Category Archives: Neuroscience

Scientists Linked Artificial and Biological Neurons in a Networkand Amazingly, It Worked – Singularity Hub

Scientists have linked up two silicon-based artificial neurons with a biological one across multiple countries into a fully-functional network. Using standard internet protocols, they established a chain of communication whereby an artificial neuron controls a living, biological one, and passes on the info to another artificial one.

Whoa.

Weve talked plenty about brain-computer interfaces and novel computer chips that resemble the brain. Weve covered how those neuromorphic chips could link up into tremendously powerful computing entities, using engineered communication nodes called artificial synapses.

As Moores law is dying, we even said that neuromorphic computing is one path towards the future of extremely powerful, low energy consumption artificial neural network-based computingin hardwarethat could in theory better link up with the brain. Because the chips speak the brains language, in theory they could become neuroprosthesis hubs far more advanced and natural than anything currently possible.

This month, an international team put all of those ingredients together, turning theory into reality.

The three labs, scattered across Padova, Italy, Zurich, Switzerland, and Southampton, England, collaborated to create a fully self-controlled, hybrid artificial-biological neural network that communicated using biological principles, but over the internet.

The three-neuron network, linked through artificial synapses that emulate the real thing, was able to reproduce a classic neuroscience experiment thats considered the basis of learning and memory in the brain. In other words, artificial neuron and synapse chips have progressed to the point where they can actually use a biological neuron intermediary to form a circuit that, at least partially, behaves like the real thing.

Thats not to say cyborg brains are coming soon. The simulation only recreated a small network that supports excitatory transmission in the hippocampusa critical region that supports memoryand most brain functions require enormous cross-talk between numerous neurons and circuits. Nevertheless, the study is a jaw-dropping demonstration of how far weve come in recreating biological neurons and synapses in artificial hardware.

And perhaps one day, the currently experimental neuromorphic hardware will be integrated into broken biological neural circuits as bridges to restore movement, memory, personality, and even a sense of self.

One important thing: this study relies heavily on a decade of research into neuromorphic computing, or the implementation of brain functions inside computer chips.

The best-known example is perhaps IBMs TrueNorth, which leveraged the brains computational principles to build a completely different computer than what we have today. Todays computers run on a von Neumann architecture, in which memory and processing modules are physically separate. In contrast, the brains computing and memory are simultaneously achieved at synapses, small hubs on individual neurons that talk to adjacent ones.

Because memory and processing occur on the same site, biological neurons dont have to shuttle data back and forth between processing and storage compartments, massively reducing processing time and energy use. Whats more, a neurons history will also influence how it behaves in the future, increasing flexibility and adaptability compared to computers. With the rise of deep learning, which loosely mimics neural processing as the prima donna of AI, the need to reduce power while boosting speed and flexible learning is becoming ever more tantamount in the AI community.

Neuromorphic computing was partially born out of this need. Most chips utilize special ingredients that change their resistance (or other physical characteristics) to mimic how a neuron might adapt to stimulation. Some chips emulate a whole neuron, that is, how it responds to a history of stimulationdoes it get easier or harder to fire? Others imitate synapses themselves, that is, how easily they will pass on the information to another neuron.

Although single neuromorphic chips have proven to be far more efficient and powerful than current computer chips running machine learning algorithms in toy problems, so far few people have tried putting the artificial components together with biological ones in the ultimate test.

Thats what this study did.

Still with me? Lets talk network.

Its gonna sound complicated, but remember: learning is the formation of neural networks, and neurons that fire together wire together. To rephrase: when learning, neurons will spontaneously organize into networks so that future instances will re-trigger the entire network. To wire together, downstream neurons will become more responsive to their upstream neural partners, so that even a whisper will cause them to activate. In contrast, some types of stimulation will cause the downstream neuron to chill out so that only an upstream shout will trigger downstream activation.

Both these propertieseasier or harder to activate downstream neuronsare essentially how the brain forms connections. The amping up, in neuroscience jargon, is long-term potentiation (LTP), whereas the down-tuning is LTD (long-term depression). These two phenomena were first discovered in the rodent hippocampus more than half a century ago, and ever since have been considered as the biological basis of how the brain learns and remembers, and implicated in neurological problems such as addition (seriously, you cant pass Neuro 101 without learning about LTP and LTD!).

So its perhaps especially salient that one of the first artificial-brain hybrid networks recapitulated this classic result.

To visualize: the three-neuron network began in Switzerland, with an artificial neuron with the badass name of silicon spiking neuron. That neuron is linked to an artificial synapse, a memristor located in the UK, which is then linked to a biological rat neuron cultured in Italy. The rat neuron has a smart microelectrode, controlled by the artificial synapse, to stimulate it. This is the artificial-to-biological pathway.

