Category Archives: Neuroscience

Neuroscience

Uncovering the Hidden Risks of Young-Onset Dementia – Neuroscience News

Summary: A new study reveals 15 risk factors for young-onset dementia, challenging the notion that genetics are the sole cause. These factors, ranging from education and socioeconomic status to lifestyle and health issues, offer hope for prevention.

With around 370,000 new cases each year, this research sheds light on a condition often overlooked. International collaboration and big data played a crucial role in advancing our understanding of dementia.

Key Facts:

Source: University of Exeter

Researchers have identified a wide range of risk factors for young-onset dementia. The findings challenge the notion that genetics are the sole cause of the condition, laying the groundwork for new prevention strategies.

The largescale study identified 15 risk factors, which are similar to those for late-onset dementia. For the first time, they indicate that it may be possible to reduce the risk of young-onset dementia by targeting health and lifestyle factors.

Relatively little research has been done on young-onset dementia, though globally there are around 370,000 new cases of young-onset dementia each year.

Published inJAMA Neurology, the new research by the University of Exeter and Maastricht University followed more than 350,000 participants younger than 65 across the United Kingdom from the UK Biobank study. The team evaluated a broad array of risk factors ranging from genetic predispositions to lifestyle and environmental influences.

The study revealed that lower formal education, lower socioeconomic status, genetic variation, lifestyle factors such as alcohol use disorder and social isolation, and health issues including vitamin D deficiency, depression, stroke, hearing impairment and heart disease significantly elevate risk of young-onset dementia

Professor David Llewellyn of the University of Exeter emphasized the importance of the findings: This breakthrough study illustrates the crucial role of international collaboration and big data in advancing our understanding of dementia. Theres still much to learn in our ongoing mission to prevent, identify, and treat dementia in all its forms in a more targeted way.

This is the largest and most robust study of its kind ever conducted. Excitingly, for the first time it reveals that we may be able to take action to reduce risk of this debilitating condition, through targeting a range of different factors.

Dr Stevie Hendriks, Researcher at Maastricht University, said: Young-onset dementia has a very serious impact, because the people affected usually still have a job, children, and a busy life. The cause is often assumed to be genetic, but for many people we dont actually know exactly what the cause is. This is why we also wanted to investigate other risk factors in this study.

Sebastian Khler, Professor of Neuroepidemiology at Maastricht University, said: We already knew from research on people who develop dementia at older age that there are a series of modifiable risk factors.

In addition to physical factors, mental health also plays an important role, including avoiding chronic stress, loneliness and depression. The fact that this is also evident in young-onset dementia came as a surprise to me, and it may offer opportunities to reduce risk in this group too.

The studys support was supported by Alzheimers Research UK, The Alan Turing Institute/Engineering and Physical Sciences Research Council, Alzheimer Nederland, Gieskes Strijbis Fonds, the Medical Research Council, the National Institute for Health and Care Research (NIHR) Applied Research Collaboration South West Peninsula (PenARC), the National Health and Medical Research Council, the National Institute on Aging, and Alzheimer Netherlands.

Dr Janice Ranson, Senior Research Fellow at the University of Exeter, said: Our research breaks new ground in identifying that the risk of young-onset dementia can be reduced.We think this could herald a new era in interventions to reduce new cases of this condition.

Dr Leah Mursaleen, Head of Clinical Research at Alzheimers Research UK, which co-funded the study, said: Were witnessing a transformation in understanding of dementia risk and, potentially, how to reduce it on both an individual and societal level.

In recent years, theres been a growing consensus that dementia is linked to 12 specific modifiable risk factors such as smoking, blood pressure and hearing loss. Its now accepted that up to four in 10 dementia cases worldwide are linked to these factors.

This pioneering study shines important and much-needed light on factors influencing the risk of young-onset dementia. This starts to fill in an important gap in our knowledge. It will be important to build on these findings in broader studies.

Author: Louise Vennells Source: University of Exeter Contact: Louise Vennells University of Exeter Image: The image is credited to Neuroscience News

Original Research: Closed access. Risk factors for young-onset dementia in the UK Biobank: A prospective population-based study by David Llewellyn et al. JAMA Neurology

Abstract

Risk factors for young-onset dementia in the UK Biobank: A prospective population-based study

Importance

There is limited information on modifiable risk factors for young-onset dementia (YOD).

Objective

To examine factors that are associated with the incidence of YOD.

