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Tag: Neuro

  • Increased risk of depression and anxiety when in higher education

    Increased risk of depression and anxiety when in higher education

    Newswise — Young people who are in higher education in England face a small increased risk of depression and anxiety, compared to their peers who are not attending higher education, finds a new study led by UCL researchers.

    The research paper, published in The Lancet Public Health, is the first to find evidence of higher levels of depression and anxiety among higher education students compared with their peers.

    The authors found that by age 25, the difference had disappeared between graduates and non-graduates.

    Lead author Dr Gemma Lewis (UCL Psychiatry) said: “In recent years in the UK we have seen an increase in mental health problems among young people, so there has been an increased focus on how to support students. Here we have found concerning evidence that students may have a higher risk of depression and anxiety than their peers of the same age who are not in higher education.

    “The first couple of years of higher education are a crucial time for development, so if we could improve the mental health of young people during this time it could have long term benefits for their health and wellbeing, as well as for their educational achievement and longer-term success.”

    The researchers used data from the Longitudinal Studies of Young People in England (LSYPE1 and LSYPE2). The first study included 4,832 young people born in 1989-90, who were aged 18-19 in the years 2007-9. The second study included 6,128 participants born in 1998-99, who were aged 18-19 in the years 2016-18 (i.e., prior to the disruption of the COVID-19 pandemic). In both studies, just over half attended higher education.

    Participants in the studies have completed surveys about their general mental health, to investigate symptoms of depression, anxiety, and social dysfunction, at multiple time points over the years.

    The researchers found a small difference in symptoms of depression and anxiety at age 18-19 between students (including those at university and other higher education institutions) and non-students.

    This association persisted after adjustment for potentially confounding factors including, among others, socioeconomic status, parents’ education, and alcohol use.

    The analysis suggests that if the potential mental health risks of attending higher education were eliminated, the incidence of depression and anxiety could potentially be reduced by 6% among people aged 18-19.

    First author Dr Tayla McCloud (UCL Psychiatry) said: “Based on our findings, we cannot say why students might be more at risk of depression and anxiety than their peers, but it could be related to academic or financial pressure. This increased risk among students has not been found in studies in the past, so if the association has only recently emerged, it may be related to increased financial pressures and worries about achieving high results in the wider economic and social context.

    “We would have expected higher education students to have better mental health than their non-student peers as they tend to be from more privileged backgrounds on average, so these results are particularly concerning. More research is needed to clarify the mental health risks facing students.

    “Improving our understanding of modifiable risk factors for depression and anxiety is a global health priority, and it is clear that supporting the mental health of our young people is vitally important.”

    The study was commissioned and funded by England’s Department for Education.

    Notes to editors

    For more information or to speak to the researchers involved, please contact Chris Lane, UCL Media Relations. T: +44 (0)20 7679 9222 / +44 (0)7717 728 648, E: [email protected]   

    Dr Tayla McCloud; Mr Strahil Kamenov; Prof Claire Callender; Prof Glyn Lewis; Dr Gemma Lewis, ‘The association between higher education attendance and common mental health problems among young people in England: evidence from two population-based cohorts’ will be published in The Lancet Public Health on Thursday 28 September 2023, 23:30 UK time / 18:30 US Eastern time and is under a strict embargo until this time.

    The paper will be published at https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(23)00188-3/fulltext and the DOI will be 10.1016/S2468-2667(23)00188-3.

    Mental health and wellbeing support for UCL students:

    • Prevention is a key competent to mental health and wellbeing support at UCL with a year-round events programme, including workshops on perfectionism, imposter syndrome, importance of sleep and personal safety and activities such as sunrise walks, meditation, laugher workshops and many more, equipping students with the tools to manage their own mental health and wellbeing throughout the evitable highs and lows of student life.
    • All undergraduate first-years are assigned a Student Adviser. Student Advisers sit within the academic department and offer 1-2-1 support for students, to help transition into university life and offer support for wellbeing or student experience matters.  
    • All UCL students can access up to six free sessions of counselling through our Student Psychological and Counselling Services.
    • UCL offers 24/7 free, confidential counselling services in over 35 languages, accessed via UCL’s 24/7 Student Support Line. Students can speak to an adviser who can help through any issues, including but not limited to feeling anxious or stressed, money worries, cultural differences, homesickness, addiction, relationship difficulties, bereavement, bullying, harassment and/or sexual harassment – anything impacting mental health, wellbeing or time at UCL. 
    • The advisers reflect the diverse range of backgrounds needed from our students, with options to speak to a male/female adviser, a BAME adviser or an adviser with additional training in LGBTQ+ related issues. 
    • Current students can also make a same day appointment with UCL’s Support and Wellbeing Team by askUCL or phoning the team directly on +44 (0) 20 3108 8836.
    • More information on our support and wellbeing services available for students: https://www.ucl.ac.uk/students/support-and-wellbeing
    • Report + Support is UCL’s online tool for current and former students and staff to report bullying, harassment and sexual misconduct, and it includes the option to report anonymously or on the record.
    • UCL is one of five universities nationally that qualified for the University Mental Health Charter Award which recognises its commitment to continuous improvement in mental health and wellbeing.

