reporting studies that used optimal designs for discovery of possible sex differences. When we accounted for papers in our sample that did not disclose sample size of the sexes, used an unbalanced design or did not use both sexes throughout all the studies within the paper, we found that only 16% of papers used a design that was optimal for discovery of sex differences. Some researchers may argue that investigating both males and females is only important in the first study of the paper and thus the use of both sexes in further experiments, beyond the initial study is not required. However, there are numerous examples where a trait may not show sex differences but the neural mechanisms underlying that trait do show significant differences between males and females32,33,34,35. Thus, using males and females in one experiment does not preclude the fact that sex differences may be seen in further related experiments that uncover mechanism. The use of what we consider to be the most advantageous design for discovery of sex differences was employed in just under 20% of papers sampled in 2019. Thus, although it appears on the face of it that most papers sampled report studies using males and females, the majority of these studies do not incorporate sex in a design that we consider optimal for discovery of possible sex differences.

Our findings also demonstrated that 25% of the papers sampled that report studies using both males and females do not report sample size, consistent with the findings from Woitowich and colleagues22. Perhaps more concerning is that in the neuroscience papers sampled, this trend increased between 2009 to 2019 with almost 50% not reporting the sample size of males and females used in 2019. This trend is troubling as readers are unable to judge how effectively males and females were used in the study.

As others have reported21,22,23,26,27, most publications do not report studies that analyse by sex. In our analysis, only 6% of the papers in our total sample that reported studies that used males and females also used sex as a discovery variable, which did not increase in the 2019 compared to the 2009 sample. This translates into only 4% of all the publications examined in our sample from both years and both disciplines that used sex as a discovery variable, matching a previous estimate21. The most common statistical method for analysing sex that was used by papers in our sample was controlling for sex using a covariate. A covariate removes the linear association of the factor of sex against the dependent variable, removing any linear variation due to sex. In our view, this is in opposition to the intention of SABV or SGBA, as we believe that the goal of these mandates is not to remove the variation due to sex but to determine whether or not sex is a variable that could be causing differences in outcomes. The use of sex as a covariate can result in the reduction of power and the loss of important information when a sex difference is present36. Mersha and colleagues36 show that 26 more single-nucleotide polymorphisms (SNPs) were identified in a sex-stratified analysis compared to when sex was used as a covariate. Put another way, when sex was used as a discovery variable 47 SNPs were identified that were associated with asthma but if sex was used as a covariate only 21 SNPs were identified36. They also found that effect sizes were larger when a sex-stratified analysis was used, contrary to popular opinion that power would be negatively affected with the addition of sex as a discovery variable. Some argue that design and sample sizes are not sufficiently powered to consider sex-stratified analyses, but if the sex effects are large, or in opposing directions, the resulting power with the inclusion of sex as a discovery variable, will improve as others have demonstrated25,26,36,37. Taken together, our survey of the literature suggests that researchers are underestimating the power of using sex as a discovery variable in their research.

Similar to other reports in neuroscience and other biological disciplines23,24,27,37, we found that papers we identified as female-only (i.e., reporting studies that used females only) were a small percentage of the sample (3%)38,39. Our findings are comparable with others showing that 5% of neuroscience papers sampled were female-only in 200937 and in 201723. While the consideration of sex and gender in studies is important, in our view, single-sex studies are still needed. In particular, given the dearth of information on womens health, disparities in diagnosis7, and continued underrepresentation of women in clinical trials13, one could argue that female-only studies are needed more so than male-only studiesor at least that single-sex studies should be conducted and published in equivalent proportions. Indeed, mandates such as SABV and SGBA were instigated in part because of the lack of knowledge of how females differed in their response to treatments and disease17. There are female-specific experiences that affect female health, such as menstruation, hormonal contraceptives, pregnancy and menopause that need to be studied40,41,42,43. Unfortunately, as highlighted by the current study, the percentage of papers that use only females remains consistently low and has not increased in 2019 compared with 2009 in our sample. Funders and researchers should work to correct this imbalance.