Design, Setting, and Participants

This prospective cohort study used data from the UK Biobank, with baseline assessment between 2006 and 2010 and follow-up until March 31, 2021, for England and Scotland, and February 28, 2018, for Wales. Participants younger than 65 years and without a dementia diagnosis at baseline assessment were included in this study. Participants who were 65 years and older and those with dementia at baseline were excluded. Data were analyzed from May 2022 to April 2023.

Exposures

A total of 39 potential risk factors were identified from systematic reviews of late-onset dementia and YOD risk factors and grouped into domains of sociodemographic factors (education, socioeconomic status, and sex), genetic factors (apolipoprotein E), lifestyle factors (physical activity, alcohol use, alcohol use disorder, smoking, diet, cognitive activity, social isolation, and marriage), environmental factors (nitrogen oxide, particulate matter, pesticide, and diesel), blood marker factors (vitamin D, C-reactive protein, estimated glomerular filtration rate function, and albumin), cardiometabolic factors (stroke, hypertension, diabetes, hypoglycemia, heart disease, atrial fibrillation, and aspirin use), psychiatric factors (depression, anxiety, benzodiazepine use, delirium, and sleep problems), and other factors (traumatic brain injury, rheumatoid arthritis, thyroid dysfunction, hearing impairment, and handgrip strength).

Main Outcome and Measures

Multivariable Cox proportional hazards regression was used to study the association between the risk factors and incidence of YOD. Factors were tested stepwise first within domains and then across domains.

Results

Of 356052 included participants, 197036 (55.3%) were women, and the mean (SD) age at baseline was 54.6 (7.0) years. During 2 891 409 person-years of follow-up, 485 incident YOD cases (251 of 485 men [51.8%]) were observed, yielding an incidence rate of 16.8 per 100000 person-years (95% CI, 15.4-18.3). In the final model, 15 factors were significantly associated with a higher YOD risk, namely lower formal education, lower socioeconomic status, carrying 2 apolipoprotein 4 allele, no alcohol use, alcohol use disorder, social isolation, vitamin D deficiency, high C-reactive protein levels, lower handgrip strength, hearing impairment, orthostatic hypotension, stroke, diabetes, heart disease, and depression.

Conclusions and Relevance

In this study, several factors, mostly modifiable, were associated with a higher risk of YOD. These modifiable risk factors should be incorporated in future dementia prevention initiatives and raise new therapeutic possibilities for YOD.

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Uncovering the Hidden Risks of Young-Onset Dementia - Neuroscience News

Neuroscience

Enhancing Motor Learning with Visual-Motor Illusions – Neuroscience News

Summary: Researchers found that visual aids creating illusions of movement, like screens showing a hands motion, can enhance motor performance and early-stage motor learning. Functional near-infrared spectroscopy revealed distinct brain activity changes in motor learning regions compared to traditional third-person motion observation. These findings may have implications for innovative treatments for hemiplegic stroke patients.

Key Facts:

Source: Tokyo Metropolitan University

Researchers from Tokyo Metropolitan University showed that visual aids which create the illusion of movement, like a screen placed in front of ones hand showing the hand move, can improve motor performance and the early stages of motor learning.

Compared to observing third-person motions, functional near-infrared spectroscopy data also showed greater changes in brain activity in regions associated with motor learning. Findings like this might inform new treatment strategies for hemiplegic stroke patients.

Visual-motor illusion (VMI) is the curious illusion of watching your body move even while it is still. Imagine having a tablet screen placed in front of your hand. Your hand is hidden behind the tablet, and your hand is not moving. Now, imagine the screen playing a video of your hand moving; your eyes are telling you that your hand is moving, but it is not moving at all.

This unsettling situation is instantly resolved if you put the screen somewhere else; watching the screen now simply entails action observation (AO). Previous work has already shown that VMI and AO entail different responses in the brain, but the wider implications of VMI remained unclear.

Now, a team of scientists led by Assistant Professor Katsuya Sakai from Tokyo Metropolitan University have shown that VMI can improve motor performance and early-stage motor learning. Volunteers were set a specific task, rolling two metal ball around in one hand. After some initial testing, a visual aid was used which showed hands performing this exact action.

One group had the visual aid placed in front of their hand to invoke VMI, while another group simply watched the same video normally. Performance could be measured by the number of complete rolls that people managed.