    About UCL – London’s Global University

    UCL is a diverse global community of world-class academics, students, industry links, external partners, and alumni. Our powerful collective of individuals and institutions work together to explore new possibilities.

    Since 1826, we have championed independent thought by attracting and nurturing the world’s best minds. Our community of more than 50,000 students from 150 countries and over 16,000 staff pursues academic excellence, breaks boundaries and makes a positive impact on real world problems.

    The Times and Sunday Times University of the Year 2024, we are consistently ranked among the top 10 universities in the world and are one of only a handful of institutions rated as having the strongest academic reputation and the broadest research impact.

    We have a progressive and integrated approach to our teaching and research – championing innovation, creativity and cross-disciplinary working. We teach our students how to think, not what to think, and see them as partners, collaborators and contributors.  

    For almost 200 years, we are proud to have opened higher education to students from a wide range of backgrounds and to change the way we create and share knowledge.

    We were the first in England to welcome women to university education and that courageous attitude and disruptive spirit is still alive today. We are UCL.

    www.ucl.ac.uk | Follow @uclnews on Twitter | Read news at www.ucl.ac.uk/news/ | Listen to UCL podcasts on SoundCloud | View images on Flickr | Find out what’s on at UCL Minds

    University College London

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  • Protein p53 regulates learning, memory, sociability in mice

    Protein p53 regulates learning, memory, sociability in mice

    BYLINE: Jenna Kurtzweil

    Newswise — Researchers have established the protein p53 as critical for regulating sociability, repetitive behavior, and hippocampus-related learning and memory in mice, illuminating the relationship between the protein-coding gene TP53 and neurodevelopmental and psychiatric disorders like autism spectrum disorder.

    “This study shows for the first time that p53 is linked directly to autism-like behavior,” said Nien-Pei Tsai, an associate professor of molecular and integrative biology at the University of Illinois Urbana-Champaign and a researcher at the Beckman Institute for Advanced Science and Technology.

    In living systems, genes act as a biological version of binary code, using the letters A, C, G, and T instead of ones and zeroes to spell out cellular marching orders. Some genes — called coding genes — instruct cells to create proteins with specific functions. For example, the gene TP53 instructs cells to create the protein p53; its job is to regulate how other genes are expressed.

    In this study, Tsai and his colleagues lowered hippocampal p53 levels in mice, looking for changes in gene expressions related to behavior. They observed that the decreased p53 levels:

    • Promoted repetitive behavior in mice.
    • Reduced sociability in mice.
    • Impaired hippocampus-dependent learning and memory, especially in male mice.

    The researchers also observed that p53 levels were elevated after a period of active communication between hippocampal neurons called long-term potentiation. Flexible neuron firing — known as plasticity — is related to positive learning and memory outcomes.

    In a 2018 study, Tsai and his colleagues identified p53 as a key protein involved in the irregular brain cell activity seen in ASD and epilepsy. In future studies, they aim to explore how p53 coordinates the expression of those autism-linked genes to guide behavior.

    Editor’s notes:

    The paper associated with this study is titled “Tumor suppressor p53 modulates activity-dependent synapse strengthening, autism-like behavior and hippocampus-dependent learning” and appears in the journal Molecular Psychiatry.

    Research reported in this press release was supported by the National Institutes of Health under award numbers R01NS105615, R01MH124827, and R21MH122840. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.

    Access the free paper online: https://www.nature.com/articles/s41380-023-02268-9

    Beckman Institute for Advanced Science and Technology, University of Illinois at Urbana-Champaign

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  • Study Seeks to Explain How Smell is Impacted in Individuals with Autism

    Study Seeks to Explain How Smell is Impacted in Individuals with Autism

    Newswise — A new study by a researcher at New York Institute of Technology College of Osteopathic Medicine (NYITCOM) could help explain how the sense of smell is impacted in individuals with autism.