Our current study indicated that the rationale for excluding females used most often was to reduce variability. To exclude females based on greater variation than males is not valid, as two studies have found that the within-sex variability, on a variety of measures, is not statistically different between males and females in rats and mice44,45. Moreover, our findings and others37, reveal that it is a common belief that females will have more variability due to their hormones, however it is important to note that both males and females have diurnal fluctuations in cortisol or corticosterone in humans and rodents, respectively46,47. Furthermore, human males have diurnal fluctuations in testosterone levels that vary significantly with age46 Researchers should be encouraged to consider that many hormones vary with diet, age, housing conditions, and experience across both sexes48,49,50. Thus, variability within females should not be considered a limiting factor to the use of females in research51.

There have been calls in the literature for editors and reviewers of manuscripts to ensure that published reports use both males and females and report on outcomes51. SAGER guidelines were developed by the European Association of Science Editors to improve sex and gender in research reporting in 201631, and indeed, some journals have adopted SAGER guidelines including over 500 Elsevier journals52. Among the guidelines, it is recommended that authors include the sex or gender in the title and abstract, background information on sex and gender effects on the variables of interest in the paper and in the results to disaggregate and analyse the data by sex or gender. However, the percentage of journals that have adopted SAGER is low with one study finding under 10% of journals in psychology had adopted the guidelines53 and in those journals the guidelines were only adopted for the title, abstract and methods but not on reporting of analyses or data by sex or gender53. However, as can be seen from the present data, the publishing of this information, particularly with respect to the analyses of sex as a discovery variable is limited, and a more concerted effort needs to be adopted.

We note several limitations to this work. We only examined three journals for each of the two disciplines, however we did a comprehensive search of eligible research papers within each journal, culminating in over 3000 papers reviewed. Previous studies have either surveyed 841 articles across the same 2 years22 or examined 6000 articles across 4 years27. We, like others27, selected journals based on high ranking by ISI, with some overlap in journals chosen. However, our comprehensive search of these six journals gave values that were not appreciably different from those that used fewer papers within more journals, or those that carried out analysis of more publication years. This suggests that the different survey methods used across these bodies of work yield similar results.

A final consideration is that for biomedical research at NIH, the SABV consideration was instituted in 2016, which may not have given enough time to fully realise the potential in the 2019 sample examined. However, the fact that, in the neuroscience journals sampled here, there was a 70% increase in 2019 in the percentage of papers with studies using both males and females, suggests there is greater inclusion of studies using males and females. However, this increased use of both sexes in studies is unfortunately not yet resulting in using sex as a discovery variable in analyses.

Given that there is excellent uptake in the use of both males and females in research, what is driving the lack of optimal design and analyses for discovery of sex differences? It seems possible that researchers themselves are not aware that they are not using best practices, perhaps due to the lack of consensus on how to use sex in analyses and the required sample size in the literature17. In one manuscript on this topic it was reported that three-quarters of researchers say they report the sex in their papers54, and 50% of these researchers said they analysed their findings by sex54. Our results from the literature survey show that although 40% of papers we sampled included analysis by sex in some fashion, only 6% used sex as a discovery variable. Taken together, the findings here, along with prior data5, suggest that researchers may be considering analyses that are suboptimal or not reporting analyses even when they have done them. Thus, it is possible that researchers believe that the addition of both sexes without thorough analyses is enough to satisfy the initiatives.

Researchers themselves may need more training in sex and gender analyses. Qualitative analyses from structured interviews with US-based researchers55 found that while researchers indicated they had a good knowledge of SABV they incorrectly used the terms sex and gender when discussing their views, indicating a lack of knowledge. The misuse of the terms sex and gender has also been noted in grant submissions as well as in the biological literature56,57,58. Gender is a psychosocial construct that includes gender identity and societal expectations for roles and behaviour based on gender identity. Gendered effects can be realised when considering a number of intersectional variables, such as race, ethnicity or age, along with sex and gender identity59. Thus, perhaps more training for researchers may be needed to ensure fruitful addition of sex and gender in research.