Meanwhile, the rat neuron in Italy also has electrodes that listen in on its electrical signaling. This signaling is passed back to another artificial synapse in the UK, which is then used to control a second artificial neuron back in Switzerland. This is the biological-to-artificial pathway back. As a testimony in how far weve come in digitizing neural signaling, all of the biological neural responses are digitized and sent over the internet to control its far-out artificial partner.

Heres the crux: to demonstrate a functional neural network, just having the biological neuron passively pass on electrical stimulation isnt enough. It has to show the capacity to learn, that is, to be able to mimic the amping up and down-tuning that are LTP and LTD, respectively.

Youve probably guessed the results: certain stimulation patterns to the first artificial neuron in Switzerland changed how the artificial synapse in the UK operated. This, in turn, changed the stimulation to the biological neuron, so that it either amped up or toned down depending on the input.

Similarly, the response of the biological neuron altered the second artificial synapse, which then controlled the output of the second artificial neuron. Altogether, the biological and artificial components seamlessly linked up, over thousands of miles, into a functional neural circuit.

SoIm still picking my jaw up off the floor.

Its utterly insane seeing a classic neuroscience learning experiment repeated with an integrated network with artificial components. That said, a three-neuron network is far from the thousands of synapses (if not more) needed to truly re-establish a broken neural circuit in the hippocampus, which DARPA has been aiming to do. And LTP/LTD has come under fire recently as the de facto brain mechanism for learning, though so far they remain cemented as neuroscience dogma.

However, this is one of the few studies where you see fields coming together. As Richard Feynman famously said, What I cannot recreate, I cannot understand. Even though neuromorphic chips were built on a high-level rather than molecular-level understanding of how neurons work, the study shows that artificial versions can still synapse with their biological counterparts. Were not just on the right path towards understanding the brain, were recreating it, in hardwareif just a little.

While the study doesnt have immediate use cases, practically it does boost both the neuromorphic computing and neuroprosthetic fields.

We are very excited with this new development, said study author Dr. Themis Prodromakis at the University of Southampton. On one side it sets the basis for a novel scenario that was never encountered during natural evolution, where biological and artificial neurons are linked together and communicate across global networks; laying the foundations for the Internet of Neuro-electronics. On the other hand, it brings new prospects to neuroprosthetic technologies, paving the way towards research into replacing dysfunctional parts of the brain with AI chips.

Image Credit: Gerd Altmann from Pixabay

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Scientists Linked Artificial and Biological Neurons in a Networkand Amazingly, It Worked - Singularity Hub

Global Motor Neuron Diseases Treatment Market by Top Key players: NIH, UCL Institute of Neurology, National Neuroscience Institute, The University of…

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Exploring future spinal cord injury therapies – Drug Target Review

Drug Target Review explores five of the latest research developments in the field of spinal cord injury (SCI) repair.

MRIs of Lumbar & Thoracic spine showing how a fracture of thoracic spine gets worse over time.

Researchers have shown that increasing energy supply to injured spinal cord neurons can promote axon regrowth and motor function restoration after a spinal cord injury (SCI).

We are the first to show that spinal cord injury results in an energy crisis that is intrinsically linked to the limited ability of damaged axons to regenerate, said Dr Zu-Hang Sheng, study co-senior author, senior principal investigator at the US National Institute of Neurological Disorders and Stroke (NINDS).

According to the team, energy levels are damaged because the mitochondria that produce adenosine triphosphate (ATP) for neurons are located in the axons. When damaged, the mitochondria are unable to produce ATP at the same level.

Nerve repair requires a significant amount of energy, said Dr Sheng. Our hypothesis is that damage to mitochondria following injury severely limits the available ATP and this energy crisis is what prevents the regrowth and repair of injured axons.

The scientists suggest that this is compounded by the anchoring of mitochondria in adult cells alongside the axons, so once damaged they are hard to replace.

Using a murine model, called a Syntaphilin knockout, where mitochondria are free to move along the axons, the researchers showed that when mitochondria are more mobile, mice have significantly more axon regrowth across the site of SCI compared to control animals. The paper also demonstrated that newly-grown axons made appropriate connections beyond the injury site, leading to functional recovery of motor tasks.

They hypothesised that increasing mitochondrial transport and thus the available energy to the injury site could enable repair of damaged nerve fibres.

When fed creatine, a compound that enhances the formation of ATP, both the control and knockout mice had increased axon regrowth following injury, compared to mice fed saline instead. More robust nerve regrowth was seen in the knockout mice that received creatine.

