Category Archives: Neuroscience

Neuroscience

How Imagination Fuels Empathy and Prosocial Behavior – Neuroscience News

Summary: A new study highlights the significant role of imagination in evoking empathy and driving prosocial behavior. While empathy is multifaceted, this research focuses on two aspects: personal distress and compassionate concern.

The study reveals that vividly imagining someone elses problems increases personal distress, motivating individuals to offer help.

These findings break new ground in understanding the connection between mental experiences and actions, shedding light on why certain situations and individuals elicit more empathy than others.

Key Facts:

Source: McGill University

In a world grappling with deep-seated division and social upheaval, empathy has become more critical than ever.

But science suggests when it comes to evoking empathy, our imagination is more powerful than we previously thought. A new study, led by McGill researchers, reveals how the different ways to experience empathy affect our willingness to help others.

Empathy is the ability to understand the situation of another person and is vital for prosocial behaviours. However, we know that empathy isnt just one thing we can experience it very differently, either as personal distress or compassionate concern for that other person, explains McGill psychology professor Signy Sheldon, and the studys co-author.

Until now, research in empathy has largely focused on how imagining helping another person can promote compassion, but not on how imagining another persons situation affects empathy, which is usually our first mental course of action.

These findings, published inthe journalEmotionbreak new ground by showing how another form of empathy, personal distress, is more prominent when imagining those situations and may actually be a catalyst for taking action to help.

The joint effort between McGill and Albany University discovered that when we vividly imagine someone elses problems in our minds, it makes us feel their pain more and motivates us to lend a helping hand.

The findings bring us closer to cracking the code of human behaviour and the link between our mental experiences and prosocial actions. These results are important for understanding why some situations and even people seem more empathetic than others.

If you hear your friend has lost a loved one or a neighbors car was stolen, what happens in your mind? Do you take on the pain of your friend or do you feel concern and compassion?

The research involved three online experiments where participants were asked to truly visualize themselves in another persons shoes.

Our experiments revealed that when people simulated distressful scenarios of other individuals, they felt much more personal distress than when these scenarios were not simulated. Interestingly, we also found imagining these scenarios in such a way increased the willingness to help that individual, says Sheldon, Canada Research Chair in Cognitive Neuroscience of Memory.

As imagining others situations is linked to episodic memory, this discovery raises significant questions about the link between memory capacity and empathy, which is an important avenue for further research.

Author: Keila DePape Source: McGill University Contact: Keila DePape McGill University Image: The image is credited to Neuroscience News

Original Research: Closed access. From memory to motivation: Probing the relationship between episodic simulation, empathy, and helping intentions by Signy Sheldon et al. Emotion

Abstract

From memory to motivation: Probing the relationship between episodic simulation, empathy, and helping intentions

Research has documented a strong link between constructingepisodic simulationsvivid imaginations of specific eventsand empathy. To date, most studies have used episodic simulations of helping someone to facilitate affective empathy and promote helping intentions, but have not studied how episodic simulations of anothers distressing situation affect empathy.

Moreover, affective empathy encompasses bothpersonal distress(i.e., an egocentric experience of distress in response to anothers circumstances) and empathic concern (i.e., compassion for another), but we do not know how episodic simulations affect each component.

To address these questions, we ran three experiments testing how different episodic simulations influenced personal distress and empathic concern, and thereby willingness to help.

In Experiment 1 (N= 216), we found that participants who constructed episodic simulations of anothers situation reported increased personal distress (but not empathic concern) and increased helping intentions compared to a control group; additional analyses revealed that personal distress mediated the simulation effect on helping.

Furthermore, in Experiment 2 (N= 213), we contrasted episodic simulation of helping versus the distressing scenario; we found no differences in personal distress or helping intentions, but simulating helping led to higher empathic concern.

Experiment 3 (N= 571) included both simulation conditions and a control condition; we fully replicated our findings, additionally showing that simulating a helping interaction increased personal distress, empathic concern, and helping intentions relative to the control condition, which consisted of prior work.

Taken together, our work illustrates how distinct forms of episodic simulation differentially guide empathic responding and highlights the importance of personal distress in motivating helping.

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How Imagination Fuels Empathy and Prosocial Behavior - Neuroscience News

Neuroscience

Peptide PACAP’s Key Role in Alcohol Addiction – Neuroscience News

Summary: Alcohol, the worlds most common addictive substance, leads to $249 billion in annual costs and 88,000 deaths in the U.S. Alcohol use disorder affects millions but is under-treated.

Researchers discovered a key player in alcohol addiction: pituitary adenylate cyclase activating polypeptide (PACAP). This peptide, found in the bed nucleus of the stria terminalis (BNST), is linked to heavy alcohol drinking and withdrawal.

Inhibiting PACAP in the BNST significantly reduces alcohol consumption, offering a potential target for novel treatments.

Key Facts:

Source: Boston University

Alcohol is the most common addictive substance in the world. Every year in the U.S. excessive alcohol use costs $249 billion and causes approximately 88,000 deaths, as well as various chronic diseases and social issues.

Alcohol use disorder, a highly prevalent, chronic, relapsing disorder, affects more than 14 million people in the U.S. alone, in addition to being severely under-treated, with only three modestly effective pharmacological therapies available.

Chronic exposure to alcohol has been shown to produce profound neuroadaptations in specific brain regions, including the recruitment of key stress neurotransmitters, ultimately causing changes in the body that sustain excessive drinking. The area of the brain known as the bed nucleus of the stria terminalis (BNST) is critically involved in the behavioral response to stress as well as in chronic, pathological alcohol use.