One could argue that the mandates do not go far enough and are limited to a few agencies in the EU, Canada, and the US. There are also no repercussions when authors do not publish or analyse by sex. Indeed, NIH funding did not significantly affect the percentage of papers that reported studies that analysed by sex with a net increase of just 3% (to 9%) overall23. Our data indicate that there is a non-significant increase in the sampled papers that reported studies that used sex as a discovery variable from research groups based in the US, Canada, and the EU in the 2019 sample studied compared with 2009, pointing to an overall potential benefit of the current mandates that exist in those countries. However, it is important to underscore that the percentage of these papers was low even when the research groups were based in those countries, and that there are no reporting requirements from these funding agencies.

What can funders do to promote more work on sex differences? One solution is to have funding dedicated specifically for SABV and SGBA proposals and not as a supplement to regular funding. Evidence suggests that this approach has been successful in cardiovascular research. For example, the American Heart Association (US) has dedicated funding for sex differences, and as a result sex and gender-based research and analyses in cardiovascular disease has flourished60. Our view is that funders should make these funds a significant portion of the budget to provide enough incentive to encourage researchers to think deeply about incorporation of sex in research. Dedicated funding would not only generate proposals and knowledge dedicated to the analyses of sex differences, but they would also have the by-product of creating the next generation of researchers that integrate sex into their research. One can also look at how significant funding to amyotrophic lateral sclerosis (ALS) and AIDS has advanced research in these areas. In 2014, the ice bucket challenge raised greater than $115M in the US and this attention leveraged dedicated funding from other sources tripling ALS research budgets in 5 years61. This bolus of funding doubled the number of ALS publications, led to a 50% increase in investigators interested in ALS, and has dramatically accelerated the number of clinical trials in ALS62. Scientific evidence takes time to build, but fruits of discovery with the increased funding are paying off with promising new treatments63. Its hard not to get excited about the possibilities if this type of funding is extended to fill the sex disparities in health research. AIDS research is another success story with dramatic advancements in AIDS research that came with dedicated funding. Worldwide HIV/AIDS research funding more than doubled from 2000 to 2019 to >1B64. With these dedicated funds have come advancements in therapeutics such that individuals with HIV can live relatively full lives65. To make significant progress, funders need to have dedicated funding for SABV, which would have a cascading effect to get more researchers interested in SABV, ensure consideration of sex and gender as discovery variables, increase the number of discoveries and train the next generation of SABV researchers.

What can publishers do to promote publications using sex-based analyses? When journals adopt SAGER guidelines, it is up to the authors, reviewers and editors to ensure the guidelines are met. In over a third of submissions to a neuroendocrinology journal, authors and reviewers failed to notice that neither sex nor gender had been disclosed66. This suggests, not surprisingly, that not every reviewer is prompted to think about the consideration of sex in experimental design and analyses upon reviewing a paper. Training modules from funders or scholarly organisations with an SABV focus may help, but working on a similar premise as above, enticing researchers to explore the influence of sex and gender in their data may be a more fruitful approach. If journals, especially those with higher visibility, adopt calls for papers using sex and gender-based analyses this may serve as a catalyst to ensure more researchers consider possible sex differences and further promote the notion that this research is important to publish.

Lastly, others have found that the presence of inferred-female first or last authors (inferred from names) was associated with the use and analyses of both sexes in research28,29 consistent with our own data. Recently, there have been concerted efforts to promote diversity in science67 and these findings suggest that increasing sex and gender diversity among authors of scientific research is another fruitful path to improve the percentage of papers reporting use of sex as a discovery factor in analyses.

