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Summary: Oxytocin, a hormone connected with bonding and love, could help to heal damage following a heart attack. Researchers found oxytocin stimulates stem cells from the hearts outer layer and migrates into the middle layer where it develops into muscle cells that generate heart contractions. This could be used to promote the regeneration of heart cells following a heart attack.
Source: Frontiers
The neurohormone oxytocin is well-known for promoting social bonds and generating pleasurable feelings, for example from art, exercise, or sex. But the hormone has many other functions, such as the regulation of lactation and uterine contractions in females, and the regulation of ejaculation, sperm transport, and testosterone production in males.
Now, researchers from Michigan State University show that in zebrafish and human cell cultures, oxytocin has yet another, unsuspected, function: it stimulates stem cells derived from the hearts outer layer (epicardium) to migrate into its middle layer (myocardium) and there develop into cardiomyocytes, muscle cells that generate heart contractions. This discovery could one day be used to promote the regeneration of the human heart after a heart attack.
The results are published inFrontiers in Cell and Developmental Biology.
Here we show that oxytocin, a neuropeptide also known as the love hormone, is capable of activating heart repair mechanisms in injured hearts in zebrafish and human cell cultures, opening the door to potential new therapies for heart regeneration in humans, said Dr Aitor Aguirre, an assistant professor at the Department of Biomedical Engineering of Michigan State University, and the studys senior author.
Stem-like cells can replenish cardiomyocytes
Cardiomyocetes typically die off in great numbers after a heart attack. Because they are highly specialized cells, they cant replenish themselves. But previous studies have shown that a subset of cells in the epicardium can undergo reprogramming to become stem-like cells, called Epicardium-derived Progenitor Cells (EpiPCs), which can regenerate not only cardiomyocytes, but also other types of heart cells.
Think of the EpiPCs as the stonemasons that repaired cathedrals in Europe in the Middle Ages, explained Aguirre.
Unfortunately for us, the production of EpiPCs is inefficient for heart regeneration in humans under natural conditions.
Zebrafish could teach us how to regenerate hearts more efficiently
Enter the zebrafish: famous for their extraordinary capacity for regenerating organs, including the brain, retina, internal organs, bone, and skin. They dont suffer heart attacks, but its many predators are happy to take a bite out of any organ, including the heart so zebrafish can regrow their heart when as much as a quarter of it has been lost.
This is done partly by proliferation of cardiomyocytes, but also by EpiPCs. But how do the EpiPCs of zebrafish repair the heart so efficiently? And can we find a magic bullet in zebrafish that could artificially boost the production of EpiPCs in humans?
Yes, and this magic bullet appears to be oxytocin, argue the authors.
To reach this conclusion, the authors found that in zebrafish, within three days after cryoinjury injury due to freezing to the heart, the expression of the messenger RNA for oxytocin increases up to 20-fold in the brain.
They further showed that this oxytocin then travels to the zebrafish epicardium and binds to the oxytocin receptor, triggering a molecular cascade that stimulates local cells to expand and develop into EpiPCs.
These new EpiPCs then migrate to the zebrafish myocardium to develop into cardiomyocytes, blood vessels, and other important heart cells, to replace those which had been lost.
Similar effect on human tissue cultures
Crucially, the authors showed that oxytocin has a similar effect on human tissuein vitro. Oxytocin but none of 14 other neurohormones tested here stimulates cultures of human Induced Pluripotent Stem Cells (hIPSCs) to become EpiPCs, at up to twice the basal rate: a much stronger effect than other molecules previously shown to stimulate EpiPC production in mice.
Conversely, genetic knock-down of the oxytocin receptor prevented the the regenerative activation of human EpiPCs in culture. The authors also showed that the link between oxytocin and the stimulation of EpiPCs is the important TGF- signaling pathway, known to regulate the growth, differentiation, and migration of cells.
Aguirre said: These results show that it is likely that the stimulation by oxytocin of EpiPC production is evolutionary conserved in humans to a significant extent. Oxytocin is widely used in the clinic for other reasons, so repurposing for patients after heart damage is not a long stretch of the imagination. Even if heart regeneration is only partial, the benefits for patients could be enormous.
Aguirre concluded: Next, we need to look at oxytocin in humans after cardiac injury. Oxytocin itself is short-lived in the circulation, so its effects in humans might be hindered by that. Drugs specifically designed with a longer half-life or more potency might be useful in this setting.
Overall, pre-clinical trials in animals and clinical trials in humans are necessary to move forward.
Author: Mischa DijkstraSource: FrontiersContact: Mischa Dijkstra FrontiersImage: The image is in the public domain
Original Research: Open access.Oxytocin promotes epicardial cell activation and heart regeneration after cardiac injury by Aitor Aguirre et al. Frontiers in Cell and Developmental Biology
Abstract
Oxytocin promotes epicardial cell activation and heart regeneration after cardiac injury
Cardiovascular disease (CVD) is one of the leading causes of mortality worldwide, and frequently leads to massive heart injury and the loss of billions of cardiac muscle cells and associated vasculature.
Critical work in the last 2decades demonstrated that these lost cells can be partially regenerated by the epicardium, the outermost mesothelial layer of the heart, in a process that highly recapitulates its role in heart development.
Upon cardiac injury, mature epicardial cells activate and undergo an epithelial-mesenchymal transition (EMT) to form epicardium-derived progenitor cells (EpiPCs), multipotent progenitors that can differentiate into several important cardiac lineages, including cardiomyocytes and vascular cells.
In mammals, this process alone is insufficient for significant regeneration, but it might be possible to prime it by administering specific reprogramming factors, leading to enhanced EpiPC function.
Here, we show that oxytocin (OXT), a hypothalamic neuroendocrine peptide, induces epicardial cell proliferation, EMT, and transcriptional activity in a model of human induced pluripotent stem cell (hiPSC)-derived epicardial cells.
In addition, we demonstrate that OXT is produced after cardiac cryoinjury in zebrafish, and that it elicits significant epicardial activation promoting heart regeneration. Oxytocin signaling is also critical for proper epicardium development in zebrafish embryos.
The above processes are significantly impaired when OXT signaling is inhibited chemically or genetically through RNA interference. RNA sequencing data suggests that the transforming growth factor beta (TGF-) pathway is the primary mediator of OXT-induced epicardial activation.