Researchers from Boston University Chobanian & Avedisian School of Medicine have identified that a peptide called pituitary adenylate cyclase activating polypeptide (PACAP), is involved in heavy alcohol drinking. In addition, they have discovered that this peptide acts in the BNST area.

Using an established experimental model for heavy, intermittent alcohol drinking, the researchers observed that during withdrawal this model showed increased levels of the stress neuropeptide PACAP selectively in the BNST, compared to the control model.

Interestingly, a similar increase was also observed in the levels of another stress neuropeptide closely related to PACAP, the calcitonin gene-related peptide, or CGRP. Both peptides have been implicated in stress as well as pain sensitivity, but their role in alcohol addiction is less established.

The researchers then used a virus in a transgenic model to block the neural pathways containing PACAP that specifically arrive to the BNST. We found that inhibiting PACAP to the BNST dramatically reduced heavy ethanol drinking, explained co-corresponding author Valentina Sabino, PhD, co-director of the Schools Laboratory of Addictive Disorders as well as professor of pharmacology, physiology & biophysics.

According to the researchers, these results provide evidence that this protein mediates the addictive properties of alcohol. We found a key player, PACAP, driving heavy alcohol drinking, which can be targeted for the development of novel pharmacological therapies, added co-corresponding author Pietro Cottone, PhD, associate professor of pharmacology, physiology & biophysics and co-director of the Laboratory of Addictive Disorders.

These findings appear online in the journaleNeuro.

Funding: Funding for this study was to grants number AA026051 (PC), AA025038 (VS), and AA024439 (VS) from the National Institute on Alcohol and Alcoholism (NIAAA), the Boston University Undergraduate Research Opportunities Program (UROP), the Boston University Micro and Nano Imaging Facility and the Office of the Director of the National Institutes of Health (S10OD024993).

Author: Gina DiGravio Source: Boston University Contact: Gina DiGravio Boston University Image: The image is credited to Neuroscience News

Original Research: Closed access. Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) of the Bed Nucleus of the Stria Terminalis Mediates Heavy Alcohol Drinking in Mice by Valentina Sabino et al. eNeuro

Abstract

Pituitary Adenylate Cyclase Activating Polypeptide (PACAP) of the Bed Nucleus of the Stria Terminalis Mediates Heavy Alcohol Drinking in Mice

Alcohol use disorder (AUD) is a complex psychiatric disease characterized by periods of heavy drinking and periods of withdrawal. Chronic exposure to ethanol causes profound neuroadaptations in the extended amygdala, which cause allostatic changes promoting excessive drinking.

The bed nucleus of the stria terminalis (BNST), a brain region involved in both excessive drinking and anxiety-like behavior, shows particularly high levels of pituitary adenylate cyclase activating polypeptide (PACAP), a key mediator of the stress response.

Recently, a role for PACAP in withdrawal-induced alcohol drinking and anxiety-like behavior in alcohol-dependent rats has been proposed; whether the PACAP system of the BNST is also recruited in other models of alcohol addiction and whether it is of local or non-local origin is currently unknown.

Here, we show that PACAP immunoreactivity is increased selectively in the BNST of C57Bl/6J mice exposed to a chronic, intermittent access to ethanol.

While PAC1R expressing cells were unchanged by chronic alcohol, the levels of a peptide closely related to PACAP, the calcitonin gene related neuropeptide (CGRP), were found to also be increased in the BNST.

Finally, using a retrograde chemogenetic approach in PACAP-ires-Cre mice, we found that the inhibition of PACAP neuronal afferents to the BNST reduced heavy ethanol drinking.

Our data suggest that the PACAP system of the BNST is recruited by chronic, voluntary alcohol drinking in mice and that non-locally originating PACAP projections to the BNST regulate heavy alcohol intake, indicating that this system may represent a promising target for novel AUD therapies.

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Peptide PACAP's Key Role in Alcohol Addiction - Neuroscience News

Neuroscience

Two leading standards bodies launch Neuroscience Community, powering a global data network that will speed up … – EurekAlert

image:

GA4GH & INCF launch Neuroscience Community

Credit: Global Alliance for Genomics and Health / Stephanie Li

The Global Alliance for Genomics and Health (GA4GH) and the International Neuroinformatics Coordinating Facility (INCF) launched a new group to lay the groundwork for connecting global neuroscience and genomic data.

Answering data-driven questions in neuroscience means dealing with complexity: in types of data, data management systems, the number and variety of conditions, ethical and legal requirements, and the genetic and biological conditions themselves. Even just aligning industry standards for neuroimaging and genomics can be a struggle.

To improve life for people with neurological conditions, we need to tackle the complexity together.

The newGA4GH & INCF Neuroscience Communityunites collaborators from around the world to share best practices and improve standards that will expand responsible use of neuroscientific data, including genomic data. Interested organisations canjoin today.

A parent wants to understand why their autistic five-year-old wakes up multiple times a night, but doctors cant explain. A person with early-onset Parkinsons struggles to find a cocktail of medications that wards off the symptoms but doesnt make them sleepy, irritable, and confused on the job. Someone has tried every treatment for severe depression that their insurance will pay for, but nothing works.

For people with neurological conditions and their families, the healthcare system can seem to offer more headache than help.

Those with illnesses like Parkinsons, addiction, depression, and epilepsy often report worse quality of life than others. So domany neurodivergent people, including autistic people and those with ADHD.For example, people with epilepsy are at greater risk ofdying early. Many autistic children facegastrointestinalandsleepproblems.

Progress has been slow to tailor healthcare for neurodivergent people and neurological patients. In part, thats because researchers need lots and lots of data and many differenttypesof data to answer neuroscience questions.