We hope these data are a call to the research community to not only include males and females in their research but to ensure appropriate methods of integration and analyses are used as well. If researchers are merely including a few animals of the opposite sex in one of many experiments this will not allow for discovery of the impact of sex as a biological variable. Nor will the non-robust adoption of sex in experiments harness the additional power that the analyses of sex can afford36. Research shows us that the use of sex as a discovery variable can lead to fruitful knowledge, and can enable conclusions that the different mechanisms between males and females require distinct treatment25. Indeed, inclusion of sex in analyses and design will improve not only the health of females but of males as well68. We lose collectively, not just in knowledge gained, but also in our search of more effective treatments when sex is not considered in the design and analyses of our studies. We call on funders, reviewers and researchers to recognise that sex and gender matter across all disciplines. The community needs to be aware that there are many types of sex differences19,69 and that some sex differences are revealed due to perturbations in environment, genotype, or disease19,70,71 so it is important to continually examine and analyse both sexes throughout the studies. It is imperative that more attention is paid to the appropriate design and analyses of sex and gender in the literature. We need to study how mandates can improve adherence in both study design and dissemination. To ensure precision medicine, we need the community of funders, researchers and publishers to embrace the addition of SABV, SGBA and SAGER to improve the health of women, men and gender-diverse individuals.

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An analysis of neuroscience and psychiatry papers published from 2009 and 2019 outlines opportunities for increasing discovery of sex differences -...

We Are More Satisfied With Life as We Age, Thanks to Oxytocin – Neuroscience News

Summary: A new study links higher levels of oxytocin to greater life satisfaction as we age.

Source: Frontiers

A new study has linked life satisfaction to the chemistry in our brains.

People that release more of the neurochemical oxytocin are kinder to others and tend to be more satisfied with their lives. In addition, oxytocin release increases with age, showing why, on average, people are more caring as they get older.

These findings are consistent with many religious philosophies, where satisfaction with ones life is enhanced by helping others.

People whose brains release more of the neurochemical oxytocin are kinder to others and are more satisfied with their lives. This is the finding of new research, published inFrontiers in Behavioral Neuroscience,that also discovered that oxytocin release increases with age, showing why, on average, people are more caring as they get older.

The findings of our study are consistent with many religions and philosophies, where satisfaction with ones life is enhanced by helping others, reported first author Dr Paul J Zak of Claremont Graduate University.

Participants in our study who released the most oxytocin were more generous to charity when given the opportunity and performed many other helping behaviors. The change in oxytocin was also positively related to participants empathy, religious participation, and gratitude.

Oxytocin

Oxytocin is a neurochemical widely known for its role in social attachment, interpersonal trust, and generosity. Zak and his colleagues wanted to understand if the release of oxytocin changed with age, as is found with some other neurochemicals that influence feelings and behaviors.

We have previously shown a link between how kind and generous people are, known as prosocial behaviors, and the release of oxytocin, said Zak.

Seniors spend more time volunteering and donate a larger proportion of their income to charity than do younger people, so we wanted to see if there was a neurochemical basis for these behaviors.

The researchers recruited more than 100 people for the study, ranging between the ages of 18 and 99. They were each shown a video about a little boy with cancer, which previous work had confirmed to induce oxytocin release in the brain. Blood was taken before and after the video to measure the change in oxytocin.

Participants had the option to donate some of their earnings from the study to a childhood cancer charity, and this was used to measure their immediate prosocial behavior. We also collected data on their emotional states, to provide information on their overall satisfaction with life, explained Zak.

Be kind, love life

People who released the most oxytocin in the experiment were not only more generous to charity, but also performed many other helping behaviors. This is the first time a distinct change in oxytocin has been related to past prosocial behaviors, reported Zak.

We also found that the release of oxytocin increased with age and was positively associated with life satisfaction.

The finding that helping behaviors improve the quality of life is consistent with many faith traditions and philosophies. Serving others appears to prime the brain to release more oxytocin in a positive feedback loop of increased empathy and gratitude.