We were very encouraged by these results, said Dr Sheng. The regeneration that we see in our knockout mice is very significant and these findings support our hypothesis that an energy deficiency is holding back the ability of both central and peripheral nervous systems to repair after injury.

Dr Sheng highlighted that despite the promising results of the study published in Cell Metabolism, genetic manipulation was required for the best regrowth as creatine produced only modest regeneration. He concluded that further research is required to develop therapeutic compounds that are more effective in entering the nervous system and increasing energy production for the treatment of SCI.

Experiments exploring the role of immune and glial cells in wound healing and neural repair has revealed that Plexin-B2, an axon guidance protein, is essential for their organisation after SCI.

The researchers suggest their findings could aid in the development of therapies that target axon guidance pathways for treatment of SCI.

An artists impression of a macrophage.

The paper published in Nature Neuroscience reveals that Plexin-B2 on macrophages and microglia is essential for the process of corralling, where microglia and macrophages are mobilised and form a protective barrier around the site of SCI, separating healthy and necrotic tissue. In this study, researchers found that corralling begins early in the healing process and requires the ability of Plexin-B2 to steer immune cells away from colliding cells.

When they deleted Plexin-B2 from the microglia and macrophages in tissues, it led to tissue damage, inflammatory spillover and hindered axonal regeneration.

The lead investigator Dr Hongyan Jenny Zou, Professor of Neurosurgery and Neuroscience at the Icahn School of Medicine at Mount Sinai, US, said the results were quite unexpected.

She concluded that understanding the signalling pathways and interactions of glial cells with each other and the injury environment is fundamental to improving neural repair after a traumatic brain or spinal cord injury.

Another studyexploring the interactions of macrophages and microglia has revealed that in the central nervous system (CNS), microglia interfere with macrophages preventing them from moving out of damaged regions of the CNS.

We expected the macrophages would be present in the area of injury, but what surprised us was that microglia actually encapsulated those macrophages and surrounded them almost like police at a riot. It seemed like the microglia were preventing them from dispersing into areas they should not be, said Jason Plemel, a medical researcher at Canadas University of Alberta and a member of the Neuroscience and Mental Health Institute.

A microglial cell stained with Rio Hortegas silver carbonate method under the microscope.

Plemel said that more research is required to ascertain why this is happening, but they found that both the immune cells that protect the CNS, microglia and the immune cells of the peripheral immune system, macrophages, are present early after demyelination and microglia continue to accumulate at the expense of macrophages.

When we removed the microglia to understand what their role was, the macrophages entered into uninjured tissue. This suggests that when there is injury, the microglia interfere with the macrophages in our CNS and act as a barrier preventing their movement.

The scientists said that this observation was only possible because they were able to distinguish between microglia and macrophages, which has historically not been possible. Using this technique, they established than one type of microglia responded to demyelination. The results were published in Science Advances.

The indication of at least two different populations of microglia is an exciting confirmation for us, said Plemel. We are continuing to study these populations and hopefully, in time, we can learn what makes them unique in terms of function. The more we know, the closer we get to understanding what is going on (or wrong) when there is neurodegeneration or injury and being able to hypothesise treatment and prevention strategies.

Researchers suggest subpially-injecting neural precursor cells (NSCs) may reduce the risk of further injury associated with current spinal cell delivery techniques.

NSCs have the potential to differentiate into many neural cell types depending on the environment and have been the subject of investigation in both the field of SCI repair and neurodegenerative disease therapies.

subpially-injected cells are likely to accelerate and improve treatment potency in cell-replacement therapies for several spinal neurodegenerative disorders

However, the senior author of this study Dr Martin Marsala, professor in the Department of Anesthesiology at University of California (UC) San Diego School of Medicine, US, explained the current delivery techniques involve direct needle injection into the spinal parenchyma the primary cord of nerve fibres running through the vertebral column, so there is an inherent risk of (further) spinal tissue injury or intraparenchymal bleeding.

The novel technique Dr Marsala proposed in a paper published in Stem Cells Translational Medicine, is to inject these cells into the spinal subpial space an area between the pial membrane and the superficial layers of the spinal cord.

This injection technique allows the delivery of high cell numbers from a single injection, Dr Marsala explained. Cells with proliferative properties, such as glial progenitors, then migrate into the spinal parenchyma and populate over time in multiple spinal segments as well as the brain stem. Injected cells acquire the functional properties consistent with surrounding host cells.

The research collaborators suggest that subpially-injected cells are likely to accelerate and improve treatment potency in cell-replacement therapies for several spinal neurodegenerative disorders. This may include spinal traumatic injury, amyotrophic lateral sclerosis and multiple sclerosis, said study senior author Dr Joseph Ciacci, a neurosurgeon at UC San Diego Health.