Though both groups showed improvement, the VMI group showed more improvement than the AO group, both immediately after the video was shown to volunteers, and one hour afterwards. This not only shows improvement in performance but highlights that early-stage learning has also improved i.e. the changes can persist.

To understand what is happening in the brain, the team used functional near-infrared spectroscopy, a non-invasive technique that helps track activity in specific parts of the brain using external probes. They were able to find key differences between AO and VMI volunteers in parts of the brain associated with learning new movements.

Importantly, these changes were found to persist an hour after the visual stimuli, matching what they found from performance on the task. This was also in line with previous findings from the group showing how connectivity in parts of the brain responsible for motor execution was enhanced by VMI.

The team note that there is still a lot of work to be done. For example, these findings come from a study on healthy individuals, and there is yet to be any assessment of mid to long-term motor performance.

However, the insights gleaned from this study shed light on a unique strategy to improve motor performance and learning, which may one day be applied to the rehabilitation of hemiplegic stroke patients and guide the development of new treatments.

Funding: This work was supported by JSPS KAKENHI Grant Number 22K17569.

Author: GO TOTSUKAWA Source: Tokyo Metropolitan University Contact: GO TOTSUKAWA Tokyo Metropolitan University Image: The image is credited to Neuroscience News

Original Research: Open access. Differences in the early stages of motor learning between visualmotor illusion and action observation by Katsuya Sakai et al. Scientific Reports

Abstract

Differences in the early stages of motor learning between visualmotor illusion and action observation

The visual-motor illusion (VMI) induces a kinesthetic illusion by watching ones physically-moving video while the body is at rest. It remains unclear whether the early stages (immediately to one hour later) of motor learning are promoted by VMI. This study investigated whether VMI changes the early stages of motor learning in healthy individuals.

Thirty-six participants were randomly assigned to two groups: the VMI or action observation condition. Each condition was performed with the left hand for 20min.

The VMI condition induced a kinesthetic illusion by watching ones ball-rotation task video. The action observation condition involved watching the same video as the VMI condition but did not induce a kinesthetic illusion. The ball-rotation task and brain activity during the task were measured pre, post1 (immediately), and post2 (after 1h) in both conditions, and brain activity was measured using functional near-infrared spectroscopy.

The rate of the ball-rotation task improved significantly at post1 and post2 in the VMI condition than in the actionobservation condition. VMI condition lowers left dorsolateral prefrontal cortex and right premotor area activity from post1 to pre compared to the actionobservation condition. In conclusion, VMI effectively aids early stages ofmotor learning in healthy individuals.

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Enhancing Motor Learning with Visual-Motor Illusions - Neuroscience News

Neuroscience

Tips from neuroscience to form healthy habits and break unhealthy ones – The Washington Post

Sharing your goal with friends to stay accountable or making a more public commitment, on social media for example, can be helpful tools for some people, Bermdez said.

Reframing the benefits of a goal can also be a powerful tool. If your goal is exercise-focused but the physical and psychological benefits arent motivation on their own, reframing time spent exercising as, Oh, this is a chance for me to catch up with my podcasts or with the music that I love, or its a chance for me to go outside, can be helpful, Bermdez said. Conversely, to break a habit, focus on the negatives of the tempting action, he said, because it will start to look increasingly less appealing.

Bermdez said its important to monitor if the strategy youve chosen is working and, if not, to be open to trying others. You may even need to reevaluate the goal itself.

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Tips from neuroscience to form healthy habits and break unhealthy ones - The Washington Post

Neuroscience

SYNGAP1 findings illuminate links between mutations, intellectual disability – The Transmitter: Neuroscience News and Perspectives

Brain communication relies on a complex set of connections, coordinated by important synaptic proteins. Mutations in one such protein, SYNGAP1, which is critical for brain plasticity, can lead to neurodevelopmental conditions.

SYNGAP1-related intellectual disability (SRID) makes up about 1 percent of intellectual disability cases. It is characterized by seizures, developmental delays and problems with motor coordination. About half of people with SRID have autism.

Recently, a flurry of new SYNGAP1 findings and the development of novel mouse models have expanded scientific understanding of the protein and gene. Together, this work may point to multiple therapeutic possibilities for SRID.

I think its an exciting time, says Gavin Rumbaugh, professor of neuroscience at UF Scripps Biomedical Research in Jupiter, Florida. There is a lot of increased interest in SYNGAP.