Zak would like to repeat this study in a more ethnically and geographically diverse sample of people to see if the findings hold for different cultures.

We would also like to conduct a longer-term measurement of neurophysiology using noninvasive wearable technologies to see what specific activities raise peoples satisfaction with life, he concluded.

Author: Suzanna BurgelmanSource: FrontiersContact: Suzanna Burgelman FrontiersImage: The image is in the public domain

Original Research: Open access.Oxytocin Release Increases With Age and Is Associated With Life Satisfaction and Prosocial Behaviors by Paul J Zak et al. Frontiers in Behavioral Neuroscience

Abstract

Oxytocin Release Increases With Age and Is Associated With Life Satisfaction and Prosocial Behaviors

Helping behaviors and life satisfaction generally increase after middle-age. Identifying the neural substrates of prosocial behaviors in older adults may offer additional insights into these changes over the lifespan.

The present study examines the endogenous release of the neuromodulator oxytocin (OT) in participants aged 1899 and its relationship to prosocial behaviors. OT has been shown to influence trust, altruism, charity, and generosity, yet the effect of age on OT release has not been well-established.

Blood samples before and after a video stimulus were obtained from 103 participants in order to examine the impact of OT on prosocial behaviors.

We found that OT release following a social prime increased with age (r= 0.49,p= 0.001) and that OT moderated the relationship between age and donations to charity.

We tested for robustness by examining three additional prosocial behaviors, money and goods donated to charity during the past year and social-sector volunteering. OT moderated the impact of age on all three prosocial behaviors (ps< 0.05).

The analysis also showed that participants change in OT was positively associated with satisfaction with life (p= 0.04), empathic concern (p= 0.015), dispositional gratitude (p= 0.019), and religious commitment (p= 0.001).

Our findings indicate that the neural chemistry that helps sustain social relationships and live a fulfilled life appear to strengthen with age.

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Psychopaths Can Feel Emotions and Can Be Treated – Neuroscience News

Summary: Contrary to popular belief, those suffering from psychopathy are able to experience emotions, but they do have a blunted emotional response if their attention is directed toward something else. In essence, psychopaths feel emotions, but ignore them if they feel they might interfere with attaining personal goals.

Source: The Conversation

On any given day, millions of Americans curl up to watch their favorite crime shows. Whether it is FBI on CBS, Dexter on Showtime, Mindhunter on Netflix, Killing Eve on BBC, reruns of Law & Order, or any of a myriad of other similar shows, they draw huge audiences with their vivid portrayals of villains whose behaviors are perplexingly cruel. Ill confess: I am part of that audience. My students even make fun of how much crime television I, aresearcher who studies criminal behavior, watch.

I justify some of my TV time as work, providing material for my undergraduate lecture course and for my seminars on the nature of the criminal mind. But I am also captivated by the characters in these dramas, despite or because of how unrealistic many of them are.

One of the most common character types on crime TV is the psychopath: the person who commits brutal murders, acts recklessly and sits stone-cold in front of law enforcement officers. Although the shows are obviously fiction, their plotlines have become familiar cultural touchstones.

People watch Agent Hotchner on Criminal Minds label any character who is disturbingly violent as someone with psychopathy. They hear Dr. Huang on Law & Order: SVU refer to a youthful offender who hurt a young girl as an adolescent with psychopathy who he suggests is incapable of responding to treatment.

Such portrayals leave viewers with the impression that individuals with psychopathy are uncontrollably evil, unable to feel emotions, and incorrigible.

But extensive research, including years of work in my ownlab, demonstrates that the sensationalized conceptions of psychopathy used to drive those narratives are counterproductive and just plain wrong.

Psychopathy isclassified by psychologistsas a personality disorder defined by a combination of charm, shallow emotions, absence of regret or remorse, impulsivity and criminality. About 1% of the general population meets the diagnostic criteria of psychopathy, a prevalence roughly twice that of schizophrenia.