Our research reveals for the first time an evolutionary conserved brain-controlled mechanism inducing cellular reprogramming and regeneration of the injured mammalian and zebrafish heart, a finding that could contribute to translational advances for the treatment of cardiac injuries.
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Love Hormone Oxytocin Could Mend a Broken Heart - Neuroscience News
Summary: SARS_CoV_2, the virus responsible for COVID-19 infects and replicates in astrocytes, reducing neural viability.
Source: FAPESP
A Brazilian study published in the journalPNASdescribes some of the effects infection by SARS-CoV-2 can have on the central nervous system.
A preliminary version (not yet peer-reviewed) posted in 2020 was one of the first to show that the virus that causes COVID-19 can infect brain cells, especially astrocytes. It also broke new ground by describing alterations in the structure of the cortex, the most neuron-rich brain region, even in cases of mild COVID-19.
The cerebral cortex is the outer layer of gray matter over the hemispheres. It is the largest site of neural integration in thecentral nervous systemand plays a key role in complex functions such as memory, attention, consciousness, and language.
The investigation was conducted by several groups at the State University of Campinas (UNICAMP) and the University of So Paulo (USP). Researchers at the Brazilian Biosciences National Laboratory (LNBio), DOr Institute (IDOR) and the Federal University of Rio de Janeiro (UFRJ) also contributed to the study.
Two previous studies detected the presence of the novel coronavirus in the brain, but no one knew for sure if it was in the bloodstream,endothelial cells[lining the blood vessels] or nerve cells. We showed for the first time that it does indeed infect and replicate in astrocytes, and that this can reduce neuron viability, Daniel Martins-de-Souza, one of the leaders of the study, told Agncia FAPESP. Martins-de-Souza is a professor at UNICAMPs Biology Institute and a researcher affiliated with IDOR.
Astrocytes are the most abundant central nervous system cells. Their functions include providing biochemical support and nutrients for neurons; regulating levels of neurotransmitters and other substances that may interfere with neuronal functioning, such as potassium; maintaining the blood-brain barrier that protects the brain from pathogens and toxins; and helping to maintain brain homeostasis.
Infection of astrocytes was confirmed by experiments using brain tissue from 26 patients who died of COVID-19. The tissue samples were collected during autopsies conducted using minimally invasive procedures by Alexandre Fabro, a pathologist and professor at the University of So Paulos Ribeiro Preto Medical School (FMRP-USP). The analysis was coordinated by Thiago Cunha, also a professor in FMRP-USP and a member of the Center for Research on Inflammatory Diseases (CRID).
The researchers used a technique known as immunohistochemistry, a staining process in which antibodies act as markers of viral antigens or other components of the tissue analyzed.
For example, we can insert one antibody into the sample to turn the astrocytes red on binding to them, another to mark the SARS-CoV-2 spike protein by making it green, and a third to highlight the viruss double-stranded RNA, which only appears during replication, by turning it magenta, Martins-de-Souza explained.
When the images produced during the experiment were overlaid, all three colors appeared simultaneously only in astrocytes.
According to Cunha, the presence of the virus was confirmed in five of the 26 samples analyzed. Alterations suggesting possible damage to the central nervous system were also found in these five samples.
We observed signs of necrosis and inflammation, such as edema [swelling caused by a buildup of fluid], neuronal lesions and inflammatory cell infiltrates, he said.
The capacity of SARS-CoV-2 to infect brain tissue and its preference for astrocytes were confirmed by Adriano Sebolella and his group at FMRP-USP using the method of brain-derived slice cultures, an experimental model in which human brain tissue obtained during surgery to treat neurological diseases such as drug-refractory epilepsy, for example, is cultured in vitro and infected with the virus.
Persistent symptoms
In another part of the research, conducted in UNICAMPs School of Medical Sciences (FCM), 81 volunteers who had recovered from mild COVID-19 were submitted to magnetic resonance imaging (MRI) scans of their brains.
These scans were performed 60 days after diagnostic testing on average. A third of the participants still had neurological or neuropsychiatric symptoms at the time. They complained mostly of headache (40%), fatigue (40%), memory alterations (30%), anxiety (28%), loss of smell (28%), depression (20%), daytime drowsiness (25%), loss of taste (16%) and low libido (14%).
We posted a link for people interested in participating in the trial to register, and were surprised to get more than 200 volunteers in only a few days. Many were polysymptomatic, with widely varying complaints. In addition to the neuroimaging exam, theyre being evaluated neurologically and taking standardized tests to measure performance in cognitive functions such as memory, attention and mental flexibility. In the article we present the initial results, said Clarissa Yasuda, a professor and member of the Brazilian Research Institute for Neuroscience and Neurotechnology (BRAINN).
Only volunteers diagnosed with COVID-19 by RT-PCR and not hospitalized were included in the study. The assessments were carried out after the end of the acute phase, and the results were compared with data for 145 healthy uninfected subjects.
The MRI scans showed that some volunteers had decreased cortical thickness in some brain regions compared with the average for controls.
We observed atrophy in areas associated, for example with anxiety, one of the most frequent symptoms in the study group, Yasuda said. Considering that the prevalence of anxiety disorders in the Brazilian population is 9%, the 28% we found is an alarmingly high number. We didnt expect these results in patients who had had the mild form of the disease.
In neuropsychological tests designed to evaluate cognitive functioning, the volunteers also underperformed in some tasks compared with the national average. The results were adjusted for age, sex and educational attainment, as well as the degree of fatigue reported by each participant.
The question were left with is this: Are these symptoms temporary or permanent? So far, weve found that some subjects improve, but unfortunately many continue to experience alterations, Yasuda said.
Whats surprising is that many people have been reinfected by novel variants, and some report worse symptoms than they had since the first infection. In view of the novel virus, we see longitudinal follow-up as crucial to understand the evolution of the neuropsychiatric alterations over time and for this understanding to serve as a basis for the development of targeted therapies.
Energy metabolism affected
In IB-UNICAMPs Neuroproteomics Laboratory, which is headed by Martins-de-Souza, experiments were performed on brain tissue cells from people who died of COVID-19 and astrocytes cultured in vitro to find out how infection by SARS-CoV-2 affects nervous system cells from the biochemical standpoint.