    Individuals with autism have an “insistence on sameness,” and often avoid unfamiliar elements, including new smells and foods, which can impact their quality of life. While many studies have focused on the behavioral features of autism, additional research is needed to help explain its sensory aspects.

    Now, research published in The Journal of Neuroscience, authored by NYITCOM Assistant Professor of Biomedical Sciences Gonzalo Otazu, Ph.D., analyzes a mouse model of autism and reports differences in the neurological processes responsible for smell.

    The findings reinforce one of Otazu’s earlier studies, which was published in the journal Nature Communications in February. In this earlier study, his team trained two groups of mice—one group with a mutation in a gene linked to autism (CNTNAP2 knockout mice) and one neurotypical group (wild-type mice)—to recognize familiar scents. Both groups succeeded in doing so. Then, they were tasked with identifying these scents when new, unfamiliar odors were introduced in the background. While the neurotypical mice were able to “filter out” new background odors and identify target scents, the CNTNAP2 knockout mice struggled to do so.

    In this latest study, Otazu repeated a similar process in mice with a mutation in the SHANK3 gene, a leading autism candidate gene, and found that the same deficit appeared in this mouse model. 

    Otazu and his co-authors write: 

    “People and mice with mutations in a single copy in the synaptic gene SHANK3 show features seen in autism spectrum disorders, including social interaction deficits…Here we used a recently developed task to show that these mice could identify odors in the presence of known background odors as well as wild-type mice. However, their performance fell below wild-type mice when challenged with novel background odors. This deficit was also previously reported in the CNTNAP2 mouse model of autism suggesting that odor detection in novel backgrounds is a general deficit across mouse models of autism.”

    New York Institute of Technology, New York Tech

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  • Donlin Long, First Head of Johns Hopkins Medicine’s Neurosurgery Department and Pain Treatment Pioneer, Dies at 89

    Donlin Long, First Head of Johns Hopkins Medicine’s Neurosurgery Department and Pain Treatment Pioneer, Dies at 89

    Newswise — Donlin M. Long, founding chair of the Johns Hopkins University School of Medicine’s Department of Neurosurgery and a pioneer in the treatment of chronic pain, died Sept. 19. He was 89.

    Highly regarded for his neurosurgical skills, extensive impact on pain reduction research and neurological studies and mentorship of medical students, residents and fellows, Long is credited with establishing the Department of Neurosurgery at Johns Hopkins in 1973, which until then had been a division of the Department of Surgery.

    “Don Long was a true renaissance man and an innovative, master neurosurgeon who nurtured generations of neurosurgical leaders who have transformed our field,” said Henry Brem, M.D., the Harvey Cushing Professor of Neurosurgery and Director of the Department of Neurosurgery at the Johns Hopkins University School of Medicine. “Dr. Long was compassionate and a great role model.”

    When Long joined Johns Hopkins, he organized, what were called at the time, “centers of expertise,” providing patients with one-stop access to specialists in neurology, neurosurgery, orthopaedics and other specialties.

    Long also popularized the concept of competency-based training for neurosurgeons. By the time he stepped down as department director in August of 2000, the full-time neurosurgical faculty had more than doubled, the surgical caseload had increased substantially, rising to some 3,500 annually at The Johns Hopkins Hospital and Johns Hopkins Bayview Medical Center, seven centers of expertise had been created, bringing together experts on everything from chronic pain and vascular diseases to skull base surgery and spinal diseases, and research funding had grown exponentially to $5.5 million a year.

    Descended from New England Quakers, Long was born on April 14, 1934, in Rolla, Missouri. His father was a chemist for the state health department and his mother was a schoolteacher. The family soon moved to Jefferson City. He obtained his undergraduate degree in 1955 and his medical degree in 1959 from the University of Missouri.

    As an intern at the University of Minnesota, Long originally planned to become a cardiac surgeon, but changed to neurosurgery after watching pioneer neurosurgeon Lyle French operate.

    As a resident at Minnesota, Long and fellow resident Joseph Galicich did the research that led to the now-universal use of steroids to reduce postoperative brain swelling. While earning his 1964 doctorate in neuroanatomy, he also did landmark research on the biological structure of the blood vessels in the brain.

    Using a then-new device, the electron microscope, he was able to make the first photographs of the cells that form the inner lining of the brain’s blood vessels, providing images that revealed why brain swelling led to a breakdown of what is known as the blood/brain barrier. This is a special system of cells that form the lining of the brain’s tiniest blood vessels and separate the brain from the central nervous system, protecting it from harmful substances in the bloodstream.