The team now intend to move their experiments from rats to larger pre-clinical animal models, more anatomically similar to humans. The goal is to define the optimal cell dosing and timing of cell delivery after spinal injury, which is associated with the best treatment effect, concluded Dr Marsala.

Dr Mohamad Khazaei is the recipient of the STEM CELLS Translational Medicines (SCTM) Young Investigator Award for his work on SCI.

The award recognises advancements in the field of stem cells and regenerative medicine made by young researchers. The recipient is the principal author of an article published in SCTM that, over the course of a year, is deemed to have the most impact.

Dr Khazaeis work focuses on bringing cell-based strategies, such as NSC transplantation, into the therapeutic pipeline through generating and differentiating novel cell types using genetic and cell engineering approaches.

While we currently lack effective regenerative medicine treatment options for spinal cord injuries, Dr Khazaeis work to create a cell transplantation therapy utilising neural precursor cells is novel and provides a promising approach, said Dr Anthony Atala, Editor-in-Chief of SCTM and director of the Wake Forest Institute for Regenerative Medicine.

His winning paper details how Dr Khazaei and his team used neurons and oligodendrocytes to obtain better functional recovery after SCI.

Related topicsCell Regeneration, CNS, Disease research, Drug Delivery, Drug Discovery, Drug Targets, Neurons, Neurosciences, Regenerative Medicine, Research & Development, Therapeutics

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Exploring future spinal cord injury therapies - Drug Target Review

Experts discover toolkit to repair DNA breaks associated with ageing, cancer and Motor Neurone Disease – University of Sheffield News

9 March 2020

A new toolkit to repair damaged DNA that can lead to ageing, cancer and motor neurone disease (MND) has been discovered by scientists at the Universities of Sheffield and Oxford.

Published in Nature Communications, the research shows that a protein called TEX264, together with other enzymes, is able to recognise and eat toxic proteins that can stick to DNA and cause it to become damaged. An accumulation of broken, damaged DNA can cause cellular ageing, cancer and neurological diseases such as MND.

Until now, ways of repairing this sort of DNA damage have been poorly understood, but scientists hope to exploit this novel repair toolkit of proteins to protect us from ageing, cancer and neurological disease.

The findings could also have implications for chemotherapy, which deliberately causes breaks in DNA when trying to kill cancerous cells. Scientists believe targeting the TEX264 protein may offer a new way to treat cancer.

Professor Sherif El-Khamisy, Co-Founder and Deputy Director of the Healthy Lifespan Institute at the University of Sheffield and a professor from the Department of Molecular Biology and Biotechnology and the Neuroscience Institute at the University of Sheffield, who co-led the research said: Failure to fix DNA breaks in our genome can impact our ability to enjoy a healthy life at an old age, as well as leave us vulnerable to neurological diseases like motor neurone disease (MND).

We hope that by understanding how our cells fix DNA breaks, we can help meet some of these challenges, as well as explore new ways of treating cancer in the future.

Professor Kristijan Ramadan from the University of Oxford, who co-led the research, said: Our finding of TEX264, a protein that forms the specialised machinery to digest toxic proteins from our DNA, significantly changes the current understanding of how cells repair the genome and so protect us from accelerated ageing, cancer and neurodegeneration. I believe this discovery has a great potential for cancer therapy in the future and we are already pursuing our research in this direction.

Professor Ramadan added: I am very proud of my research team who initially discovered the involvement of TEX264 in DNA repair.

Oxfords research was supported by funding bodies, including the Medical Research Council. Backing was also received from the Oxford Institute for Radiation Oncology and Department of Oncology.

Professor El-Khamisys lab is funded by the Wellcome Trust and the Lister Institute of Preventative Medicine.

The work forms part of the research taking place at the University of Sheffields Healthy Lifespan Institute and the Neuroscience Institute.

The Healthy Lifespan Institute brings together 120 world-class researchers from a wide range of disciplines with the aim of slowing down the ageing process and tackling the global epidemic of multi-morbidity the presence of two or more chronic conditions in a bid to help everyone live healthier, independent lives for longer and reduce the cost of care.

The Neuroscience Institute aims to translate scientific discoveries from the lab into pioneering treatments that will benefit patients living with neurodegenerative disorders.

The next step of the research will be to test if the behaviour and properties of protein TEX264 is altered in ageing and in neurological disorders such as MND.

The University of SheffieldWith almost 29,000 of the brightest students from over 140 countries, learning alongside over 1,200 of the best academics from across the globe, the University of Sheffield is one of the worlds leading universities.