The autopsy samples were obtained via collaboration with the group led by Paulo Saldiva, a professor at the University of So Paulos Medical School (FM-USP). The proteome (all proteins present in the tissue) was mapped using mass spectrometry, a technique employed to identify different substances in biological samples according to their molecular mass.
When the results were compared with those of uninfected subjects, several proteins with altered expression were found to be abundant in astrocytes, which validated the findings obtained by immunohistochemistry, Martins-de-Souza said.
We observed alterations in various biochemical pathways in the astrocytes, especially pathways associated withenergy metabolism.
The next step was to repeat theproteomic analysisin cultured astrocytes infected in the laboratory. The astrocytes were obtained from induced pluripotent stem cells (iPSCs). The method consists of reprogramming adult cells (derived from skin or other easily accessible tissues) to assume a stage of pluripotency similar to that of embryo stem cells.
This first part was conducted in the IDOR laboratory of Stevens Rehen, a professor at UFRJ. Martins-de-Souzas team then used chemical stimuli to make the iPSCs differentiate into neural stem cells and eventually into astrocytes.
The results were similar to those of the analysis of tissue samples obtained by autopsy in that they showed energy metabolism dysfunction, Martins-de-Souza said.
We then performed a metabolomic analysis [focusing on the metabolites produced by the cultured astrocytes], which evidenced glucose metabolism alterations. For some reason, infected astrocytes consume more glucose than usual, and yet cellular levels of pyruvate and lactate, the main energy substrates, decreased significantly.
Lactate is one of the products of glucose metabolism, and astrocytes export this metabolite to neurons, which use it as an energy source. The researchers in vitro analysis showed that lactate levels in the cell culture medium were normal but decreased inside the cells. Astrocytes appear to strive to maintain the energy supply to neurons even if this effort weakens their own functioning, Martins-de-Souza said.
As an outcome of this process, the functioning of the astrocytes mitochondria (energy-producing organelles) was indeed altered, potentially influencing cerebral levels of such neurotransmitters as glutamate, which excites neurons and is associated with memory and learning, or gamma-aminobutyric acid (GABA), which inhibits excessive firing of neurons and can promote feelings of calm and relaxation.
In another experiment, we attempted to culture neurons in the medium where the infected astrocytes had grown previously and measured a higher-than-expected cell death rate. In other words, this culture medium conditioned by infected astrocytes weakened neuron viability, Martins-de-Souza said.
The findings described in the article confirm those of several previously published studies pointing to possible neurological and neuropsychiatric manifestations of COVID-19.
Results of experiments on hamsters conducted at the Institute of Biosciences (IB-USP), for example, reinforce the hypothesis that infection by SARS-CoV-2 accelerates astrocyte metabolism and increases the consumption of molecules used to generate energy, such as glucose and the amino acid glutamine.
The results obtained by the group led by Jean Pierre Peron indicate that this metabolic alteration impairs the synthesis of a neurotransmitter that plays a key role in communication among neurons.
Unanswered questions
According to Martins-de-Souza, there is no consensus in the scientific literature on how SARS-CoV-2 reaches the brain.
Some animal experiments suggest the virus can cross the blood-brain barrier. Theres also a suspicion that it infects the olfactory nerve and from there invades the central nervous system. But these are hypotheses for now, he said.
One of the discoveries revealed by thePNASarticle is that the virus does not use the protein ACE-2 to invade central nervous system cells, as it does in the lungs.
Astrocytes dont have the protein in their membranes. Research by Flvio Veras [FMRP-USP] and his group shows that SARS-CoV-2 binds to the protein neuropilin in this case, illustrating its versatility in infecting different tissues, Martins-de-Souza said.
At UNICAMPs Neuroproteomics Laboratory, Martins-de-Souza analyzed nerve cells and others affected by COVID-19, such as adipocytes, immune system cells and gastrointestinal cells, to see how the infection altered the proteome.
Were now compiling the data to look for peculiarities and differences in the alterations caused by the virus in these different tissues. Thousands of proteins and hundreds of biochemical pathways can be altered, with variations in each case. This knowledge will help guide the search for specific therapies for each system impaired by COVID-19, he said.
Were also comparing the proteomic differences observed inbrain tissuefrom patients who died of COVID-19 with proteomic differences weve found over the years in patients with schizophrenia. The symptoms of both conditions are quite similar. Psychosis, the most classic sign of schizophrenia, also occurs in people with COVID-19.
The aim of the study is to find out whether infection by SARS-CoV-2 can lead to degeneration of the white matter in the brain, made up mainly of glial cells (astrocytesand microglia) and axons (extensions of neurons).
Weve observed a significant correspondence [in the pattern of proteomic alterations] associated with the energy metabolism and glial proteins that appear important in both COVID-19 and schizophrenia. These findings may perhaps provide a shortcut to treatments for the psychiatric symptoms of COVID-19, Martins-de-Souza pondered.
Marcelo Mori, a professor at IB-UNICAMP and a member of the Obesity and Comorbidities Research Center (OCRC), the study was only possible thanks to the collaboration of researchers with varied and complementary backgrounds and expertise.
It demonstrates that first-class competitive science is always interdisciplinary, he said. Its hard to compete internationally if you stay inside your own lab, confining yourself to the techniques with which youre familiar and the equipment to which you have access.
Author: Press OfficeSource: FAPESPContact: Press Office FAPESPImage: The image is in the public domain
Original Research: Open access.Morphological, cellular, and molecular basis of brain infection in COVID-19 patients by Fernanda Crunfli et al. PNAS
Abstract
Morphological, cellular, and molecular basis of brain infection in COVID-19 patients
Although increasing evidence confirms neuropsychiatric manifestations associated mainly with severe COVID-19 infection, long-term neuropsychiatric dysfunction (recently characterized as part of long COVID-19 syndrome) has been frequently observed after mild infection.