    Once he came to Johns Hopkins, Long continued his groundbreaking research into chronic pain, where he designed the first external transcutaneous electrical nerve stimulator — now universally known simply as TENS — for stimulating peripheral nerves to ease pain.

    In 1981, he and Johns Hopkins colleagues announced the invention of the first battery-powered, rechargeable, implantable electronic stimulator. It became a standard tool in pain management around the world.

    In addition, Long collaborated with colleagues at the Johns Hopkins Applied Physics Laboratory to invent an implantable medication pump, now a standard device used for the administration of insulin in the treatment of patients with diabetes.

    Long is survived by his wife of 64 years, Harriett Page Long; three children, Dr. Kimberley Page Riley and her spouse Dr. Lee Hunter Riley, III, Elisabeth Merchant Long, and David Bradford Long and his spouse Dr. Elizabeth Selvin; and four grandchildren, Lauren Palmer Riley, Thomas Hunter Riley, Benjamin Logan Selvin Long and Eli Duncan Selvin Long.

    Read the full obituary for Donlin M. Long at the Johns Hopkins Department of Neurosurgery website: In Memoriam: Donlin M. Long | Johns Hopkins Neurology and Neurosurgery

    Johns Hopkins Medicine

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  • UCI researchers announce publication of an open-label clinical trial suggesting that N-acetylglucosamine restores neurological function in Multiple Sclerosis patients.

    UCI researchers announce publication of an open-label clinical trial suggesting that N-acetylglucosamine restores neurological function in Multiple Sclerosis patients.

    Newswise — Irvine, CA – Sept. 11, 2023 – UCI researchers have found that a simple sugar, N-acetylglucosamine, reduces multiple inflammation and neurodegeneration markers in people who suffer from multiple sclerosis (MS). In addition, they also found this dietary supplement improved neurological function in 30% of patients.

    According to the World Health Organization, MS affects more than 1.8 million people, and while there are treatments to prevent relapses and improve quality of life, there is no cure.

    The study, N-acetylglucosamine inhibits inflammation and neurodegeneration markers in multiple sclerosis: a mechanistic trial, was published in the Journal of Neuroinflammation. Michael Demetriou, MD, PhD, Chief of the Division of Multiple Sclerosis and Neuroimmunology at UCI, is the lead investigator of the study. Michael Y. Sy, MD, PhD, Director of the Neuroimmunology Fellowship at UCI School of Medicine, is the first author, and Barbara Newton, MD, Project Scientist at UCI, is the second author.

    A major issue with current therapies in MS is the inability to treat chronic-active neuroinflammation in the brain and the associated failure to repair the loss of myelin that covers and protects axons, the electrical wires of the brain. Over time, this leads to permanent nerve cell damage and slow progressive loss of neurological function in patients.

    “Our previous studies in mice and humans implicated N-acetylglucosamine in suppressing brain inflammation, promoting the re-growth of the myelin sheath and slowing brain degeneration,” said Michael Demetriou, MD, PhD, Professor of Neurology and Microbiology & Molecular Genetics at the UCI School of Medicine.

    The new paper reports on the first clinical trial of N-acetylglucosamine in MS patients to directly investigate these potential activities. The trial was developed and performed exclusively in the Demetriou Lab at the UCI School of Medicine and UCI’s Institute of Clinical and Translational Science.

    Researchers found that N-acetylglucosamine was safe and reduced multiple inflammation and neurodegeneration markers in MS patients despite the patients already being on the FDA approved immunomodulatory therapy Glatiramer Acetate, known to impact these pathways outside the brain.  

    “We also observed a sustained reduction in neurological disability in 30% of the patients, an activity which has not been observed with current FDA approved therapies,” said Michael Y. Sy, MD, PhD, Associate Professor of Neurology, UCI School of Medicine. “They at best slow progression, not improve function.”

    The data suggest that N-acetylglucosamine reduced untreated chronic-active neuroinflammation and/or promoted myelin repair.  However, the researchers stress that the trial was unblinded and therefore future blinded studies and additional parameters are essential to validate N-acetylglucosamine’s potential to improve residual chronic-active brain inflammation, myelin repair, neurodegeneration and neurological function in MS.

    “Future studies demonstrating that N-acetylglucosamine can restore neurological function in MS patients would be a gamechanger and provide something that no other current therapy can do,” said Dr. Demetriou, MD, PhD.