The exact causes of psychopathy have not been identified, but most scholars conclude that bothgenetics and environmentare contributing factors.

Psychopathy imposes ahigh coston individuals and on society as a whole.

People with psychopathy commit two to three times as much crime overall as others who engage in antisocial behavior and account for roughly 25% of the incarcerated population. They also commit new crimes after being released from incarceration or supervision at amuch higher ratethan other types of offenders.

My colleagues and I have found that people with psychopathy tend tostart using substancesat an earlier age and try more types of substances than others. There also is some evidence that people with psychopathy tendnot to respond wellto conventional therapeutic strategies.

Reality is significantly more nuanced and encouraging than the grim media narratives. Contrary to most portrayals, psychopathy is not synonymous with violence. It is true that individuals with psychopathy are more likely to commit violent crime than are individuals without the disorder, but violent behavior is not a requirement for a diagnosis of psychopathy.

Someresearchersargue that key traits of psychopathy are present in individuals who show no violent behavior but who tend toward impulsive and risky behaviors, take advantage of others and show little concern for the consequences of their actions. Those traits can be observed in politicians, CEOs and financiers.

Many crime shows, as well as many mainstream news stories, associate psychopathy with a lack of emotion, particularly of fear or remorse. Whether a character is standing calmly over a lifeless body or giving the classic psychopathic stare, viewers are accustomed to seeing people with psychopathy as almost robotic. The belief that people with psychopathy are emotionless is widespread not only among laypeople but among psychologists as well.

There is an element of truth here: Considerableresearchhas found that individuals with psychopathy exhibit a reduced ability to process emotions and to recognize the emotions of others. But my colleagues and I are finding evidence that individuals with psychopathy actually can identify and experience emotions under the right circumstances.

In my lab, we are conducting experiments that reveal a complex relationship between psychopathy and emotions.

In onestudy, we examined the supposed lack of fear of individuals with psychopathy using a simple lab test. We showed a group of participants the letter n and colored boxes on a screen. Seeing a red box meant a participant might get an electric shock; green boxes meant that they would not. The color of the box therefore signaled a threat.

As a brief aside, the shocks were not harmful, just slightly uncomfortable, and this study was approved by appropriate human subject protection review boards.

On some trials, we asked the participant to tell us the color of the box (forcing them to focus on the threat). On other trials, we asked the participant to tell us the case of the letter (forcing them to focus on the nonthreat), although the box was still displayed.

We could see that individuals with psychopathy displayed fear responses based on theirphysiologicalandbrainreactions when they had to focus on the shock threat.

However, they showed a deficit in fear responses when they had to tell us the case of the letter and the box was secondary to that task. Evidently, individuals with psychopathy are capable of experiencing emotion; they just have a blunted emotional response when their attention is directed toward something else.

This is an extreme version of the kind of processing we all do. In routine decision-making, we rarely focus explicitly on emotion. Rather, we use emotional information as a background detail that informs our decisions.

The implication is that individuals with psychopathy have a kind of mental myopia: The emotions are there, but they are ignored if they might interfere with attaining a goal.

Research in my lab and in others has uncovered additional evidence that individuals with psychopathy are capable of experiencing and labeling emotions in the context ofobserving emotionalscenesorfaces, thepainofothers,andexperiences of regret. Here, too, individuals with psychopathy are able to process emotion when focusing on the emotion, but they display deficits when emotion is hard to detect or is secondary to their objective.

Manystudieshave shown that individuals with psychopathy are great at using information and regulating their behavior if it is directly relevant to their objective; for instance, they can act charming and ignore emotions to con someone. But when information is beyond their immediate focus of attention, they often display impulsive behavior (such as quitting a job without a new one lined up) and egregious decision-making (such as seeking publicity for a crime while they are wanted by police).

They have difficulty processing emotion, but unlike the common characters on television, they are not inherently cold-blooded.