We show the spectrum of cerebral impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, ranging from long-term alterations in mildly infected individuals (orbitofrontal cortical atrophy, neurocognitive impairment, excessive fatigue and anxiety symptoms) to severe acute damage confirmed in brain tissue samples extracted from the orbitofrontal region (via endonasal transethmoidal access) from individuals who died of COVID-19. In an independent cohort of 26 individuals who died of COVID-19, we used histopathological signs of brain damage as a guide for possible SARS-CoV-2 brain infection and found that among the 5 individuals who exhibited those signs, all of them had genetic material of the virus in the brain.
Brain tissue samples from these five patients also exhibited foci of SARS-CoV-2 infection and replication, particularly in astrocytes.
Supporting the hypothesis of astrocyte infection, neural stem cellderived human astrocytes invitro are susceptible to SARS-CoV-2 infection through a noncanonical mechanism that involves spikeNRP1 interaction. SARS-CoV-2infected astrocytes manifested changes in energy metabolism and in key proteins and metabolites used to fuel neurons, as well as in the biogenesis of neurotransmitters. Moreover, human astrocyte infection elicits a secretory phenotype that reduces neuronal viability.
Our data support the model in which SARS-CoV-2 reaches the brain, infects astrocytes, and consequently, leads to neuronal death or dysfunction. These deregulated processes could contribute to the structural and functional alterations seen in the brains of COVID-19 patients.
Originally posted here:
Study Reveals Main Target of COVID-19 in Brain and Describes Effects of Virus on Nervous System - Neuroscience News
Summary: During brain development, oligodendrocyte precursor cells (OPCs) contribute to the neural pruning process, helping to shape the healthy development of the brain.
Source: CSHL
When the brain first wires itself up in early development, it creates more connections than it actually needs.
Some of these connections, or synapses, will transmit critical signals as young animals begin to sense their surroundings. Others will be eliminated as the brain matures.
Only those that the animal needs to understand and interact with the world are left.
Cold Spring Harbor Laboratory (CSHL) Assistant Professor Lucas Cheadle and colleagues have discovered that cells called oligodendrocyte precursor cells (OPCs) contribute to this pruning process. This helps shape a healthybrainduring early development.
Understanding this vital part of brain development may reveal new strategies for treating neurodevelopmental conditions like schizophrenia andautism spectrum disorder(ASD).
The discovery was sparked while using high-powered microscopes to examine the brains of adult mice. Cheadles team noticed that many OPCs were actively engulfing the connection points between neurons.
The team suspected the cells might be busy eliminating synapses that the brain did not need. Cheadle and his team wondered if OPCs did the same thing in younger brains. A young animals experiences have a particularly profound impact on shaping neural circuits duringearly development.
The researchers raised young mice in the dark. When the mice were first exposed to light, OPCs began engulfingsynapsesin response. The cells were operating in their brains vision-processing circuitry.
OPCs seem to be especially poised to regulate brain connections associated with experiences, Cheadle says. These cells are very responsive to new experiences. They can take that information and use it to shape brain connections.
Published inNature Neuroscience, the Cheadle teams discovery reveals an unexpected role for OPCs. Several kinds of cells help shapeneural circuitsby eliminating unnecessary connections. OPCs had previously only been known for producing cells that surround and support neurons.
Cheadle says, This is a cell type thats really poised to sort of serve as an intermediary between whats going on in the world out there and whats happening inside of our brains.
Cheadle hopes this new information will help understand neurodevelopmental disorders better. He plans to investigate whether faulty OPC pruning plays a role in conditions like schizophrenia and ASD.
Author: Press OfficeSource: CSHLContact: Press Office CSHLImage: The image is credited to Cheadle lab/Imaris software/CSHL, 2022
Original Research: Open access.Oligodendrocyte precursor cells engulf synapses during circuit remodeling in mice by Yohan S. S. Auguste et al. Nature Neuroscience
Abstract
Oligodendrocyte precursor cells engulf synapses during circuit remodeling in mice
Oligodendrocyte precursor cells (OPCs) give rise to myelinating oligodendrocytes throughout life, but the functions of OPCs are not limited to oligodendrogenesis.
Here we show that OPCs contribute to thalamocortical presynapse elimination in the developing and adult mouse visual cortex. OPC-mediated synapse engulfment increases in response to sensory experience during neural circuit refinement.
Our data suggest that OPCs may regulate synaptic connectivity in the brain independently of oligodendrogenesis.
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The Unexpected Cells Helping to Shape Young Brains - Neuroscience News
Summary: Powerful hierarchical situations make it easier for individuals to commit harmful actions. The reason for this, researchers say, is because empathy and agency become split across multiple individuals.
Source: KNAW
Researchers from the Netherlands Institute for Neuroscience show that powerful hierarchical situations make it easier to commit harmful actions, asagency and empathy are split across multiple individuals.
There are numerous historical examples where horrific acts and mass destruction have occurred as a result of a hierarchical structure. A superior communicates a plan and a subordinate carries it out. The superior then bears responsibility for the decision but is distanced from the results, while the subordinate experiences authorship over the action but may experience reduced responsibility for its outcomes. And in our daily lives too, hierarchy is acquired throughout our society.
In many organizations, orders are embedded in an even longer chain of commands in which a given commander often merely relays on the orders received from a superior. But what effect does this have on our actions?
A new study from the social brain lab looked at how your position within a hierarchical structure (commander or intermediary) influences the sense of agency and empathy for pain. The aim was to understand how these two different neurocognitive processes differ in commanders and intermediaries.
And guess what? Commanders and intermediaries show reduced activation in empathic brain regions when pain is inflicted on the victim compared to people who can decide and act for themselves.
The results were published in the journaleNeuro.
The team used functional MRI (fMRI) and electroencephalogram (EEG) techniques in order to perform their experiments. fMRI measures brain activity by tracking changes in blood flow over time. The changes visible on the scan are related to change in oxygen levels: when areas of the brain are active, they will need more oxygen, causing them to light up.
Using EEG, brain activity is measured electrically. During this test, small sensors are attached to the scalp to pick up the electrical signals produced by the brain.
Reduced empathy
The fMRI study shows that activity in empathy-related brain regions was low in both the commander and the intermediary, compared to someone who delivered the shock directly of their own free will.
During the both studies, pain was administered by a human or robot.
The EEG results show that the sense of agency did not differ between commanders and intermediaries, regardless of whether the execution was performed by a robot or a human. However, it turned out that the neural response to the pain of the victim were higher when participants commanded a robot compared to a human.