A member of the UKs prestigious Russell Group of leading research-led institutions, Sheffield offers world-class teaching and research excellence across a wide range of disciplines.

Unified by the power of discovery and understanding, staff and students at the university are committed to finding new ways to transform the world we live in.

Sheffield is the only university to feature in The Sunday Times 100 Best Not-For-Profit Organisations to Work For 2018 and for the last eight years has been ranked in the top five UK universities for Student Satisfaction by Times Higher Education.

Sheffield has six Nobel Prize winners among former staff and students and its alumni go on to hold positions of great responsibility and influence all over the world, making significant contributions in their chosen fields.

Global research partners and clients include Boeing, Rolls-Royce, Unilever, AstraZeneca, Glaxo SmithKline, Siemens and Airbus, as well as many UK and overseas government agencies and charitable foundations.

For further information please contact:

Shemina DavisMediaRelations ManagerThe University of Sheffield0114 222 5339shemina.davis@sheffield.ac.uk

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Experts discover toolkit to repair DNA breaks associated with ageing, cancer and Motor Neurone Disease - University of Sheffield News

Study: Cough That Spreads Tuberculosis Has Pain-Linked Trigger – University of Texas at Dallas

Mycobacterium tuberculosis, which causes TB, produces a fatty acid called sulfolipid-1 that triggers a pain-response cough to spread the disease, according to a study published March 5 in the journal Cell. M. tuberculosis bacteria are shown in the close-up view.

Tuberculosis is distinguished primarily by the persistent cough that serves to spread the disease. Stopping whatever triggers that cough could greatly reduce the transmission of the disease, which annually kills more than 1.3 million people worldwide.

Researchers from The University of Texas at Dallas Center for Advanced Pain Studies worked with colleagues from UTSouthwestern Medical Center to pinpoint a molecule that the tuberculosis bacterium manufactures to induce coughing.

Their findings, published online March 5 in the journal Cell, could help reduce the impact of tuberculosis, which remains one of the top 10 causes of death worldwide, according to the World Health Organization.

Tuberculosis deaths have been greatly reduced in the United States, but it is still a huge issue in many parts of the world, and we would love to have an impact on stopping the spread of the disease, said Dr. Ted Price BS97, Eugene McDermott Professor of neuroscience in the School of Behavioral and Brain Sciences (BBS) and one of five UTDallas authors of the Cell paper. Discovering the mechanism through which TB causes cough affords just such an opportunity, and our collective team has the appropriate expertise to tackle this problem, which we have started to accomplish through this work.

From left: School of Behavioral and Brain Sciences faculty members Drs. Ted Price, Gregory Dussor and Michael Burton were among the authors of the paper published March 5 in Cell.

The idea that nociceptors the nerve cells that respond to pain stimuli cause the coughing associated with TB runs counter to existing suppositions that link the cough to infection-induced lung inflammation or irritation.

No one had ever shown that TB produces an irritant that acts directly on the sensory innervation of the lungs, Price said. We have now shown this directly through our collaborative work on this project.

In testing on rodents, researchers sought to identify the components or products of the Mycobacterium tuberculosis that cause coughing or trigger nociceptors. Ultimately, they identified a fatty acid called sulfolipid-1 (SL-1) as a pain-response trigger. They then reproduced that response in isolated human nociceptor cells. Finally, the researchers altered a strain of Mycobacterium tuberculosis to not produce SL-1. Rodents infected with this version developed other tuberculosis symptoms, but not coughing.

If researchers can show that suppressing cough does not worsen the condition of tuberculosis patients, the spread of the disease might be prevented by developing a drug that inhibits SL-1 production, Price said.

No one had ever shown that TB produces an irritant that acts directly on the sensory innervation of the lungs. We have now shown this directly through our collaborative work on this project.

Dr. Ted Price BS97, Eugene McDermott Professor of neuroscience in the School of Behavioral and Brain Sciences

People with active tuberculosis can cough for months and spread disease even when they are receiving appropriate treatment, said corresponding author Dr. Michael Shiloh, associate professor of internal medicine and microbiology at UTSouthwestern. Someday, doctors may give antibiotics in conjunction with a medication that prevents coughing, which in turn could prevent spread.

Additional UTDallas authors were Dr. Gregory Dussor, associate professor of cognition and neuroscience and Fellow, Eugene McDermott Professor; Dr. Michael Burton, assistant professor in BBS; Dhananjay Naik, a doctoral student in cognition and neuroscience; and Galo Mejia, a graduate student in innovation and entrepreneurship and a research assistant in BBS. Other UTSouthwestern authors included Dr. Connie Hsia, professor of internal medicine; Dr. Tian Qin, assistant professor of biochemistry and a Eugene McDermott Scholar in Biomedical Research; Dr. Laurent Gautron, assistant professor of internal medicine; and first author Cody Ruhl, a graduate student and member of Shilohs lab.