The image of the fearless killer draws on an outdated scientific conception of psychopathy. Instead, it appears that people with psychopathy can access emotions the emotional information just gets stifled by the focus on goals.

One of the most damaging fallacies about psychopathy in fiction, in the news and in some of the old scientific literature is that it is a permanent, unchanging condition. This idea reinforces the compelling good-versus-evil trope, but the latest research tells a quite different story.

Traits of psychopathy naturally decrease over time for many young people, starting in late adolescence into adulthood. Samuel Hawes, a psychologist at Florida International University, and his collaboratorstracked more than 1,000 individualsfrom childhood to adulthood, repeatedly measuring their traits of psychopathy.

Although a small group showed persistently high levels of psychopathic traits, more than half of the boys who initially had high levels of those traits trended downward over time and no longer presented with them later in adolescence.

With proper intervention, the prospects for improvement get better. We are finding thatyouths with traits of psychopathyand adults with psychopathy can change and respond to treatments that are tailored to their needs.

Several studies have documented the effectiveness ofspecific treatmentsdesigned to help youths learn to identify and respond to emotions. Parenting interventions that focuses on enhancing the emotional warmth of the caregiver and helping youths identify emotions seems to reduce symptoms and problematic behavior.

In a series of experiments, we have been investigating video games designed totrain the brainsof individuals with psychopathy by helping them improve the way they integrate information.

For example, we show a group of participants a face and instruct them to respond on the basis of the emotion they see and the direction in which the eyes are looking, coaching them to integrate all features of the face. Or we play a game in which we show participants a series of cards and see if they can pick up when we shift the rules, switching which one is a winning or losing card. The participants are not told when the shift will happen, so they have to learn to pay attention to subtle contextual changes as they go.

Our preliminary data shows that lab-based tasks like these can change the brains and real-world behavior of individuals with psychopathy.

Such studies open the possibility of reducing the social and personal harm caused by psychopathy. I believe society needs to retire the myths that individuals with psychopathy are fundamentally violent, emotionless and incapable of change.

The behavior of individuals with psychopathy is fascinating so much so that it does not need to be embellished to make for dramatic plotlines. We should work harder to aid individuals with psychopathy so that they can notice more information in their environment and use more of their emotional experience. Pop culture can help rather than hinder those goals.

Author: Arielle Baskin-SommersSource: The ConversationContact: Arielle Baskin-Sommers The ConversationImage: The image is in the public domain

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Psychopaths Can Feel Emotions and Can Be Treated - Neuroscience News

MIVI Neuroscience Launches Largest Study Yet of its Aspiration Catheter for Thrombus Removal – Diagnostic and Interventional Cardiology

April 21, 2022 MIVI Neuroscience, Inc., innovator of the next generation of neurointerventional medical devices, today announced the first patient enrollments in a multicenter clinical study to assess the safety and performance of the Q Aspiration Catheter used in a combined aspiration with stent-retriever technique for thrombus removal in patients who have suffered an acute ischemic stroke.

The AQUAS Registry is a prospective registry of 250 subjects conducted across up to 12 high-volume, comprehensive stroke centers in Europe. It is the largest study of a MIVI device to date. The study is expected to conclude within 12 months.

In the United States, approximately 50% of ischemic stroke interventions employ a combined technique; the other 50% use only an aspiration catheter. In both cases, we want the physician to reach for the Q Aspiration Catheter because it offers the highest aspiration power available and a simpler setup, said Bob Colloton, CEO of MIVI Neuroscience. This registry is a massive undertaking, involving a large group of stroke experts, patients, and two important partners: study organizer Angionautix and Acandis, manufacturer of the stent retriever that will be used with our catheter. We believe that the Q Aspiration Catheter is the physicians best choice, and the AQUAS Registry will provide us with additional data on its safety and performance.