     

    UCI School of Medicine:

    Each year, the UCI School of Medicine educates more than 400 medical students and nearly 150 PhD and MS students. More than 700 residents and fellows are trained at the UCI Medical Center and affiliated institutions. Multiple MD, PhD and MS degrees are offered. Students are encouraged to pursue an expansive range of interests and options. For medical students, there are numerous concurrent dual degree programs, including an MD/MBA, MD/MPH, or an MD/MS degree through one of three mission-based programs: the Health Education to Advance Leaders in Integrative Medicine (HEAL-IM), the Program in Medical Education for Leadership Education to Advance Diversity-African, Black and Caribbean (PRIME LEAD-ABC), and the Program in Medical Education for the Latino Community (PRIME-LC). The UCI School of Medicine is accredited by the Liaison Committee on Medical Accreditation and ranks among the top 50 nationwide for research. For more information, visit medschool.uci.edu.

     

    Conflict of Interest Disclosures:

    MS and MD are named as inventors on a patent application that describes GlcNAc as a biomarker for progressive multiple sclerosis. MD is named as an inventor on a patent for use of GlcNAc in multiple sclerosis.

    DOI: 10.1186/s12974-023-02893-9

    University of California, Irvine

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  • UTHealth Houston study: Unruptured brain aneurysms may be missed in routine clinical care, but AI-powered algorithm can help

    UTHealth Houston study: Unruptured brain aneurysms may be missed in routine clinical care, but AI-powered algorithm can help

    Newswise — Unruptured cerebral aneurysms of sizes and locations that require attention may be frequently missed in routine clinical care, but a machine learning algorithm could minimize missed care opportunities, according to a new study from UTHealth Houston.

    The research, published today in Stroke: Vascular and Interventional Neurology, was led by senior author Sunil A. Sheth, MD, associate professor in the Department of Neurology with McGovern Medical School at UTHealth Houston, as well as co-first authors Hyun Woo Kim, MD, vascular and interventional neurology fellow at UTHealth Houston, and Anjan Nagesh Ballekere, MS, research coordinator in the neurology department.

    Approximately 30,000 people living in the U.S. experience a ruptured aneurysm annually. The estimated prevalence of unruptured cerebral aneurysms is 3.2%. Currently, many of these aneurysms are found incidentally on brain imaging, performed often for unrelated reasons, and getting an accurate count remains challenging.

    “We have already seen the tremendous benefit that machine learning can bring to patients suffering from acute stroke,” said Sheth, who is also director of the vascular neurology program at McGovern Medical School. “In this study, we see a similar possibility for substantially improving the way in which we identify, counsel, and help patients with brain aneurysms.”

    The team studied a prospectively maintained registry that included eight certified stroke centers. They identified patients who underwent computed tomography (CT) angiography for evaluation of possible stroke from March 14, 2021, to Nov. 31, 2021. A machine learning algorithm called Viz Aneurysm analyzed imaging to identify unruptured brain aneurysms at least 4 millimeters in size.

    Of the 1,191 CT angiograms performed during the study period, 50 were flagged by the machine learning algorithm as possibly demonstrating an unruptured cerebral aneurysm. Among those, 36 true aneurysms were identified from the 31 CT angiograms, with four cases of multiple aneurysms.

    Twenty-four of the 36 aneurysms (67%) were previously not referred for follow-up, with a median size of 4.4 millimeters. Among them, five aneurysms measured greater than 7 millimeters and had an average risk of rupture of 2.4% over five years. In other words, only 33% of unruptured cerebral aneurysms – many of which require attention and may warrant treatment – were originally referred for follow-up in routine clinical care.

    “Before Viz Aneurysm, the referral rate of unruptured cerebral aneurysms were significantly lower than we expected,” Kim said. “We believe that machine learning algorithm screening and alerting clinicians to studies that may harbor cerebral aneurysms could improve rates of detection and follow-ups.”

    Overall, the most common locations of aneurysms included the internal carotid artery (46%).

    The researchers said machine learning algorithms have the potential to improve the identification of unruptured cerebral aneurysms by flagging CT angiograms suspected of aneurysm, and coordinating the potential follow-up with referral and communication options for the entire care team in the same application.

    “We hope to continue and improve upon this work in order to benefit patients,” Ballekere said. “This will help improve quality of care for acute stroke patients when implemented.”