To fully understand just one neurological patient or research participant, you need brain images, genomic sequences, gene expression data, socio-cultural factors, test results showing how they metabolise drugs, their overall health history and their familys, and biomarker data like health and weight. Then add a detailed work-up of their phenotype, or the traits, behaviours, and symptoms they show, said neuroscientist Randy McIntosh, Co-Lead of the GA4GH & INCF Neuroscience Community, Deputy Chair of the INCF Governing Board, and professor at Simon Fraser University.

Now multiply that amount of data by thousands of people, which you need to get real predictive power in a study, he said.

A single organisation is unlikely to collect or manage so much data. Yet sharing data between groups is difficult, in part for an important reason: stewarding someones data means taking great care to protect their privacy, wishes, and legal rights.

One solution is data visiting.

Instead of downloading a data file and transferring it to a faraway scientist, data visiting means that a scientist visits the data where it lives. These days, data visiting is done virtually: algorithms or other computer tools travel to an institutions trove of data, or a secure environment where many institutions share their data, and run tests. Then they send the results to scientists with proper access permissions.

To visit the most data possible, you need a federated network where you can study data housed in many different locations, all at once.

No matter your access method, you need to use data responsibly. Groups like the Wellcome-funded Brain Research International Data Governance & Exchange Program (BRIDGE) a Neuroscience Community member are studying how to properly follow laws and regulations when making data available worldwide. BRIDGE works with partners in Brazil, the US, South Africa, Switzerland, and the UK to develop resources for governing neuroscience data.

Conditions and diseases dont respect borders. If we want the lives of people with neurological conditions to improve, we cant just look at data from one hospital or even one country. We have to study diverse data from around the world. With data visiting powered by federation and Global Alliance for Genomics and Health standards, clinicians and researchers can vastly expand their pool of data while data stewards rest easy knowing they are protecting rights and following regulations, said Peter Goodhand, CEO of GA4GH.

The GA4GH & INCF Neuroscience Community will connect international partners to develop the standards, collaborations, and systems needed to power data visiting across a global network.

The community will help get answers faster for patients and people everywhere, while respecting the human rights of people who donate their data. (Read the communitysin-progress charter.)

For nearly two decades, INCF has developed standards and best practices to make neuroscience data FAIR: findable, accessible, interoperable, and reusable. Now we are eager to work with partners from genomics, like GA4GH, to ensure that our standards development efforts progress together and lead to the best possible science, said Mathew Abrams, Director of Science and Training for INCF.

The GA4GH & INCF Neuroscience Community will expand neuroscience and genomic data networking around the world ramping up what many members are already doing.

In Ontario, Canada, for example, several Neuroscience Community members run projects to link data across the province and the globe.

Take software company DNAstack. Working closely with the Autism Sharing Initiative (a GA4GH Driver Project), the company developed the Neuroscience AI network with its existing Omics AI software. The network makes it easier to find, analyse, and apply artificial intelligence to autism and other neuroscience datasets.

Then Azadeh Kushki, a researcher at Holland Bloorview Kids Rehabilitation Hospital also a Neuroscience Community member arrived. She used Neuroscience AI to make an important discovery: neurodivergent kids might be prescribed medication differently based on their ethnicity and family income.

The finding relied on a machine learning model trained on a federated network that follows GA4GH standards. Thanks to the Neuroscience Community, other groups will learn how to apply this powerful technique.

Another Neuroscience Community member, the Ontario Brain Institute, scaled up even further. Its Brain-CODE platform includes not only neurodevelopmental but also concussion, mental health, cerebral palsy, epilepsy, and neurodegenerative data. Brain-CODE houses data from more than 20,000 people who agreed to give researchers and other third parties access.

For more than 10 years, the Ontario Brain Institute has fostered an integrated approach for neuroscience discovery to improve brain health. By combining ideas and expertise from patients, researchers, and industry, weve created a powerful ecosystem of innovation using data, analytics, and AI. But we cant do this alone. With the GA4GH & INCF Neuroscience Community, we have a genuinely international opportunity to combine efforts and reach breakthroughs faster, said Francis Jeanson, Head of the Centre for Analytics at Ontario Brain Institute and Co-Lead of the GA4GH & INCF Neuroscience Community.

The new Neuroscience Community is one of severalCommunities of Interestfounded in recent years by GA4GH. These groups bring together global experts who focus on a specific topic, and who are eager to connect across borders and find a path to better data use.

Great work is happening all over the world to understand neurological conditions, including their genomic underpinnings. The GA4GH & INCF Neuroscience Community will ensure that all those experts are sharing best practices, developing interoperable standards, and building connections across data, said Angela Page, GA4GH Director of Strategy and Engagement. People with neurological conditions have advocated for and deserve a global data network that will lead to better healthcare and improved quality of life.

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About GA4GH

The Global Alliance for Genomics and Health (GA4GH) is an international, not-for-profit alliance formed in 2013 to accelerate progress in human health by expanding responsible use of genomic data. Bringing together 500+ leading organisations working in healthcare, research, patient advocacy, life science, and information technology, the GA4GH community creates frameworks and standards that power the responsible, broad, and democratised use of genomic and related health data.

About INCF

The International Neuroinformatics Coordinating Facility (INCF) network serves as a forum to collaboratively coordinate global neuroinformatics activities that guide and oversee the development of standards, best practices, ontologies, and other unifying activities. The mission of INCF network is to promote the uptake of FAIR data management practices in neuroscience through the development of standards and best practices that support open, FAIR, and citable neuroscience. INCF also provides training on how standards and best practices facilitate reproducibility and enables the publishing of the entirety of research output, including data and code.