The work of UTDallas researchers was supported in part by grants from the National Institute of Neurological Disorders and Stroke, a component of the National Institutes of Health (R01NS104200, R01NS065926). The Burroughs Wellcome Fund and The Welch Foundation also supported the study.

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Study: Cough That Spreads Tuberculosis Has Pain-Linked Trigger - University of Texas at Dallas

Washington University to break ground on neuroscience research hub – St. Louis American

Washington University in St. Louis will begin construction this month on what will be one of the largest neuroscience research buildings in the country. Located on the School of Medicine campus, the 11-story, state-of-the-art research facility will merge, cultivate and advance some of the worlds leading neuroscience research.

The 609,000-square-foot facility and interconnected projects initially will bring together over 100 research teams focused on solving the many mysteries of the brain and the bodys nervous system. Those teams, comprising some 875 researchers, will come from a wide array of disciplines, including the medical schools neurology, neuroscience, neurosurgery, psychiatry and anesthesiology departments.

Washington University is one of the premier institutions in the world in neuroscience research, with faculty known for their contributions to the understanding of normal brain development, how nerve cells communicate, neuroimaging, neurological diseases such as Alzheimers disease, and surgical treatments for cerebral palsy, among other contributions, said Chancellor Andrew D. Martin.

With this new building, we are able to offer the neuroscience community a central home and a laboratory environment that can inspire entirely new concepts that allow us to grasp a much deeper understanding of the brain and have a global impact on health and science.

The School of Medicine has a long history as one of the worlds foremost centers for neuroscience research, including as a leading institution in the study of Alzheimers disease. Its scientists have identified key molecules involved in sculpting nervous system development and triggers of neurodegenerative diseases, mapped connections from brain region to brain region, and developed pioneering surgical treatments for nerve injuries, among other groundbreaking discoveries.

David H. Perlmutter, MD, executive vice chancellor for medical affairs, the George and Carol Bauer Dean of the School of Medicine, and the Spencer T. and Ann W. Olin Distinguished Professor, said the new facility will open the door to bold new research initiatives and partnerships.

Understanding the brain is key to addressing some of the most devastating afflictions that affect mankind, Perlmutter said.

So many of us have been touched by the inexorable decline of our loved ones due to diseases and conditions such as Alzheimers and Parkinsons, brain trauma, glioblastoma and severe mental illness, and we have learned that the development of effective therapies has proven formidable. As scientists, we believe that a deeper understanding of cognition and emotional regulation can help us address major public health problems such as obesity, substance abuse, depression and suicide.

The initiative will increase synergy and facilitate greater collaboration between scientists in the medical schools neuroscience-focused departments and researchers in related disciplines, especially those whose work requires close collaboration with neuroscientists.

Collaboration across disciplines will be key to advancing our understanding of this new frontier in medicine, Perlmutter said.

For example, new studies have recognized the importance of the microbiome and its interaction with our immune system in shaping the development and function of the brain. Work on synaptic connections in the nervous system is also critical to the development of machine intelligence and socially interactive robots that could solve many of the most important challenges of modern society. This building will be dedicated to advancing our global leadership position in solving these very big problems with imagination and rigor.

The new research center to be located at 4370 Duncan Ave. also is expected to inspire health-minded entrepreneurial pursuits and synergy with visionary business developers situated within a stones throw of the new research center. The building and related construction, which will be built at an expected cost of $616 million, will sit at the eastern edge of the Medical Campus, in the 200-acre Cortex Innovation Community, one of the fastest-growing business, innovation and technology hubs in the United States, and home to numerous biotech startups founded by Washington University faculty, staff and students.

We are constructing the building at the intersection of Cortex and the Medical Campus to encourage efforts by Washington University neuroscientists to transform their research into innovations that can move rapidly to improve medical care and quality of life for people with neurological conditions, said Jennifer K. Lodge, the universitys vice chancellor for research.

Among Washington Universitys achievements in the field of neuroscience, two Nobel Prizes in Physiology or Medicine have been won by scientists at the university. In 1944, Joseph Erlanger and Herbert Gasser won the Nobel for their work studying nerve fibers. They showed that the conduction velocity of nerve impulses is faster in thick nerve fibers than in thin fibers, and identified numerous other properties of sensory and motor nerves. And in 1986, Stanley Cohen and Rita Levi-Montalcini won the Nobel for discovering chemical growth factors essential for cell growth and development in the body. In the 1950s, they discovered nerve growth factor, a protein crucial for building networks of nerves.