For example, past research has indicated that the protein acts as an enzyme to modulate the synaptic connections between neurons. But SYNGAP1 protein may also regulate synaptic plasticity and cognition by physically controlling the number of neurotransmitter receptors at excitatory synapses, according to a preprint posted on bioRxiv in August.

Other work suggests a new role for the gene and protein. In the past, they have primarily been recognized for their effects on synapse functioning. But now SYNGAP1 joins several autism-linked genes that code for synaptic proteins that also shape the developing brain.

A mutation that decreases SYNGAP1 protein levels may exert significant effects on the development of the cortical layers in a human organoid model by disrupting the differentiation of supporting cells that serve as a scaffold for neurons to migrate during development, Rumbaugh and his colleagues have found. Their study was published in Nature Neuroscience in November.

Its very important to use model systems to test the function of the proteins associated with disease at different developmental time points and in different cell types, says lead investigator Giorgia Quadrato, assistant professor of stem cell biology and regenerative medicine at the University of South California in Los Angeles.

A

In developing human neurons cultured in a dish, a lack of SYNGAP1 leads to increased cell size and dendrite length, and speeds up the onset of synaptic activity.

But it was unclear whether or how small mutations in the gene the situation typically seen in people with SRID affect the levels and function of the SYNGAP1 protein, synaptic plasticity and behavior in animals. To address this, lead investigator Richard Huganir and his team at Johns Hopkins University in Baltimore, Maryland, developed two new mouse models.

Each model is based on mutations in the SYNGAP1 gene as they appear in two people a young boy and girl. Its much better to have [models] with patient-based mutations for future therapeutics, says Huganir, professor of neuroscience.

Using CRISPR, the group introduced the two faulty versions of SYNGAP1 into different sets of healthy mice. Both mutations reduced SYNGAP1 protein levels by about 50 percent compared with those of wildtype mice. And the mice showed changes in the expression of genes involved in synaptic plasticity.

Brain slices revealed that the SYNGAP1 mice also had impaired long-term potentiation, the process by which synapses strengthen to facilitate learning and memory. In line with that finding, these mice less frequently went into the arms of a y-shaped maze they had not recently explored than did wildtype rodents.

That behavior indicates the mice might not recall the arm they were in last, which generally reflects deficits in working memory. The mice also displayed hyperactive and repetitive behaviors, typical characteristics in SRID. The results were published in PNAS in September.

I think its an exciting time. There is a lot of increased interest in SYNGAP.

A

The mice showed altered SYNGAP1 functioning that in turn affected synapse functioning, which, would suggest it could increase your risk for developing some sort of mental health disorder, Rumbaugh adds.

This work also reveals that a decrease in SYNGAP1 protein may be a crucial mechanism for the development of SRID. Researchers are already looking for ways to restore the SYNGAP1 protein to treat people with SRID and other neurodevelopmental conditions.

For example, one antisense oligonucleotide a short molecule of DNA or RNA increased the levels of SYNGAP1 in mice in a study published in Neuron in March. Yet another approach to intervention could involve new molecular technology that binds to mRNA and regulates gene expression. The resulting tool brings together the protein-producing machinery for a specific gene, according to a study published in Nature Communications in October.

With this technology, it is possible to elevate SYNGAP1 protein levels in neurons derived from induced pluripotent stem cells that lack one copy of the gene. The approach may open a new avenue for treating conditions such as SRID that are caused by the absence of a functional gene.

[SRID] kids have no direct treatments, says study investigator Bryan Dickinson, professor of chemistry at the University of Chicago in Illinois. There is a critical unmet medical need.

The new mouse strains also offer important therapeutic possibilities. These are actual patient mutations, and that is really cool, says Jill Silverman, professor of psychiatry and behavioral sciences at the University of California, Davis MIND Institute, who was not involved in any of the recent studies.

Its very innovative and important for precision medicine, Silverman says. The sky is the limit.

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SYNGAP1 findings illuminate links between mutations, intellectual disability - The Transmitter: Neuroscience News and Perspectives

Neuroscience

How to keep neuroscience’s past racism from being its future – STAT – STAT

De-Shaine Murray is working at the cutting edge of neurotechnology. As a postdoctoral fellow at Yale, he is developing a device to monitor the brain following traumatic brain injury or stroke.