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Two leading standards bodies launch Neuroscience Community, powering a global data network that will speed up ... - EurekAlert

Neuroscience

Fruit Fly Study Sheds Light on Aggression’s Neural Roots – Neuroscience News

Summary: Researchers have discovered new insights into persistent aggression in female fruit flies, challenging existing theories.

A new study shows that certain neural cells sustain aggressive behavior for up to 10 minutes, suggesting factors beyond recurrent neural connections are at play.

These findings could aid understanding of human aggression and related neurological conditions, highlighting the need for revised models of aggression in the brain.

Key Facts:

Source: HHMI

Its one of those days. On the drive home from work, the car in the next lane cuts you off. You slam on the brakes, lay on the horn, and yell choice words at the offending driver. When you walk into your house half an hour later, youre still angry, and snap at your partner when they ask about your day.

Fruit flies may not have to worry about the lingering effects of road rage, but they also experience states of persistent aggression. In the case of female fruit flies, this behavior is a survival mechanism, causing the flies to headbutt, shove, and fence other female fruit flies to guard prime egg-laying territory on a ripe banana.

Now, researchers at Janelia and the California Institute of Technology are homing in on the neurons, circuits, and mechanisms responsible for this tenacious behavior.

In anew study, the researchers report theyve teased out the cell types contributing to a persistent aggressive state in female fruit flies, showing that some cells associated with aggression can cause flies to remain angry for up to 10 minutes.

They also found that this persistent state may not be solely due to a recurrent connection between the aggression-associated cells, as had been thought. In a recurrent connection, signals loop back and feed into the same neural circuit, which could cause a behavior to persist.

Instead, the new research suggests persistent aggression could be regulated by other factors, including neuromodulators affecting neuronal activity, neurons downstream from the aggression-associated cells, or other circuits in the fly brain. Considering their findings, scientists may need to develop a new model that considers these other factors in addition to recurrent connections to explain this enduring behavior.

It is interesting for the field because we talk about these recurrent connections as being key for the persistent state, and thats really what we thought, says Katie Schretter, a postdoc in the Rubin Lab who led the research. But now it seems less clear in this case.

Understanding persistent internal states like aggression could help researchers better uncover how the brain makes decisions for instance, whether to stay mad or move on and the individual circuits involved in these choices. Figuring out the underlying mechanisms behind aggression could also help scientists better understand aggressive behavior in humans, including behaviors that can occur alongside neurodegenerative or psychiatric diseases.

For our society, its important to be able to decrease aggression and figure out how to stop persistent aggression, Schretter says. Figuring out how the circuit works can help us figure out how we might decrease it.

Fighting fruit flies

Scientists had previously identified cell types associated with aggression in the brains of female fruit flies. They found that activating these cells caused the flies to fight. Given this, the team, led by Schretter, Cal Tech graduate student Hui (Vivian) Chiu, Janelia Senior Group Leader Gerry Rubin, and HHMI Investigator David Anderson, wanted to look at these cells to see how their signals might feed back into each other to generate a persistent aggressive state.

The researchers separated female flies with a barrier and then activated the different cell types associated with aggression for 30 seconds at a time. They kept the flies separated for specific periods of time, up to 30 minutes, before removing the barrier and letting them interact.

The team hypothesized that recurrent connections between certain aggression-associated cell types could cause the flies to remain aggressive for longer periods of time.

They found that one cell type associated with aggression aIPg contributes to persistent aggression. When these cells were activated, the flies would fight for up to 10 minutes after the barrier was removed. But another cell type previously found to be involved in aggression pC1d did not cause this same enduring anger.

pC1d also didnt affect whether aIPg caused persistent aggression, and neither pC1d nor aIPg showed persistent neuronal activity. These findings suggest that a persistent aggressive state doesnt depend on a recurrent connection between the two cell types.

Previous research had shown that stimulating another cell associated with aggression pC1e also does not cause persistent behavior on its own. However, Schretter and colleagues were surprised to find that when pC1d and pC1e were stimulated simultaneously, the flies remained persistently aggressive.

Taken together, the results suggest that the persistent aggressive state may be maintained by a mechanism different from what the researchers had originally thought. Instead of being due to a recurrent connection between aIPg and pC1d, as they had hypothesized, persistent aggression could involve pC1e.

But it could also include other factors, such as a neuromodulator acting on the circuit or the effect of neurons downstream from aIPg, pC1d, and pC1e. Or aggression could be controlled by another circuit altogether.

Schretter says investigating these other models to explain persistent aggression is the next step.

Its exciting to see what else could lengthen that persistence, because there could be other circuits that are also involved, she says. It is basically open for us to go after, so it is a fun place to be.

Author: Nanci Bompey Source: HHMI Contact: Nanci Bompey HHMI Image: The image is credited to the CDC and is in the public domain

Original Research: Open access. Cell type-specific contributions to a persistent aggressive internal state in femaleDrosophila by Katie Schretter et al. eLife

Abstract

Cell type-specific contributions to a persistent aggressive internal state in femaleDrosophila

Persistent internal states are important for maintaining survival-promoting behaviors, such as aggression. In femaleDrosophila melanogaster, we have previously shown that individually activating either aIPg or pC1d cell types can induce aggression.

Here we investigate further the individual roles of these cholinergic, sexually dimorphic cell types, and the reciprocal connections between them, in generating a persistent aggressive internal state.

We find that a brief 30-second optogenetic stimulation of aIPg neurons was sufficient to promote an aggressive internal state lasting at least 10 minutes, whereas similar stimulation of pC1d neurons did not.

While we previously showed that stimulation of pC1e alone does not evoke aggression, persistent behavior could be promoted through simultaneous stimulation of pC1d and pC1e, suggesting an unexpected synergy of these cell types in establishing a persistent aggressive state.