This suggests that when there is a second human involved, the responsibility tends to be diffused and commanders pain processing of the victims pain is reduced. Diffusing such responsibility onto a robot is perhaps more difficult.
Emilie Caspar (first co-author of the paper): The law generally punished those who gave out orders more severely than those who carried out the orders. But what do people feel exactly in a hierarchical chain?
Recently, Khieu Samphan, one of the main Khmer Rouge leaders, was sentenced to life imprisonment for crimes against humanity and genocide. Yet, he claimed that he did not know what was happening during the Khmer Rouge Era, where millions of Cambodians died of execution, starvation, and diseases.
It seems that people commanding may not always experience the responsibility they should, an aspect which would nonetheless be crucial to avoid mass atrocities.
This is why it is important to understand better their subjective experience and how their brain processes the consequences of their orders, to perhaps in the future offer interventions that would prevent a diminution of responsibility in hierarchical chain
Kalliopi Ioumpa (first co-author of the paper): These results complement previous research showing that hierarchy has a measurable effect on peoples behaviour and brain activation, making them less engaged in the harm they cause.
This study can raise questions on how we can ensure that people feel responsibility despite being in a hierarchical chain. Is it easier for executors to take responsibility over their actions since they are the ones acting or for commanders because they bear the responsibility of the order?
We show how powerful hierarchical situations can facilitate committing actions that harm others, as agency and empathy are distributed across multiple individuals.
Prof Dr Christian Keysers (One of the senior author of the study heading the lab in which it was performed): Times are changing. The solder at the forefront, whose empathy sometimes prevented the worst atrocities, is increasingly replaced by drones that feel no empathy. Has this removed any empathy from the chain of command? Indeed, we find that merely commanding someone to deliver pain reduces how much your brain processes the pain you command compared to directly triggering the pain.
What was really exciting to see, however, is that knowing that you command a machine, that you cannot defer the responsibility to, restores some of the reactions to the pain in commanders.
Perhaps there is hope, after all, that the empathy we reduce at the forefront might be replaced at least in part by an increase is the sense of responsibility at higher levels in the hierarchy
Information about the authors:
The study was performed by Dr Emilie Caspar and PhD student Kalliopi Ioumpa under the supervision of Dr Christian Keysers and Dr Valeria Gazzola, who lead together the Social Brain Lab at the Netherlands Institute for Neuroscience, a research institute of the Royal Netherlands Academy of Arts and Sciences. Dr Emilie Caspar has since become an associate professor at Ghent University.
Author: Eline FeenstraSource: KNAWContact: Eline Feenstra KNAWImage: The image is credited to Kalliopi Ioumpa Netherlands Institute for Neuroscience
Original Research: Closed access.Commanding or being a simple intermediary: how does it affect moral behavior and related brain mechanisms? by Kalliopi Ioumpa et al. eNeuro
Abstract
Commanding or being a simple intermediary: how does it affect moral behavior and related brain mechanisms?
Psychology and neuroscience research have shown that fractioning operations between several individuals along a hierarchical chain allows diffusing responsibility between components of the chain, which has the potential to disinhibit antisocial actions.
Here, we present two studies, one using fMRI (Study 1) and one using EEG (Study 2), designed to help understand how commanding or being in an intermediary position impacts the sense of agency and empathy for pain. In the age of military drones, we also explored whether commanding a human or robot agent influences these measures.
This was done within a single behavioral paradigm in which participants could freely decide whether or not to send painful shocks to another participant in exchange for money.
In Study 1, fMRI reveals that activation in social cognition and empathy-related brain regions was equally low when witnessing a victim receive a painful shock while participants were either commander or simple intermediary transmitting an order, compared to being the agent directly delivering the shock.
In Study 2, results indicated that the sense of agency did not differ between commanders and intermediary, no matter if the executing agent was a robot or a human. However, we observed that the neural response over P3 was higher when the executing agent was a robot compared to a human.
Source reconstruction of the EEG signal revealed that this effect was mediated by areas including the insula and ACC. Results are discussed regarding the interplay between the sense of agency and empathy for pain for decision-making.
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What Is the Effect of Hierarchy on Moral Behavior? - Neuroscience News
Summary: Drinking at least two cups of coffee a day, even instant coffee was associated with increased longevity and a lower risk of cardiovascular disease.
Source: European Society of Cardiology
Drinking two to three cups of coffee a day is linked with a longer lifespan and lower risk of cardiovascular disease compared with avoiding coffee, according to research published today in theEuropean Journal of Preventive Cardiology,a journal of the ESC.The findings applied to ground, instant and decaffeinated varieties.
In this large, observational study, ground, instant and decaffeinated coffee were associated with equivalent reductions in the incidence of cardiovascular disease and death from cardiovascular disease or any cause, said study author Professor Peter Kistler of the Baker Heart and Diabetes Research Institute, Melbourne, Australia.
The results suggest that mild to moderate intake of ground, instant and decaffeinated coffee should be considered part of a healthy lifestyle.
There is little information on the impact of different coffee preparations on heart health and survival.
This study examined the associations between types of coffee and incident arrhythmias, cardiovascular disease and death using data from the UK Biobank, which recruited adults between 40 and 69 years of age.
Cardiovascular disease was comprised of coronary heart disease, congestive heart failure and ischaemic stroke.
The study included 449,563 participants free of arrhythmias or other cardiovascular disease at baseline. The median age was 58 years and 55.3% were women.
Participants completed a questionnaire asking how many cups of coffee they drank each day and whether they usually drank instant, ground (such as cappuccino or filtered coffee), or decaffeinated coffee. They were then grouped into six daily intake categories, consisting of none, less than one, one, two to three, four to five, and more than five cups per day.
The usual coffee type was instant in 198,062 (44.1%) participants, ground in 82,575 (18.4%), and decaffeinated in 68,416 (15.2%). There were 100,510 (22.4%) non-coffee drinkers who served as the comparator group.
Coffee drinkers were compared to non-drinkers for the incidence of arrhythmias, cardiovascular disease and death, after adjusting for age, sex, ethnicity, obesity, high blood pressure, diabetes, obstructive sleep apnoea, smoking status, and tea and alcohol consumption.