    Co-authors with McGovern Medical School included Iman Ali, third-year student; neurology residents Sergio Salazar Marioni, MD, and Arash Niktabe, MD; and neurology research coordinators Hussain Azeem and Ananya Iyyangar. Other UTHealth Houston co-authors included Rania Abdelkhaleq, MPH, third-year student at UTHealth Houston School of Public Health, and Luca Giancardo, PhD, associate professor of health data science and artificial intelligence with McWilliams School of Biomedical Informatics at UTHealth Houston. Also co-authoring the study were Omri Segev, BMedSc; Orin Bibas; and Christopher J. Love, PhD, with Viz.ai; and Dan Paz, MD, with Galilee Medical Center in Israel. Viz.ai sponsored the study in part.

    University of Texas Health Science Center at Houston

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  • Groundbreaking Program Encourages Underrepresented Minorities to Consider Career in Neurosurgery

    Groundbreaking Program Encourages Underrepresented Minorities to Consider Career in Neurosurgery

    Newswise — Today, the Congress of Neurological Surgeons (CNS) Foundation launched its Pathway to Neurosurgery program in Washington, DC. The initiative is dedicated to alleviating health care disparities by encouraging high school students from underrepresented groups to pursue a career in neurosurgery or medicine.

    High school students from the E.L. Haynes, A District of Columbia Public Charter School, were selected to participate in a full-day symposium at the CNS Annual Meeting, an international conference of neurosurgeons gathering to discuss the latest advancements in the field. The guest students will attend inspiring presentations and participate in hands-on laboratory stations to gain insight into a neurosurgeon’s daily life. At the end of the symposium, the students will be invited to apply for scholarships, and up to two will be selected for year-long mentorships with local neurosurgeons in Washington, DC.

    In recognition of this groundbreaking program, District of Columbia Mayor Muriel Bowser proclaimed Sept. 7-13 as Pathway to Neurosurgery Week.

    Elad I. Levy, MD, CNS president and professor and chair of neurosurgery at the State University of New York at Buffalo, stated, “The CNS is thrilled that Mayor Bowser has recognized the Pathway to Neurosurgery program. As CNS president, it has been a privilege to witness the growth and development of this critical mission-centric project, offering exposure to the wonders of neuroscience to these exceptional students.”

    Only 4% of practicing neurosurgeons in the U.S. are Black, 5% are Hispanic and 8% are women. In contrast, approximately 14% of the U.S. population are Black, 19% are Hispanic and 50% are women.

    “African Americans, Hispanic Americans and women are significantly underrepresented in neurosurgery, and the CNS Pathway to Neurosurgery program aims to address this problem by promoting diversity, equity and inclusion in neurosurgery. Our goal is to inspire students to consider neurosurgery as a career option to foster innovations in patient care that can improve outcomes and reduce minority health disparities,” said Tiffany R. Hodges, MD, co-chair of the CNS Diversity, Equity, and Inclusion Committee and associate professor of neurosurgery at Case Western Reserve School of Medicine.

    Edjah K. Nduom, MD, co-chair of the CNS Diversity, Equity, and Inclusion Committee and associate professor of neurosurgery at Emory University School of Medicine, added, “There are persistent racial health disparities in the United States, including in neurosurgical care, and the evidence is clear that diversifying the neurosurgical workforce is an important tool in our fight to end these disparities. The CNS Foundation is working to expand the Pathway to Neurosurgery program nationwide to harness all of the diverse talent of our people to improve health outcomes for everyone.”

    “This unique program highlights what we can achieve when we all come together. The CNS Foundation’s Pathway to Neurosurgery program will make a difference and open doors and opportunities that did not exist before,” concluded Martina Stippler, MD, chair of the CNS Foundation, vice-chief of the division of neurosurgery at Beth Israel Medical Center and associate professor of neurosurgery at Harvard University.

    Neurosurgery is a highly specialized medical field dedicated to excellence in the diagnosis, treatment and surgical management of disorders affecting the nervous system (including the brain, spinal cord and peripheral nerves). The specialty plays a critical role in improving patient outcomes and advancing scientific knowledge in the neurosciences.

    The Pathway to Neurosurgery program is supported by generous grants from Medtronic, Stryker and MicroVention.

    # # #

    Founded in 1951, the Congress of Neurological Surgeons is the global leader in neurosurgical education, serving to promote health and improve lives through innovative neurosurgical education, advancement of clinical practice & scientific exchange. The CNS Foundation’s philanthropic mission is to improve worldwide patient health by supporting innovative programs that allow neurosurgeons to collaborate globally as researchers, learners, educators, and caregivers. For more information, visit www.cns.org.