Neither aIPg nor pC1d show persistent neuronal activity themselves, implying that the persistent internal state is maintained by other mechanisms.

Moreover, inactivation of pC1d did not significantly reduce aIPg-evoked persistent aggression arguing that the aggressive state did not depend on pC1d-aIPg recurrent connectivity.

Our results suggest the need for alternative models to explain persistent female aggression.

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Fruit Fly Study Sheds Light on Aggression's Neural Roots - Neuroscience News

Neuroscience

AI Reveals Brain Differences in ADHD – Neuroscience News

Summary: Researchers utilizing artificial intelligence (AI) to analyze brain MRI scans have identified significant differences in white matter tracts of adolescents with ADHD.

The study, involving over 1,700 participants from the multi-institutional Adolescent Brain Cognitive Development Study, used diffusion-weighted imaging (DWI) and a deep-learning AI model to detect these variations.

Elevated fractional anisotropy (FA) values were found in nine white matter tracts in individuals with ADHD, providing objective biomarkers for diagnosis. This approach offers a new, quantitative way to diagnose ADHD, addressing the current reliance on subjective self-reported surveys.

Key Facts:

Source: RSNA

Using artificial intelligence (AI) to analyze specialized brain MRI scans of adolescents with and without attention-deficit/hyperactivity disorder (ADHD), researchers found significant differences in nine brain white matter tracts in individuals with ADHD. Results of the study will be presented today at theannual meetingof the Radiological Society of North America (RSNA).

ADHD is a common disorder often diagnosed in childhood and continuing into adulthood, according to the Centers for Disease Control and Prevention. In the U.S., an estimated 5.7 million children and adolescents between the ages of 6 and 17 have been diagnosed with ADHD.

ADHD often manifests at an early age and can have a massive impact on someones quality of life and ability to function in society, said study co-author Justin Huynh, M.S., a research specialist in the Department of Neuroradiology at the University of California, San Francisco, and medical student at the Carle Illinois College of Medicine at Urbana-Champaign.

It is also becoming increasingly prevalent in society among todays youth, with the influx of smartphones and other distracting devices readily accessible.

Children with ADHD may have trouble paying attention, controlling impulsive behaviors or regulating activity. Early diagnosis and intervention are key to managing the condition.

ADHD is extremely difficult to diagnose and relies on subjective self-reported surveys, Huynh said. There is definitely an unmet need for more objective metrics for diagnosis. Thats the gap we are trying to fill.

Huynh said this is the first study to apply deep learning, a type of AI, to identify markers of ADHD in the multi-institutional Adolescent Brain Cognitive Development (ABCD) Study, which includes brain imaging, clinical surveys and other data on over 11,000 adolescents from 21 research sites in the U.S. The brain imaging data included a specialized type of MRI called diffusion-weighted imaging (DWI).

Prior research studies using AI to detect ADHD have not been successful due to a small sample size and the complexity of the disorder, Huynh said.

The research team selected a group of 1,704 individuals from the ABCD dataset, including adolescents with and without ADHD. Using DWI scans, the researchers extracted fractional anisotropy (FA) measurements along 30 major white matter tracts in the brain. FA is a measure of how water molecules move along the fibers of white matter tracts.

The FA values from 1,371 individuals were used as input for training a deep-learning AI model, which was then tested on 333 patients, including 193 diagnosed with ADHD and 140 without. ADHD diagnoses were determined by the Brief Problem Monitor assessment, a rating tool used for monitoring a childs functioning and their responses to interventions.

With the help of AI, the researchers discovered that in patients with ADHD, FA values were significantly elevated in nine white matter tracts.

These differences in MRI signatures in individuals with ADHD have never been seen before at this level of detail, Huynh said. In general, the abnormalities seen in the nine white matter tracts coincide with the symptoms of ADHD.

The researchers intend to continue obtaining data from the rest of the individuals in the ABCD dataset, comparing the performance of additional AI models.

Many people feel that they have ADHD, but it is undiagnosed due to the subjective nature of the available diagnostic tests, Huynh said.

This method provides a promising step towards finding imaging biomarkers that can be used to diagnose ADHD in a quantitative, objective diagnostic framework, Huynh said.

Co-authors are Pierre F. Nedelec, M.S., M.T.M., Samuel Lashof-Regas, Michael Romano, M.D., Ph.D., Leo P. Sugrue, M.D., Ph.D., and Andreas M. Rauschecker, M.D., Ph.D.

Author: Linda Brooks Source: RSNA Contact: Linda Brooks RSNA Image: The image is credited to Neuroscience News

Original Research: The findings will be presented at the 109th Scientific Assembly and Annual Meeting of the Radiological Society of North America

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AI Reveals Brain Differences in ADHD - Neuroscience News

Neuroscience

RNA’s Pivotal Role in Fear Memory and PTSD Treatment – Neuroscience News

Summary: Researchers have revealed a groundbreaking role of RNA in fear-related learning and memory. Their study shows how noncoding RNA Gas5 influences neuronal excitability, impacting learning and memory processes.

Another study identified m6A-modified RNAs that regulate synaptic plasticity, crucial for fear extinction memory, a key factor in PTSD. These findings offer new insights into RNAs role in the brain and potential RNA-based therapies for PTSD.

Key Facts:

Source: University of Queensland

Researchers fromThe University of Queenslandhave discovered a new way ribonucleic acid (RNA) impacts fear-related learning and memory.

Professor Timothy BredyfromUQs Queensland Brain Institutesaid this is an exciting example of RNAs role in fine-tuning the cellular functions in the brain.

In a paper published inNature Communications, researchers demonstrated that a noncoding RNA known as Gas5 coordinates the trafficking and clustering of RNA molecules inside the long processes of neurons, and orchestrating neuronal excitability in real time that contributes to learning and memory.