He is also trying to fight the long legacy of racism in neuroscience. During 2020, when it was difficult to conduct research, he said, I got the chance and the ability to read more widely and to just look into the legacy of neuroscience. He found a direct line from racist pseudoscience like phrenology to disparities in neuroscience today, like how the texture of Black peoples hair can sometimes exclude them from clinical trials because electrodes are not designed for them. In 2021, he co-founded Black in Neuro, an organization dedicated to improving Black representation in neuroscience.

On this episode of the First Opinion Podcast, I spoke to him about how the past and present racism in neuroscience could be reflected in the future, especially as neurotechnology like brain implants become more common.

Im not saying that whatever electrode that you made or created is racist. But when you have someone who creates a technology but doesnt think about the wide range of users that are potentially going to use it, then thats where the problem comes in, he told me.

We also discussed the way inequities in neuroscience research are visible in stroke wards, how brain implants might jump from helping disabled people to being used for human enhancement, and more.

Our conversation was inspired by his recent First Opinion essay, Neuroscience has to grapple with a long legacy of racism if it wants to move into the future. The book I mention at the end is Lock In by John Scalzi, a great sci-fi mystery exploring themes of race, socioeconomic status, neurotechnology, and more.

Be sure to sign up for the weekly First Opinion PodcastonApple Podcasts,Spotify,Google Play, or wherever you get your podcasts. And dont forget to sign up for theFirst Opinion newsletterto read each weeks best First Opinion essays.

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How to keep neuroscience's past racism from being its future - STAT - STAT

Neuroscience

PhD in Neuroscience | Elson S. Floyd College of Medicine | Washington State University – Washington State University

WSU College of Medicine in Spokane is home to more than a dozen faculty members who are affiliated with the Neuroscience PhD program. These researchers recruit and mentor graduate students, providing outstanding opportunities for scientific training, scholarship, and collaboration. As the universitys health sciences hub, it is home to world-class health science facilities, faculty, and expertise, as well as partnerships with local and regional hospitals and research facilities.

Completing your studies through the Spokane campus provides a range of options for research areas of focus, with faculty who specialize in the following research areas:

Students complete three 8-week lab rotations during the first year to gain experience on different topics, learn a variety of techniques, and find the right mentor for continuing their research.

Spokane has the benefit of being located in the beautiful Pacific Northwest region, with ample options for outdoor sports and recreation; local shopping, dining, and events.

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PhD in Neuroscience | Elson S. Floyd College of Medicine | Washington State University - Washington State University

Neuroscience

Social and Affective Neuroscience of Autism (SANA) Lab – Yale School of Medicine

The Social and Affective Neuroscience of Autism (SANA) lab focuses on early social and affective development of children with autism and other neurodevelopmental conditions. We aim to discover biomarkers of social and emotional vulnerabilities and novel treatment targets in infancy and early childhood. Our highly interdisciplinary and collaborative research relies on integration of cutting edge clinical behavioral, neurophysiological, and imaging data in service of improving the lives of children living with complex developmental disorders. The blog will highlight our research, staff, and resources. The first blog features two studies that are actively recruiting infants and young children.

This study of emotional development will help us develop better methods for early diagnosis and intervention for behavioral and emotional challenges. It addresses an understudied yet important area by examining emotional vulnerabilities amongst infants with a family history of autism and evaluating their contribution to later emotional and behavioral difficulties. We are recruiting infants 4 months of age or younger with or without a family history of autism (e.g., siblings, parents, aunts, uncles, or cousins). Participation will include fun and family-friendly follow-up visits through 30 months of age and include assessment of social, adaptive, cognitive, and language development; studies of attention involving watching brief videos; and play-based activities to assess your childs emotional development. https://medicine.yale.edu/lab/chawarska/participate/newborns/

This study focuses on the development of repetitive movements. The study will help us better understand the causes and developmental course of repetitive behavior in children. These typically consist of rhythmic movements that do not appear to serve a specific purpose, and may include flapping, posturing, waving, rotating, or tensing of body parts. Repetitive movements are frequently observed in autism, developmental delays, ADHD, anxiety, and other conditions; they have also been reported in children otherwise developing typically. For some, repetitive movements begin to manifest in infancy; for others, they emerge during the first years and tend to persist throughout childhood and adolescence. We are recruiting children 4 years of age and younger with repetitive motor behavior, either typically developing or with autism or other neurodevelopmental conditions such as ADHD. Participation will include a visit to the lab where your child will have a comprehensive diagnostic evaluation, assessment of repetitive behavior, studies of attention, and collection of saliva samples to learn more about genetic factors involved in repetitive behavior. https://medicine.yale.edu/lab/chawarska/participate/young-children

Join a study or be seen in our clinic

Please share this information with families who may be interested.