Led by Dr. Sebastian Remollo Friedemann of Hospital Universitari Germans Trias I Pujol in Barcelona, the registry will assess the safety and performance of the Q Aspiration Catheter combined with the Acandis Aperio stent-retriever in treating ischemic stroke patients.

The QAspiration Catheter is a powerful solution for stroke treatment, said Dr. Remollo. Im looking forward to solid evidence from the study that adds to my personal experience with the product and advancing the approach to thrombus removal.

The Q Aspiration Catheter is CE-marked in Europe and under Investigational Device Exemption in the United States.

For more information: http://www.mivineuro.com

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New 1.2 million funding to advance development of investigational MND drug – University of Sheffield News

Researchers from the University of Sheffield and early-stage biopharmaceutical company Aclipse Therapeutics have been awarded 1.2 million to support the development of an investigational motor neurone disease (MND) drug.

Researchers from the University of Sheffield and early-stage biopharmaceutical company Aclipse Therapeutics have been awarded 1.2 million to support the development of an investigational motor neurone disease (MND) drug.

The funding has been awarded from the Congressionally Directed Medical Research Programs (CDMRP) at the United States Department of Defenses (DOD) U.S. Army Medical Research and Development Command (USAMRDC), as part of its FY21 Amyotrophic Lateral Sclerosis Research Program (ALSRP) Therapeutic Development Award.

The award will fund research conducted at the Sheffield Institute for Translational Neuroscience (SITraN) to further develop M102 - a potentially disease-modifying drug candidate that has shown promise in impeding the progression of MND - also known as Amyotrophic Lateral Sclerosis (ALS) or Lou Gehrigs disease.

MND is highly relevant to the health of military service members and veterans. Since September 2001, more U.S. veterans have died from ALS (an estimated 9,500 to 10,000 deaths) than from U.S. combat deaths in Iraq and Afghanistan combined. Currently, there is no cure for the disease, and there are limited treatments to slow its progression.

Aclipse is taking a dual approach for the treatment of MND. M102 activates the NRF2 (nuclear factor erythroid 2-related factor 2) and HSF1 (Heat shock factor 1) signalling pathways, which are understood to impact MND pathophysiology. Based on preclinical results to date, M102 is expected to be mechanistically superior to currently available drugs and may lead to significant slowing of disease progression in patients with both familial and sporadic MND.

Professor Dame Pamela Shaw, Director of SITraN and primary contributor to M102s development programme, said: This development funding is wonderful news for MND/ALS patients who are in urgent need of effective therapies to address this life-threatening neurodegenerative disease.

Along with my SITraN colleagues and co-principal investigators, Professor Laura Ferraiuolo and Dr Richard Mead, we spearheaded the MND/ALS biology research that led to the identification and development of M102, including the discovery of a potential precision medicine approach for its use.

This funding will allow our team to expand development of precision medicine research and drive M102 into a Phase 1 trial. We are very excited and appreciative of the funding support awarded.

Raymond K. Houck, Chief Executive Officer of Aclipse Therapeutics, said: I believe that the award reflects the DODs appreciation of the significance of ALS to the military and their belief in our unique M102 drug candidate and approach to treating ALS patients. We are very grateful for their support.

Dr Ning Shan, Chief Scientific Officer of Aclipse Therapeutics and the awards principal investigator, said: This latest award, combined with ongoing financial backing from Australias FightMND and the United Kingdoms Medical Research Council, is allowing our team to accelerate the development of M102 toward first-in-human clinical studies, which is expected to initiate in 2023, and further validates M102s novel biology and our precision medicine approach.

This work was supported by the Office of the Assistant Secretary of Defense for Health Affairs endorsed by the Department of Defense, through the Amyotrophic Lateral Sclerosis Research Program, in the amount of $1,475,101, under Award No. W81XWH2210175. Opinions, interpretations, conclusions and recommendations are those of the author and are not necessarily endorsed by the Department of Defense.

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New 1.2 million funding to advance development of investigational MND drug - University of Sheffield News