Understanding the complex world of RNA is a rapidly emerging area of neuroscience research, where we are constantly learning more about how different classes of RNA control the communication between and within brain cells, Professor Bredy said.

In this study, we found learning-related RNAs at the synapse and one, in particular, called Gas5 seems to be uniquely required for fear extinction memory.

Theres a lot more happening with these kinds of RNA molecules than we first thought and that fact they influence cellular function on a millisecond timeframe, which mirrors the real time changes in synaptic function that happen in the brain during learning, is extraordinary.

Non-coding RNA may be the missing link to understanding how the brain processes critically important inputs that lead to the formation of memory

This study builds on earlier findings this year from the Bredy Lab which identified a separate population of learning-related RNAs that accumulate near the synapse the junction between neurons that allow them to communicate.

In that paper, published in theJournal of Neuroscience, they uncovered several new synapse-specific RNA that harbour a specific chemical tag called N6-methyladenosine (m6A).

Lead authorDr Sachithrani Madugallesaid the findings highlighted the importance of m6A-modified RNAs in regulating synaptic plasticity.

Readers are proteins that bind to the chemical tag and direct it to locations and functions, Dr Madugalle said.

The readers allowed us to determine the functional role of m6A-modified RNA molecules in the formation of new memories.

By examining one such RNA, Malat1, we discovered the key proteins that interact with this RNA and support processes related to an important type of memory called fear extinction.

Fear extinction impairment is associated with post-traumatic stress disorder (PTSD).

When Malat1 is chemically decorated with m6A, this allows it to interact with different proteins in the synaptic compartment, which can then alter the mechanisms involved in the formation of fear extinction memory.

This new information may inform the development of future RNA therapies to address PTSD.

By understanding where, when, and how an RNA molecule is activated and having a precise marker will help us identify the target for therapies.

In addition, in both studies the team employed an innovative new tool that allowed them to manipulate the functional state of an RNA molecule, together with Professor Bryan Dickinson and Dr. Simone Rauch at the University of Chicago.

We are now looking for ways to harness RNA to control the aspects of synaptic function underlying memory formation and to potentially develop an RNA therapeutic for the treatment of PTSD and phobia, Professor Bredy said.

Author: Lisa Clarke Source: University of Queensland Contact: Lisa Clarke University of Queensland Image: The image is credited to Neuroscience News

Original Research: Open access. Fear extinction is regulated by the activity of long noncoding RNAs at the synapse by Sachithrani Madugalle et al. Nature Communications

Closed access. Synapse-Enriched m6A-Modified Malat1 Interacts with the Novel m6A Reader, DPYSL2, and Is Required for Fear-Extinction Memory by Sachithrani Madugalle et al. Journal of Neuroscience

Abstract

Fear extinction is regulated by the activity of long noncoding RNAs at the synapse

Long noncoding RNAs (lncRNAs) represent a multidimensional class of regulatory molecules that are involved in many aspects of brain function.

Emerging evidence indicates that lncRNAs are localized to the synapse; however, a direct role for their activity in this subcellular compartment in memory formation has yet to be demonstrated.

Using lncRNA capture-seq, we identified a specific set of lncRNAs that accumulate in the synaptic compartment within the infralimbic prefrontal cortex of adult male C57/Bl6 mice.

Among these was a splice variant related to the stress-associated lncRNA,Gas5. RNA immunoprecipitation followed by mass spectrometry and single-molecule imaging revealed that thisGas5isoform, in association with the RNA binding proteins G3BP2 and CAPRIN1, regulates the activity-dependent trafficking and clustering of RNA granules.

In addition, we found that cell-type-specific, activity-dependent, and synapse-specific knockdown of theGas5variant led to impaired fear extinction memory.

These findings identify a new mechanism of fear extinction that involves the dynamic interaction between local lncRNA activity and RNA condensates in the synaptic compartment.

Abstract

Synapse-Enriched m6A-Modified Malat1 Interacts with the Novel m6A Reader, DPYSL2, and Is Required for Fear-Extinction Memory

The RNA modification N6-methyladenosine (m6A) regulates the interaction between RNA and various RNA binding proteins within the nucleus and other subcellular compartments and has recently been shown to be involved in experience-dependent plasticity, learning, and memory.

Using m6A RNA-sequencing, we have discovered a distinct population of learning-related m6A- modified RNAs at the synapse, which includes the long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 (Malat1). RNA immunoprecipitation and mass spectrometry revealed 12 new synapse-specific learning-induced m6A readers in the mPFC of male C57/BL6 mice, with m6A-modifiedMalat1binding to a subset of these, including CYFIP2 and DPYSL2.

In addition, a cell type- and synapse-specific, and state-dependent, reduction of m6A onMalat1impairs fear-extinction memory; an effect that likely occurs through a disruption in the interaction betweenMalat1and DPYSL2 and an associated decrease in dendritic spine formation.

These findings highlight the critical role of m6A in regulating the functional state of RNA during the consolidation of fear-extinction memory, and expand the repertoire of experience-dependent m6A readers in the synaptic compartment.