A key goal for the neuroscience center is to take what we discover in our laboratories and get it out into the public sector so patients, and society as a whole, can benefit, said David Holtzman, MD, the Andrew B. and Gretchen P. Jones Professor and head of the Department of Neurology. This building and the collaborations it will grow will position us to achieve meaningful breakthroughs in science and medicine.

An internationally renowned expert on the causes of Alzheimers disease, Holtzman and his team helped develop antibodies aimed at preventing dementia by reducing deposits of the Alzheimers proteins amyloid beta and tau in the brain, and have advanced the understanding of how sleep and apolipoprotein E the most important genetic risk factor for Alzheimers contribute to brain injury. Holtzman also is involved in a project led byRandall J. Bateman, MD, the Charles F. and Joanne Knight Distinguished Professor of Neurology, to develop a blood test that can measure levels of amyloid beta and other proteins in the blood with the goal of diagnosing Alzheimers before symptoms develop.

Neuroscience research is a synergetic enterprise that depends on the expertise of people in many fields, Holtzman said. By bringing together so much knowledge, talent and passion, this new facility will make it considerably more likely that people will have the kinds of water-cooler discussions that lead to interdisciplinary game-changing ideas and projects.

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Washington University to break ground on neuroscience research hub - St. Louis American

Washington University to build neuroscience building in the Cortex – KMOV.com

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Washington University to build neuroscience building in the Cortex - KMOV.com

New UNC computational tool boosts understanding of genetic disorders affecting the brain – WRAL Tech Wire

CHAPEL HILL Scientists at the UNC School of Medicine and colleagues created a new computational tool called H-MAGMA to study the genetic underpinnings of nine brain disorders, including the identification of new genes associated with each disorder.

The research,published inNature Neuroscience, revealed that genes associated with psychiatric disorders are typically expressed early in life, highlighting the likelihood of this early period of life as critical in the development of psychiatric illnesses. The researchers also discovered that neurodegenerative disorder-associated genes are expressed later in life. Lastly, the scientists linked these disorder-associated genes to specific brain cell types.

By using H-MAGMA, we were able to link non-coding variants to their target genes, a challenge that had previously limited scientists ability to derive biologically meaningful hypotheses from genome-wide association studies of brain disorders, said study senior authorHyejung Won, PhD, assistant professor of genetics at the UNC School of Medicine and member of the UNC Neuroscience Center. Additionally, we uncovered important biology underlying the genetics of brain disorders, and we think these molecular mechanisms could serve as potential targets for treatment.

Hyejung Won, PhD UNC photo)

Brain disorders such as schizophrenia and Alzheimers disease are among the most burdensome disorders worldwide. But there are few treatment options, largely due to our limited understanding of their genetics and neurobiological mechanisms. Genome-wide association studies (GWAS) have revolutionized our understanding of the genetic architecture related to many health conditions, including brain-related disorders. GWAS is a technique that allows researchers to compare genetic sequences of individuals with a particular trait such as a disorder to control subjects. Researchers do this by analyzing the genetic sequences of thousands of people.

To date, we know of hundreds of genomic regions associated with a persons risk of developing a disorder, Won said. However, understanding how those genetic variants impact health remained a challenge because the majority of the variants are located in regions of the genome that do not make proteins. They are called non-coding genetic variants. Thus, their specific roles have not been clearly defined.

Prior research suggested that while non-coding variants might not directly encode proteins, they can interact with and regulate gene expression. That is, these variants help regulate how genes create proteins, even though these variants do not directly lead to or code for the creation of proteins.

Given the importance of non-coding variants, and that they make up a large proportion of GWAS findings, we sought to link them to the genes they interact with, using a map of chromatin interaction in the human brain, Won said. Chromatin is the tightly packed structure of DNA and proteins inside cells, folded in the nucleus in a way to maintain normal human health.

Won and colleagues used this map to identify genes and biological principles underlying nine different brain disorders, including psychiatric conditions such as schizophrenia, autism, depression, and bipolar disorder; and neurodegenerative disorders such as Alzheimers, Parkinsons, amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS).

Using the computational tool H-MAGMA, Won and colleagues could link non-coding variants to their interacting genes the genes already implicated in previous GWAS findings.

Another important question in brain disorders is to identify cellular etiology the cells involved in the root cause of disease. This is especially critical as the brain is a complex organ with many different cell types that may act differently in response to treatment. In the attempt of finding critical cell types for each brain disorder, the researchers found that genes associated with psychiatric disorders are highly expressed in glutamatergic neurons, whereas genes associated with neurodegenerative disorders are highly expressed in glia, further demonstrating how the two disorder clusters diverge from each other.