Submitted by Gitta Selva on December 20, 2023

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Social and Affective Neuroscience of Autism (SANA) Lab - Yale School of Medicine

Neuroscience

The Future of Neuroscience and AI: DeepSouth Supercomputer – Medriva

Stepping into the Future with DeepSouth

The world is on the brink of a significant breakthrough with the development of DeepSouth, the first-ever supercomputer capable of simulating the entire human brain. This trailblazing project, under the leadership of Western Sydney University in Australia, is set to revolutionize neuroscience and artificial intelligence as we know it. With an operational launch date set for 2024, DeepSouth is poised to unlock a myriad of opportunities in medicine, technology, and beyond.

DeepSouth isnt just another supercomputer it is a powerhouse that matches the human brains estimated rate of operations. With the ability to perform 228 trillion synaptic operations per second, it is set to redefine what technology can achieve. Its not just about the staggering numbers; its about how DeepSouth uses this power. The supercomputer is designed to process colossal amounts of information with minimal power, emulating the efficiency of the human brain.

What sets DeepSouth apart is its neuromorphic system. Unlike traditional computer systems, the neuromorphic system is designed to operate like networks of neurons. This unique configuration allows the supercomputer to emulate large networks of spiking neurons efficiently, requiring less power and enabling greater efficiencies. This ingenious design is what makes the simulation of the entire human brain possible.

DeepSouth is expected to be a game-changer for neuroscience and AI. By simulating the human brain, it will provide unprecedented insights into how our brains process information so efficiently. These findings could lead to breakthroughs in understanding both healthy and diseased human brains, opening new avenues for medical research and treatment. The supercomputer will also be an invaluable resource for researchers looking to prototype new engineering solutions in the AI space.

While the implications for neuroscience are profound, the potential applications of DeepSouth dont stop there. The project could lead to advances in smart devices and sensors, further enhancing the technology that forms an integral part of our lives. With AI applications becoming increasingly prevalent, the insights derived from DeepSouths brain simulations could pave the way for more sophisticated AI systems, pushing the boundaries of what technology can achieve.

As we look forward to DeepSouths operational launch in 2024, its clear that were on the cusp of a new era in technology and neuroscience. This supercomputer isnt just simulating the human brain; its unlocking the potential to understand our brains better, develop more advanced AI, and create smarter technology. The future of neuroscience and AI is bright, and DeepSouth is leading the charge.

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The Future of Neuroscience and AI: DeepSouth Supercomputer - Medriva

Neuroscience

Revolutionizing Neuroscience and AI: The DeepSouth Supercomputer – Medriva

Revolutionizing Neuroscience and AI: The DeepSouth Supercomputer

The world of neuroscience and artificial intelligence is about to experience a seismic shift with the activation of DeepSouth, the first supercomputer designed to simulate the entire human brain. Scheduled to be operational by 2024, this groundbreaking project is being developed by the International Centre for Neuromorphic Systems (ICNS) at Western Sydney University, alongside partners working in the neuromorphic field.

The DeepSouth supercomputer stands as a testament to the incredible advancements in technology and neuroscience. It utilizes a neuromorphic system to efficiently emulate large networks of spiking neurons at a staggering rate of 228 trillion synaptic operations per second, mirroring the human brains operational speed. This ambitious endeavor aims to replicate the brains functions and complexities, offering significant potential insights into neurological disorders and cognitive processes.

This remarkable project holds promise not only for the advancement of neuroscience but also for the development of more efficient AI systems. By mimicking the human brain, researchers aspire to understand better how it operates, thus facilitating the design of more efficient artificial intelligence. The DeepSouth supercomputer is also expected to contribute to the development of smart devices, sensors, and other AI applications, marking a significant leap forward in technology.

One of the essential aspects of this supercomputer is its potential to enhance our understanding of the human brainboth healthy and diseased. This knowledge could revolutionize the way we approach and treat various neurological disorders, leading to improved outcomes for patients worldwide.

The DeepSouth supercomputer is not only a technological marvel but also a profound game changer for neuroscience. It will be of immense interest to researchers studying neuroscience, as well as those prototyping new engineering solutions in the AI space. The supercomputers ability to process vast amounts of information with little power, just like our brains, could open doors to creating a brain vastly more powerful than our own.