Outcome information was obtained from medical records and death records. The median follow up was 12.5 years.
A total of 27,809 (6.2%) participants died during follow up. All types of coffee were linked with a reduction in death from any cause. The greatest risk reduction seen with two to three cups per day, which compared to no coffee drinking was associated with a 14%, 27% and 11% lower likelihood of death for decaffeinated, ground, and instant preparations, respectively.
Cardiovascular disease was diagnosed in 43,173 (9.6%) participants during follow up. All coffee subtypes were associated with a reduction in incident cardiovascular disease.
Again, the lowest risk was observed with two to three cups a day, which compared to abstinence from coffee was associated with a 6%, 20%, and 9% reduced likelihood of cardiovascular disease for decaffeinated, ground, instant coffee, respectively.
An arrhythmia was diagnosed in 30,100 (6.7%) participants during follow up. Ground and instant coffee, but not decaffeinated, was associated with a reduction in arrhythmias including atrial fibrillation.
Compared with non-drinkers, the lowest risks were observed with four to five cups a day for ground coffee and two to three cups a day for instant coffee, with 17% and 12% reduced risks, respectively.
Professor Kistler said: Caffeine is the most well-known constituent in coffee, but the beverage contains more than 100 biologically active components. It is likely that the non-caffeinated compounds were responsible for the positive relationships observed between coffee drinking, cardiovascular disease and survival.
Our findings indicate that drinking modest amounts of coffee of all types should not be discouraged but can be enjoyed as a heart healthy behavior.
Author: Justine PinotSource: European Society of CardiologyContact: Justine Pinot European Society of CardiologyImage: The image is in the public domain
Original Research: Open access.The impact of coffee subtypes on incident cardiovascular disease, arrhythmias, and mortality: long-term outcomes from the UK Biobank by Peter Kistler et al. European Journal of Preventative Cardiology
Abstract
The impact of coffee subtypes on incident cardiovascular disease, arrhythmias, and mortality: long-term outcomes from the UK Biobank
Aims
Epidemiological studies report the beneficial effects of habitual coffee consumption on incident arrhythmia, cardiovascular disease (CVD), and mortality. However, the impact of different coffee preparations on cardiovascular outcomes and survival is largely unknown. The aim of this study was to evaluate associations between coffee subtypes on incident outcomes, utilizing the UK Biobank.
Methods and results
Coffee subtypes were defined as decaffeinated, ground, and instant, then divided into 0, <1, 1, 23, 45, and >5cups/day, and compared with non-drinkers. Cardiovascular disease included coronary heart disease, cardiac failure, and ischaemic stroke. Cox regression modelling with hazard ratios (HRs) assessed associations with incident arrhythmia, CVD, and mortality. Outcomes were determined through ICD codes and death records. A total of 449563 participants (median 58 years, 55.3% females) were followed over 12.50.7 years.
Ground and instant coffee consumption was associated with a significant reduction in arrhythmia at 15cups/day but not for decaffeinated coffee.
The lowest risk was 45cups/day for ground coffee [HR 0.83, confidence interval (CI) 0.760.91,P<0.0001] and 23cups/day for instant coffee (HR 0.88, CI 0.850.92,P<0.0001). All coffee subtypes were associated with a reduction in incident CVD (the lowest risk was 23cups/day for decaffeinated,P=0.0093; ground,P<0.0001; and instant coffee,P<0.0001) vs. non-drinkers.
All-cause mortality was significantly reduced for all coffee subtypes, with the greatest risk reduction seen with 23cups/day for decaffeinated (HR 0.86, CI 0.810.91,P<0.0001); ground (HR 0.73, CI 0.690.78,P<0.0001); and instant coffee (HR 0.89, CI 0.860.93,P<0.0001).
Conclusion
Decaffeinated, ground, and instant coffee, particularly at 23cups/day, were associated with significant reductions in incident CVD and mortality. Ground and instant but not decaffeinated coffee was associated with reduced arrhythmia.
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Coffee Drinking Is Associated With Increased Longevity - Neuroscience News
Summary: The COVID-19 pandemic may have altered the trajectory of personality in individuals, especially in younger people.
Source: PLOS
Despite a long-standing hypothesis that personality traits are relatively impervious to environmental pressures, the COVID-19 pandemic may have altered the trajectory of personality across the United States, especially in younger adults, according to a new study published this week in the open-access journalPLOS ONEby Angelina Sutin of Florida State University College of Medicine, and colleagues.
Previous studies have generally found no associations between collective stressful eventssuch as earthquakes and hurricanesand personality change. However, the coronavirus pandemic has affected the entire globe and nearly every aspect of life.
In the new study, the researchers used longitudinal assessments of personality from 7,109 people enrolled in the online Understanding America Study.
They compared five-factor modelpersonality traitsneuroticism, extraversion,openness, agreeableness andconscientiousnessbetween pre-pandemic measurements (May 2014February 2020) and assessments early (MarchDecember 2020) or later (2021-2022) in the pandemic.
A total of 18,623 assessments, or a mean of 2.62 per participant, were analyzed. Participants were 41.2% male and ranged in age from 18 to 109.
Consistent with other studies, there were relatively few changes between pre-pandemic and 2020 personality traits, with only a small decline in neuroticism.
However, there were declines in extraversion, openness, agreeableness, and conscientiousness when 2021-2022 data was compared to pre-pandemic personality.
The changes were about one-tenth of a standard deviation, which is equivalent to about one decade of normative personality change.
The changes were moderated by age, with younger adults showing disrupted maturity in the form of increased neuroticism and decreased agreeableness and conscientiousness, and the oldest group of adults showing no statistically significant changes in traits.
The authors conclude that if these changes are enduring, it suggests that population-wide stressful events can slightly bend the trajectory of personality, especially in younger adults.
The authors add that there was limitedpersonality changeearly in the pandemic but striking changes starting in 2021. Of most note, the personality of young adults changed the most, with marked increases in neuroticism and declines inagreeablenessand conscientiousness.
That is, younger adults became moodier and more prone to stress, less cooperative and trusting, and less restrained and responsible.