    Congress of Neurological Surgeons

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  • Study could help explain why certain brain tumors don’t respond well to immunotherapy

    Study could help explain why certain brain tumors don’t respond well to immunotherapy

    BYLINE: Denise Heady

    Newswise — A study led by researchers at the UCLA Jonsson Comprehensive Cancer Center sheds new light on why tumors that have spread to the brain from other parts of the body respond to immunotherapy while glioblastoma, an aggressive cancer that originates in the brain, does not.

    In people with tumors that originated in other parts of the body but spread to the brain, treatment with a type of immunotherapy called immune checkpoint blockade appears to elicit a significant increase in both active and exhausted T cells — signs that the T cells have been triggered to fight the cancer. The reason the same thing doesn’t occur in people with glioblastoma is that anti-tumor immune responses are best initiated in draining lymph nodes outside of the brain, and that process does not occur very effectively in glioblastoma cases.

    To date, immunotherapy has not been effective in treating glioblastoma, but it has been shown to slow or even eradicate other types of cancer, such as melanoma, which frequently metastasizes to the brain.

    The new research, published in the Journal of Clinical Investigation, could help improve the effectiveness of immunotherapy for people with brain tumors and it could suggest new paths in the effort to help develop more effective therapies.

    “If we’re going to try to develop new therapies for solid tumors, like glioblastoma, which are not typically responsive, we need to understand the tumor types that are responsive, and learn the mechanisms by which that happens,” said the study’s senior author, Robert Prins, a professor of molecular and medical pharmacology and of neurosurgery at the David Geffen School of Medicine at UCLA.

    The researchers studied the immune cells obtained from nine people with metastatic brain tumors who had been treated with immune checkpoint blockade — which works by harnessing the body’s immune system to destroy cancer cells — and compared their observations with immune cells taken from 19 patients with brain metastases that not been treated with immunotherapy.

    They used a technique called single-cell RNA sequencing to examine the genetic material in both sets of samples, and then compared the data to previously published analyses of 25 recurrent glioblastoma tumors to better understand the effect the immunotherapy had on T cells.

    “We really were trying to figure out which immune cells are changing in the more responsive tumors in order to better explain the higher response rate to the treatment,” said the study’s co-first author, Lu Sun, a project scientist in the Geffen School of Medicine’s neurosurgery department. “No study has comprehensively examined the differential effect of immune checkpoint blockade treatment on these two types of brain tumors before.”

    In the tumors that had spread to the brain, the researchers saw that the T cells had specific characteristics associated with fighting tumors entering the brain, most likely due to a more effective priming step that occurs outside of the brain.

    Before traveling to the brain, T cells are first activated in the lymph nodes. During this process, a type of immune cells called dendritic cells share information about the tumor to T cells so they can better attack the tumor. This priming process, however, doesn’t work very effectively when doctors attempt to use immune checkpoint blockade for treating glioblastoma.

    The researchers also found that a specific subgroup of those exhausted T cells was associated with longer overall survival in people whose cancer had metastasized to the brain.

    “We found quite a significant difference between the two types of brain tumors and how they respond to immunotherapies,” said study author Dr. Won Kim, surgical director of UCLA Health’s brain metastasis program and a member of the Jonsson Cancer Center. “There was a tremendous number of T cell lymphocytes that were found within brain metastases following immunotherapy, and while the number of T cell lymphocytes also increased in glioblastoma patients, it wasn’t anywhere near the same extent.”

    Prins, who is also a researcher at the Jonsson Cancer Center, said that finding “suggests that enhancing the activation and presentation of T cells by dendritic cells could be a potential treatment strategy.”

    In future studies, the researchers plan to analyze data from a larger, more uniform group of people who were diagnosed with melanoma that had spread to the brain.

    The study’s other co-first author is Jenny Kienzler, who was a UCLA fellow in neurosurgery when the research was conducted. Other UCLA authors are Jeremy Reynoso, Alexander Lee, Eileen Shiuan, Shanpeng Li, Jiyoon Kim, Lizhong Ding, Amber Monteleone, Geoffrey Owens, Dr. Richard Everson, David Nathanson, Dr. Timothy Cloughesy, Gang Li, Dr. Linda Liau and Willy Hugo.

    The research was supported by grants from the National Institutes of Health Specialized Programs of Research Excellence in Brain Cancer, National Cancer Institute, National Institutes of Health National Center for Advancing Translational Science, Parker Institute for Cancer Immunotherapy, Brain Tumor Funder’s Collaborative and Cancer Research Institute.

    University of California, Los Angeles (UCLA), Health Sciences

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  • Can Taking Statins After a Bleeding Stroke Lower Risk of Another Stroke?

    Can Taking Statins After a Bleeding Stroke Lower Risk of Another Stroke?