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RNA's Pivotal Role in Fear Memory and PTSD Treatment - Neuroscience News

Neuroscience

Personality Predictors of Dementia; Parkinson’s Blood Test; Klotho in Alzheimer’s – Medpage Today

Personality traits were strong predictors of dementia diagnoses in a meta-analysis, but were not consistently associated with neuropathology at autopsy. (Alzheimer's and Dementia)

Neuronally derived extracellular vesicle-associated alpha-synuclein in serum correctly identified 80% of at-risk people who phenoconverted to Parkinson's disease and related dementia. (JAMA Neurology)

High-dose nicotinamide riboside eased Parkinson's motor symptoms in a phase I trial. (Nature Communications)

Injecting allogeneic neural stem cells into the brains of people with secondary progressive multiple sclerosis was tolerated in a phase I study. (Cell Stem Cell)

Klotho protein levels differed in clinical stages of Alzheimer's and were associated with amyloid and tau burden. (JAMA Network Open)

Newborn infants perceived the beat in music. (Cognition)

Short sleep and sleep variability were linked with impaired cognitive performance in older adults. (JAMA Network Open)

Liver fibrosis was associated with cognitive decline in Parkinson's disease. (Journal of Clinical Neuroscience)

Blood-based biomarkers of amyloid, tau, and neurodegeneration were tied to domain-specific neuropsychological performance in women with and without HIV. (JAMA Network Open)

Microglia with the R47H/+ mutation in TREM2 protein promoted synapse loss in mice. (GLIA)

Also in mice, salty immune cells that surrounded the brain were linked with hypertension-induced dementia. (Nature Neuroscience)

A Norwegian study found a moderate association between objectively measured hearing impairment and dementia in people ages 70 to 85. (eClinicalMedicine)

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimers, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinsons, ALS, concussion, CTE, sleep, pain, and more. Follow

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Personality Predictors of Dementia; Parkinson's Blood Test; Klotho in Alzheimer's - Medpage Today

Neuroscience

Tinnitus Linked to Auditory Nerve Loss – Neuroscience News

Summary: A new study reveals that tinnitus, a common auditory issue characterized by ringing in the ears, is associated with undetected auditory nerve loss. This finding challenges the traditional understanding that tinnitus is solely a result of brain maladaptation to hearing loss.

The study shows that individuals with normal hearing tests but experiencing tinnitus actually suffer from cochlear synaptopathy, a type of hidden hearing loss. This discovery paves the way for potential treatments, including nerve regeneration through neurotrophins, bringing hope for millions affected worldwide.

Key Facts:

Source: Mass Eye and Ear

A new study fromMass Eye and Earinvestigators shows that individuals who report tinnitus, which present as a ringing in the ears in more than one out of ten adults worldwide, are experiencing auditory nerve loss that is not picked up by conventional hearing tests.

This work is part of aP50 grantawarded by the National Institutes of Health (NIH) to Mass Eye and Ear researchers within the Eaton-Peabody Laboratories (EPL) for their work on cochlear synaptopathy, which is commonly referred to as hidden hearing loss.

The results from this study provide a better understanding on the origins of tinnitus and are published November 30th inScientific Reports.

Beyond the nuisance of having persistent ringing or other sounds in the ears, tinnitus symptoms are debilitating in many patients, causing sleep deprivation, social isolation, anxiety and depression, adversely affecting work performance, and reducing significantly their quality of life, said senior authorStphane F. Maison, PhD, CCC-A, a principal investigator at Mass Eye and Ear, a member of Mass General Brigham, and clinical director of the Mass Eye and Ear Tinnitus Clinic.

We wont be able to cure tinnitus until we fully understand the mechanisms underlying its genesis. This work is a first step toward our ultimate goal of silencing tinnitus.

Many individuals with hearing loss report a buzzing, humming, ringing or even roaring sound in their ears. Its been a longstanding idea that these symptoms, known as tinnitus, arise as a result of a maladaptive plasticity of the brain.

In other words, the brain tries to compensate for the loss of hearing by increasing its activity, resulting in the perception of a phantom sound, tinnitus. Until recently though, this idea was disputed as some tinnitus sufferers have normal hearing tests.

However, the discovery of cochlear synaptopathy back in 2009 by Mass Eye and Ear investigators brought back to life this hypothesis as it was evidenced that patients with a normal hearing test can have a significant loss to the auditory nerve.

In view of this paradigm shift in the way researchers and clinicians think about hearing loss, Maison and his team sought to determine if such hidden damage could be associated with the tinnitus symptoms experienced by a cohort of normal hearing participants.

By measuring the response of their auditory nerve and brainstem, the researchers found that chronic tinnitus was not only associated with a loss of auditory nerve but that participants showed hyperactivity in the brainstem.

Our work reconciles the idea that tinnitus may be triggered by a loss of auditory nerve, including in people with normal hearing, said Maison.

In terms of future directions, the investigators aim to capitalize on recent work geared toward the regeneration of auditory nerve via the use of drugs called neurotrophins.

The idea that, one day, researchers might be able to bring back the missing sound to the brain and, perhaps, reduce its hyperactivity in conjunction with retraining, definitely brings the hope of a cure closer to reality, Maison added.

Disclosures:The authors declare no competing interests.

Funding:This work was supported by a grant from the NIDCD (P50 DC015857) and the Lauer Tinnitus Research Center at the Mass Eye and Ear.

Author: Ryan Jaslow Source: Mass Eye and Ear Contact: Ryan Jaslow Mass Eye and Ear Image: The image is credited to Neuroscience News

Original Research: The findings will appear in Scientific Reports

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Tinnitus Linked to Auditory Nerve Loss - Neuroscience News

Neuroscience

Heartbeat’s Influence on Brain Activity – Neuroscience News

Summary: New research uncovered that the phases of a heartbeat significantly influence brain and motor system excitability.

The study utilized transcranial magnetic stimulation (TMS) on 37 healthy volunteers to observe changes in cortical and corticospinal excitability across the cardiac cycle. They found heightened excitability during the systolic phase, when blood vessels are distended.

This discovery could revolutionize treatments for depression and stroke by aligning them with the cardiac cycle for enhanced effectiveness.