Moreover, we classified biological processes central to the disorders, Won said. From this analysis, we found that the generation of new brain cells, transcriptional regulation, and immune response as being essential to many brain disorders.

Won and colleagues also generated a list of shared genes across psychiatric disorders to describe common biological principles that link psychiatric disorders.

Amongst the shared genes, we once again identified the brains early developmental process as being critical and upper layer neurons as being the fundamental cell-types involved, Won said We unveiled the molecular mechanism that underscores how one gene can affect two or more psychiatric diseases.

H-MAGMA is publicly available so that the tool can be widely applicable and available to the genetics and neuroscience community to help expand research, with the ultimate goal of helping people who suffer with brain-related conditions.

The National Institute of Mental Health, the Brain and Behavior Research Foundation, and the Simons Foundation Autism Research Initiative funded this research.

Other authors were Nancy Sey, Benxia Hu, Won Mah, Harper Fauni, Jessica McAfee, all from UNC-Chapel Hill, and Prashanth Rajarajan, Kristen Brennand, and Schahram Akbarian from Mount Sinai Health System.

(C) UNC-Chapel Hill

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New UNC computational tool boosts understanding of genetic disorders affecting the brain - WRAL Tech Wire

This $20 training bundle can teach you to improve your memory and attention – Android Central

If you suffer from either short-term or long-term memory loss issues, you're not alone. Countless people experience episodes of memory loss throughout the day that can be as trivial as forgetting to grab your keys on the way out the door or as serious as forgetting to pick your friend up from the airport, and the older you get the more pronounced these lapses tend to become.

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This $20 training bundle can teach you to improve your memory and attention - Android Central

In the Developing Brain, There’s More Than One Theory of Mind – Technology Networks

In order to understand what another person thinks and how he or she will behave we must take someone else's perspective. This ability is referred to as Theory of Mind. Until recently, researchers were at odds concerning the age at which children are able to do such perspective taking. Scientists at the Max Planck Institute for Human Cognitive and Brain Sciences (MPI CBS), University College London, and the Social Neuroscience Lab Berlin shed new light on this question in a study now published in the renowned journal PNAS. Only 4-year-olds seem to be able to understand what others think.

The study reports that this unique ability emerges around 4 years of age because of the maturation of a specific brain network which enables this. Younger children are already capable of predicting others' behaviour based on what they think, but the study shows that this prediction of behaviour relies on a different brain network. The brain seems to have two different systems to take another person's perspective, and these mature at different rates.

The researchers investigated these relations in a sample of 3- to 4-year-old children with the help of a video clips that show a cat chasing a mouse. The cat watches the mouse hiding in one of two boxes. While the cat is away the mouse sneaks over to the other box, unnoticed by the cat. Thus, when the cat returns it should still believe that the mouse is in the first location.

This cat-and-mouse game asks the viewer, "Where does the cat look for the mouse?" In the study, only 4-year-olds were able to answer correctly. Credit: MPI CBS

Using eye-tracking technology, the scientists analysed the looking behaviour of their study participants and noticed: Both, the 3- and 4-year-olds expected the cat to go to the box where the mouse had originally been. That is, they predicted correctly where the cat was going to search for the mouse based on the cat's belief.

Interestingly, when the scientists asked the children directly where the cat will search for the mouse, instead of looking at their gaze, 3-year-olds answered incorrectly. Only 4-years-olds succeeded. Control conditions ensured that this was not because the younger children misunderstood the question.

The reason for this discrepancy was a different one. The study shows that different brain structures were involved in verbal reasoning about what the cat thinks as opposed to non-verbal predictions of how the cat is going to act. The researchers refer to these brain structures as regions for implicit and explicit Theory of Mind. These cortical brain regions mature at different ages to fulfill their function. The supramarginal gyrus that supports non-verbal action prediction matures earlier, and is also involved in visual and emotional perspective taking. "This enables younger children to predict how people will act. The temporoparietal junction and precuneus through which we understand what others think - and not just what they feel and see or how they will act - only develops to fulfil this function at the age of 4 years", first author Charlotte Grosse Wiesmann from the MPI CBS explains.

"In the first three years of life, children don't seem to fully understand yet what others think", says co-author Nikolaus Steinbeis from the University College London. "But there already seems to be a mechanism a basic form of perspective taking, by which very young children simply adopt the other's view."

Reference: Wiesmann, C. G., Friederici, A. D., Singer, T., & Steinbeis, N. (2020). Two systems for thinking about others thoughts in the developing brain. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1916725117

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

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In the Developing Brain, There's More Than One Theory of Mind - Technology Networks