The activation of the DeepSouth supercomputer in 2024 is eagerly anticipated by the scientific community. As this revolutionary technology comes to life, it promises to offer unprecedented insights into the human brains workings and pave the way for substantial progress in neuroscience and artificial intelligence. The future of these fields looks incredibly promising, thanks to this groundbreaking project.

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Revolutionizing Neuroscience and AI: The DeepSouth Supercomputer - Medriva

Neuroscience

Breathing Is The Key to Memory Consolidation During Sleep – Neuroscience News

Summary: Researchers unveiled a critical link between breathing and memory consolidation during sleep. In an extensive study involving EEG and breathing analysis, they discovered that specific sleep-related brain rhythms are directly influenced by our breathing patterns.

These findings highlight the importance of respiration in reinforcing learned information while we sleep. This work could have significant implications for addressing age-related memory issues and sleep disorders.

Key Facts:

Source: LMU

How are memories consolidated during sleep?

In 2021, researchers led by Dr. Thomas Schreiner, leader of the Emmy Noether junior research group at LMUs Department of Psychology, had already shown there was a direct relationship between the emergence of certain sleep-related brain activity patterns and the reactivation of memory contents during sleep.

However, it was still unclear whether these rhythms are orchestrated by a central pacemaker. So the researchers joined up with scientists from the Max Planck Institute for Human Development in Berlin and the University of Oxford to reanalyze the data. Their results have identified respiration as a potential pacemaker.

That is to say, our breathing influences how memories are consolidated during sleep, says Schreiner.

Learning processes investigated in sleep laboratory

For their original study, the researchers showed 20 study participants 120 images over the course of two sessions. All the pictures were associated with certain words. Then the participants slept for around two hours in the sleep laboratory.

When they awoke, they were questioned about the associations they had learned. During the entire learning and sleep period, their brain activity was recorded by means of EEG, along with their breathing.

The researchers discovered that previously learned contents were spontaneously reactivated by the sleeping brain during the presence of so-called slow oscillations and sleep spindles (short phases of increased brain activity).

The precision of the coupling of these sleep-related brain rhythms increases from childhood to adolescenceand then declines again during aging, says Schreiner.

Breathing and brain activity are linked

Because respiration frequency also changes with age, the researchers then analyzed the data in relation to the recorded breathing and were able to establish a connection between them.

Our results show that our breathing and the emergence of characteristic slow oscillation and spindle patterns are linked, says Schreiner.

Although other studies had already established a connection between breathing and cognition during wake, our work makes clear that respiration is also important for memory processing during sleep.

Older people often suffer from sleep disorders, respiratory disorders, and declining memory function. Schreiner plans to further investigate whether there are connections between these phenomena and whether interventions such as the use of CPAP masks, which are already used to treat sleep apnea make sense from a cognitive perspective.

Author: Constanze Drewlo Source: LMU Contact: Constanze Drewlo LMU Image: The image is credited to Neuroscience News

Original Research: Open access. Respiration modulates sleep oscillations and memory reactivation in humans by Thomas Schreiner et al. Nature Communications

Abstract

Respiration modulates sleep oscillations and memory reactivation in humans

The beneficial effect of sleep on memory consolidation relies on the precise interplay of slow oscillations and spindles. However, whether these rhythms are orchestrated by an underlying pacemaker has remained elusive.

Here, we tested the relationship between respiration, which has been shown to impact brain rhythms and cognition during wake, sleep-related oscillations and memory reactivation in humans.

We re-analysed an existing dataset, where scalp electroencephalography and respiration were recorded throughout an experiment in which participants (N=20) acquired associative memories before taking a nap.

Our results reveal that respiration modulates the emergence of sleep oscillations. Specifically, slow oscillations, spindles as well as their interplay (i.e., slow-oscillation_spindle complexes) systematically increase towards inhalation peaks.

Moreover, the strength of respiration slow-oscillation_spindle coupling is linked to the extent of memory reactivation (i.e., classifier evidence in favour of the previously learned stimulus category) during slow-oscillation_spindles.

Our results identify a clear association between respiration and memory consolidation in humans and highlight the role of brain-body interactions during sleep.

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Breathing Is The Key to Memory Consolidation During Sleep - Neuroscience News