Key Facts:

Source; PLOS

Optimal windows exist for action and perception during the 0.8 seconds of a heartbeat, according to research published November 28thin the open access journalPLOS Biology.

The sequence of contraction and relaxation is linked to changes in the motor system and its ability to respond to stimulation, and this could have implications for treatments for depression and stroke that excite nerve cells.

The ways in which we perceive and engage with the world are influenced by internal bodily processes such as heartbeats, respiration and digestion. Cardiac activity can influence auditory and visual perception, and touch and sensory perceptions have been shown to be impaired during the systolic phase of the cardiac cycle when blood vessels are briefly distended.

Esra Al of the Max Planck Institute for Human Cognitive and Brain Sciences,Germany, and colleagues, wanted to understand whether there were changes in cortical and corticospinal excitability the ability to respond to stimuli across the cardiac cycle. 37 healthy human volunteers aged between 18 and 40 years received a series of transcranial magnetic stimulation (TMS) pulses non-invasive short magnetic pulses that stimulate nerve cells above the right side of the brain.

Motor and cortical responses as well as heartbeats were measured during the pulses and the authors found that higher excitability was recorded during the systolic phase. These simultaneous recordings of brain activity, heart activity, and muscle activity, suggest the timing of heartbeats and their neural processing are linked to changes in the excitability of the motor system.

TMS is used in treatments for depression and recovery after stroke. The research raises questions about whether these could be fine-tuned to improve results, as well as contributing to a greater understanding of brain-body interactions in health and in disease.

The authors add, Intriguingly, this study uncovers a remarkable connection between the human heart and brain, revealing distinct time windows tailored for action and perception.

Author: Claire Turner Source: PLOS Contact: Claire Turner PLOS Image: The image is credited to Neuroscience News

Original Research: Open access. Cardiac activity impacts cortical motor excitability by Esra Al et al. PLoS Biology

Abstract

Cardiac activity impacts cortical motor excitability

Human cognition and action can be influenced by internal bodily processes such as heartbeats. For instance, somatosensory perception is impaired both during the systolic phase of the cardiac cycle and when heartbeats evoke stronger cortical responses.

Here, we test whether these cardiac effects originate from overall changes in cortical excitability.

Cortical and corticospinal excitability were assessed using electroencephalographic and electromyographic responses to transcranial magnetic stimulation while concurrently monitoring cardiac activity with electrocardiography.

Cortical and corticospinal excitability were found to be highest during systole and following stronger neural responses to heartbeats. Furthermore, in a motor task, handmuscle activity and the associated desynchronization of sensorimotor oscillations were stronger during systole.

These results suggest that systolic cardiac signals have a facilitatory effect on motor excitabilityin contrast to sensory attenuation that was previously reported for somatosensory perception. Thus, it is possible that distinct time windows exist across the cardiac cycle, optimizing either perception or action.

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Heartbeat's Influence on Brain Activity - Neuroscience News

Neuroscience

The Intersection of Art and Neuroscience: Exploring the Beauty and Complexity of the Brain – Medriva

The Intersection of Art and Neuroscience

Every year, the Art of Neuroscience competition presents a unique opportunity for artists to bring the intricate beauty and complexity of the brain to life. These artistic representations, ranging from visualizations of diseased neurons and neurodegenerative diseases to creative portrayals of the brains inner workings, serve not only as a celebration of the aesthetics of science but also as a platform for communicating the technical outputs of brain research and challenging long-held societal beliefs.

One of the most remarkable aspects of this competition is its focus on portraying the real-world ramifications of complex disorders. Particularly noteworthy is the emphasis on the experiences of individuals living with Functional Neurological Disorder (FND). These artworks offer a poignant, personal perspective on the struggles and resilience of those affected by this condition, fostering empathy and understanding among viewers.

The competition also delves into the fascinating concept of an inner Mars through a meditation practice. This unusual approach to neuroscience stimulates contemplation about our brains capabilities and potential for exploration and discovery, much like the uncharted terrain of the red planet.

Another captivating aspect of this competition is the endeavor to restore the lost voices of medical history. Through their creative work, artists shed light on forgotten narratives and highlight the human stories intertwined with the development of neuroscience. This approach not only enriches our understanding of the fields history but also underscores the individual experiences that have shaped its progression.

Some submissions take a dynamic approach to neuroscience by portraying the brains malleability through a choreographed interpretation of neuroplasticity. These performances encapsulate the brains incredible ability to adapt and change, providing a vivid, kinetic demonstration of this fundamental biological process.

With the advancement of technology, digital art installations have started to play a significant role in the Art of Neuroscience competition. For instance, a collaboration between the Society for Neuroscience, ARTECHOUSE, and a team of neurobiologists has resulted in an immersive experience of a human neuron. This digital endeavor brings viewers up close and personal with the intricate structures and processes of a neuron, offering a fresh perspective on these essential components of our nervous system.

Microscopy imaging also holds a special place in the competition. The Image of the Year 2022 Americas Winner, Igor Siwanowicz, demonstrated the potential for this technique to capture the art of the natural world. His winning image of a morning glory pollen grain germinating on the flowers stigma is a testament to the power of microscopy to reveal the hidden beauty in the microscopic world surrounding us.

In conclusion, the Art of Neuroscience competition is more than just a showcase of artistic talent. Its a platform for dialogue, understanding, and exploration, illuminating the many facets of the brain and the field of neuroscience. By exploring the intersection of art and science, the competition encourages us to view these disciplines not as separate entities but as complementary perspectives that can enrich our understanding of the world and ourselves.

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The Intersection of Art and Neuroscience: Exploring the Beauty and Complexity of the Brain - Medriva