Author: Press OfficeSource: PLOSContact: Press Office PLOSImage: The image is in the public domain
Original Research: Open access.Differential personality change earlier and later in the coronavirus pandemic in a longitudinal sample of adults in the United States by Angelina Sutin et al. PLOS ONE
Abstract
Differential personality change earlier and later in the coronavirus pandemic in a longitudinal sample of adults in the United States
Five-factor model personality traits (neuroticism, extraversion, openness, agreeableness, conscientiousness) are thought to be relatively impervious to environmental demands in adulthood.
The coronavirus pandemic is an unprecedented opportunity to examine whether personality changed during a stressful global event. Surprisingly, two previous studies found that neuroticism decreased early in the pandemic, whereas there was less evidence for change in the other four traits during this period.
The present research used longitudinal assessments of personality from the Understanding America Study (N = 7,109; 18,623 assessments) to examine personality changes relatively earlier (2020) and later (20212022) in the pandemic compared to pre-pandemic levels. Replicating the two previous studies, neuroticism declined very slightly in 2020 compared to pre-pandemic levels; there were no changes in the other four traits.
When personality was measured in 20212022, however, there was no significant change in neuroticism compared to pre-pandemic levels, but there were significant small declines in extraversion, openness, agreeableness, and conscientiousness.
The changes were about one-tenth of a standard deviation, which is equivalent to about one decade of normative personality change. These changes were moderated by age and Hispanic/Latino ethnicity, but not race or education. Strikingly, younger adults showed disrupted maturity in that they increased in neuroticism and declined in agreeableness and conscientiousness.
Current evidence suggests the slight decrease in neuroticism early in the pandemic was short-lived and detrimental changes in the other traits emerged over time.
If these changes are enduring, this evidence suggests population-wide stressful events can slightly bend the trajectory of personality, especially in younger adults.
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Did the Pandemic Change Our Personalities? - Neuroscience News
Summary: Loneliness, restless sleep, and unhappiness have a significant effect on biological aging, a new study reports.
Source: Deep Longevity LTD
Molecular damage accumulates and contributes to the development of aging-related frailty and serious diseases. In some people these molecular processes are more intense than in others, a condition commonly referred to as accelerated aging.
Fortunately, the increased pace of aging may be detected before its disastrous consequences manifest by using digital models of aging (aging clocks). Such models can also be used to derive anti-aging therapies on individual and population levels.
According to the latestarticle published inAging-US, any anti-aging therapy needs to focus on ones mental health as much as on ones physical health.
An international collaboration led byDeep Longevitywith US and Chinese scientists have measured the effects of being lonely, having restless sleep, or feeling unhappy on the pace of aging and found it to be significant.
The article features a new aging clock trained and verified with blood and biometric data of 11,914 Chinese adults. This is the first aging clock to be trained exclusively on a Chinese cohort of such volume.
Aging acceleration was detected in people with a history of stroke, liver and lung diseases, smokers, and most interestingly, people in a vulnerable mental state. In fact, feeling hopeless, unhappy, and lonely was shown to increase ones biological age more than smoking.
Other factors linked to aging acceleration include being single and living in a rural area (due to the low availability of medical services).
The authors of the article conclude that the psychological aspect of aging should not be neglected either in research or in practical anti-aging applications.
According to Manuel Faria from Stanford University:
Mental and psychosocial states are some of the most robust predictors of health outcomes and quality of life yet they have largely been omitted from modern healthcare.
Alex Zhavoronkov, the CEO ofInsilico Medicine, points out that the study provides a course of action to slow down or even reverse psychological aging on a national scale.
Earlier this year, Deep Longevity released an AI-guided mental health web serviceFuturSelf.AIthat is based on a preceding publication in Aging-US.
The service offers a free psychological assessment that is processed by an AI and provides a comprehensive report on a users psychological age as well as current and future mental well-being.
Deepankar Nayak, the CEO of Deep longevity affirms, FuturSelf.AI, in combination with the study of older Chinese adults, positions Deep Longevity at the forefront of biogerontological research.
Author: Fedor GalkinSource: Deep Longevity LTDContact: Fedor Galkin Deep Lingevity LTDImage: The image is in the public domain
Original Research: The findings will appear in Aging-US
See the article here:
Being Lonely and Unhappy Accelerates Aging More Than Smoking - Neuroscience News
Summary: Researchers have identified a link between metabolism and dementia-related brain measures. Obesity related to inflammation, kidney stress, or liver stress had the biggest impact on adverse brain health.
Source: University of South Australia
Every three seconds, someone in the world is diagnosed with dementia. And while there is no known cure, changes in the brain can occur years before a dementia diagnosis.
Now, a world-first study from the University of South Australias Australian Center for Precision Health has found a link between metabolism and dementia-related brain measures, providing valuable insights about the disease.
Analyzing data from 26,239 people in the U.K. Biobank, researchers found that those with obesity related to liver stress, or to inflammation and kidney stress, had the most adverse brain findings.
The study measured associations of six diverse metabolic profiles and 39 cardiometabolic markers with MRI brain scan measures of brain volume, brain lesions, and iron accumulation, to identify early risk factors for dementia.
People with metabolic profiles linked to obesity were more likely to have adverse MRI profiles showing lower hippocampal and gray matter volumes, greater burden of brain lesions, and higher accumulation of iron.
UniSA researcher, Dr. Amanda Lumsden, says the research adds a new layer of understanding to brain health.
Dementia is a debilitating disease that affects more than 55 million people worldwide, Dr. Lumsden says.
Understanding metabolic factors and profiles associated with dementia-related brain changes can help identify early risk factors for dementia.
In this research, we found that adverse neuroimaging patterns were more prevalent among people who had metabolic types related to obesity.
These people also had the highest Basal Metabolic Rate (BMR)how much energy your body requires when resting in order to support its basic functionsbut curiously, BMR seemed to contribute to adverse brain markers over and above the effects of obesity.
Senior Investigator, UniSAs Professor Elina Hyppnen says the finding presents a new avenue for understanding brain health.
This study indicates that metabolic profiles are associated with aspects ofbrainhealth. We also found associations with many individual biomarkers which may provide clues into the processes leading todementia, Prof Hyppnen says.
Thehuman bodyis complex, and more work is now needed to find out exactly why and how these associations arise.
Author: Press OfficeSource: University of South AustraliaContact: Press Office University of South AustraliaImage: The image is in the public domain
Original Research: Open access.Metabolic profilebased subgroups can identify differences in brain volumes and brain iron deposition by Amanda L. Lumsden et al. Diabetes, Obesity, and Metabolism
Abstract
Metabolic profilebased subgroups can identify differences in brain volumes and brain iron deposition
To evaluate associations of metabolic profiles and biomarkers with brain atrophy, lesions, and iron deposition to understand the early risk factors associated with dementia.
Using data from 26239 UK Biobank participants free from dementia and stroke, we assessed the associations of metabolic subgroups, derived using an artificial neural network approach (self-organizing map), and 39 individual biomarkers with brain MRI measures: total brain volume (TBV), grey matter volume (GMV), white matter volume (WMV), hippocampal volume (HV), white matter hyperintensity (WMH) volume, and caudate iron deposition.
In metabolic subgroup analyses, participants characterized by high triglycerides and liver enzymes showed the most adverse brain outcomes compared to the healthy reference subgroup with high-density lipoprotein cholesterol and low body mass index (BMI) including associations with GMV (standardized0.20, 95% confidence interval [CI] 0.24 to 0.16), HV (standardized0.09, 95% CI 0.13 to 0.04), WMH volume (standardized0.22, 95% CI 0.18 to 0.26), and caudate iron deposition (standardized0.30, 95% CI 0.25 to 0.34), with similar adverse associations for the subgroup with high BMI, C-reactive protein and cystatin C, and the subgroup with high blood pressure (BP) and apolipoprotein B. Among the biomarkers, striking associations were seen between basal metabolic rate (BMR) and caudate iron deposition (standardized0.23, 95% CI 0.22 to 0.24 per 1 SD increase), GMV (standardized0.15, 95% CI 0.16 to 0.14) and HV (standardized0.11, 95% CI 0.12 to 0.10), and between BP and WMH volume (standardized0.13, 95% CI 0.12 to 0.14 for diastolic BP).
Metabolic profiles were associated differentially with brain neuroimaging characteristics. Associations of BMR, BP and other individual biomarkers may provide insights into actionable mechanisms driving these brain associations.
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Metabolism Linked to Brain Health - Neuroscience News
Summary: Psychostimulants increase dopamine levels, enhancing task-relevant cortical signals by acting on the striatum and the difference in dopamine synthesis capacity in the striatum explains the variability in the drugs cognitive effects.
Source: Human Brain Project
Psychostimulants are commonly used as treatments of psychiatric disorders or to improve cognition, but the benefits of these drugs are not the same for everyone, as their effects vary greatly both across individuals and within the same patient.
This large variability poses a major problem for treatment strategies in psychiatry, and the reasons behind it are still not clear.
Now, scientists of the Human Brain Project (HBP) have moved closer to understanding them.
One of these medications is methylphenidate, the active ingredient of the drugs Ritalin and Concerta that are used to treat attention deficit hyperactivity disorder (ADHD), but are also widely used by healthy people for its cognition-improving effects. Methylphenidate acts in part by increasing levels of dopamine, a neurotransmitter involved in the brains reward system.A new study by a team of researchers from Radboud University Medical Center (Netherlands) and Donders Institute for Brain, Cognition and Behavior (Netherlands) unravels the mechanisms by which methylphenidate gates both attention and reward learning.
The researchers tested the hypothesis that the effects of methylphenidate on learning based on reward or punishment depend on the baseline levels of dopamine in a persons brain.
To test this, one hundred young healthy adults received (in different sessions) methylphenidate, sulpiride (a medication used to treat symptoms of schizophrenia that acts more selectively on dopamine receptors), or a placebo, and were later scanned with functional magnetic resonance imaging (fMRI) during a reward/punishment reversal learning task. In this task, participants learned to predict whether a picture (of a face or a landscape) that is selected by the computer is followed by reward or punishment.
A reward outcome consisted of a green smiley and a + 100 sign. A punishment consisted of a red sad smiley and a -100 sign. Whether the face or the landscape was associated with reward or punishment changed frequently in the task, so to perform well people had to continue to pay attention and flexibly update their behaviour based on prediction errors.The researchers observed that the degree to which both methylphenidate and sulpiride improved reward compared with punishment learning depends on baseline dopamine synthesis capacity.
Moreover, these effects on learning were accompanied by increased activity in the striatum, a dopamine-rich region deep inside the brain, and also by increased specificity of the activity in regions of the cortex near the back of the brain that are specialised for processing faces and landscapes.Their findings provide strong support for two hypotheses related to methylphenidate: First, that dopamine enhances task-relevant cortical signals by acting on the striatum. Second, that differences between individuals in dopamine synthesis capacity in the striatum explain the variability in the drugs cognitive effects.
Author: Peter ZekertSource: Human Brain ProjectContact: Peter Zekert Human Brain ProjectImage: The image is in the public domain
Original Research: Open access.Striatal dopamine dissociates methylphenidate effects on value-based versus surprise-based reversal learning by Roshan Coolset al. Nature Communications
Abstract
Striatal dopamine dissociates methylphenidate effects on value-based versus surprise-based reversal learning
Psychostimulants such as methylphenidate are widely used for their cognitive enhancing effects, but there is large variability in the direction and extent of these effects.
We tested the hypothesis that methylphenidate enhances or impairs reward/punishment-based reversal learning depending on baseline striatal dopamine levels and corticostriatal gating of reward/punishment-related representations in stimulus-specific sensory cortex.
Young healthy adults (N=100) were scanned with functional magnetic resonance imaging during a reward/punishment reversal learning task, after intake of methylphenidate or the selective D2/3-receptor antagonist sulpiride.
Striatal dopamine synthesis capacity was indexed with [18F]DOPA positron emission tomography. Methylphenidate improved and sulpiride decreased overall accuracy and response speed.
Both drugs boosted reward versus punishment learning signals to a greater degree in participants with higher dopamine synthesis capacity. By contrast, striatal and stimulus-specific sensory surprise signals were boosted in participants with lower dopamine synthesis.
These results unravel the mechanisms by which methylphenidate gates both attention and reward learning.
Original post:
Mechanisms of Psychostimulants on Attention and Learning Revealed - Neuroscience News