    EMBARGOED FOR RELEASE UNTIL 4 P.M. ET, WEDNESDAY, AUGUST 30, 2023

    Newswise — MINNEAPOLIS – People who have had a stroke called an intracerebral hemorrhage who take cholesterol-lowering drugs called statins may have a lower risk of having another stroke, especially ischemic stroke, compared to people who also had an intracerebral hemorrhage but were not taking statins, according to a new study published in the August 30, 2023, online issue of Neurology®, the medical journal of the American Academy of Neurology.

    Intracerebral hemorrhage is caused by bleeding in the brain. Ischemic stroke is caused by a blockage of blood flow to the brain and is the most common type of stroke.

    “Previous research has had mixed results on the risk of stroke in people who are taking statins and have already had a bleeding stroke, so we evaluated this further,” said study author David Gaist, MD, PhD, of the University of Southern Denmark in Odense and a member of the American Academy of Neurology. “We looked at whether use of statins after a bleeding stroke is associated with the risk of any additional stroke, including both those caused by bleeding and by blood clots. We found that those who used statins had a lower risk of stroke, notably ischemic stroke, while there was no change in the risk of bleeding stroke.”

    For the study, researchers looked at health records in Denmark and identified 15,151 people who had a first bleeding stroke.

    People were followed from 30 days after their first bleeding stroke until the first occurrence of another stroke, death, or the end of follow-up, which on average lasted 3.3 years. Researchers used prescription data to determine information on statin use.

    Researchers then compared 1,959 people who had another stroke to 7,400 people who did not have another stroke who were similar in age, sex and other factors. Of those who had another stroke, 757 people, or 39%, took statins compared to 3,044 people, or 41%, of those who did not have a second stroke.

    After adjusting for factors like high blood pressure, diabetes and alcohol use, statin use was associated with a 12% lower risk of another stroke.

    Then they compared 1,073 people who had an ischemic stroke to 4,035 people who did not have another stroke. Of those who had an ischemic stroke, 427 people, or 40%, took statins compared to 1687 people, or 42%, of those who did not have another stroke.

    After adjusting for similar factors, statin use was associated with a 21% lower risk of an ischemic stroke after the initial bleeding stroke.

    They also compared 984 people who had another bleeding stroke to 3,755 people who did not have another stroke. Of those who had a recurrent bleeding stroke, 385 people, or 39%, took statins compared to 1,532 people, or 41%, of those who did not have another stroke.

    After adjustments, researchers did not find a link between statin use and recurrent bleeding stroke.

    “The results of our study are good news for people taking statins who have had a bleeding stroke,” Gaist added. “While we did find a lower risk of having another stroke, it is important to note that when looking at the data more closely, that lower risk was for ischemic stroke. Still, we found no increased risk for bleeding stroke. More studies are needed to confirm our findings.”

    A limitation of the study was that it only included the Danish population, which is primarily people of European ancestry, and may not be generalizable to people from other populations.

    The study was supported by Novo Nordisk Foundation.

    Learn more about stroke at BrainandLife.org, home of the American Academy of Neurology’s free patient and caregiver magazine focused on the intersection of neurologic disease and brain health. Follow Brain & Life® on Facebook, Twitter and Instagram.  

    When posting to social media channels about this research, we encourage you to use the hashtags #Neurology and #AANscience.

    The American Academy of Neurology is the world’s largest association of neurologists and neuroscience professionals, with over 40,000 members. The AAN is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Alzheimer’s disease, stroke, migraine, multiple sclerosis, concussion, Parkinson’s disease and epilepsy.

    For more information about the American Academy of Neurology, visit AAN.com or find us on Facebook, Twitter, Instagram, LinkedIn and YouTube.

    American Academy of Neurology (AAN)

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  • Half as many AF patients dying of heart attacks and strokes in the UK

    Half as many AF patients dying of heart attacks and strokes in the UK

    Newswise — Patients living with one of the UK’s most common heart rhythm conditions are 50% less likely to die from a heart attack or stroke than they were at the start of the millennium, new research has found. 

    Analysis of the health records of more than 70,000 patients newly diagnosed with atrial fibrillation (AF) showed that mortality from related cardiovascular and cerebrovascular diseases more than halved over the 16-year study period. 

    AF is associated with an increased risk of stroke. 

    The research showed that dementia now accounts for more deaths within one year of an AF diagnosis than acute stroke, heart attack and heart failure combined, demonstrating the need for more research into the link between dementia and AF. 

    The study team believe the lower mortality rate can be attributed to better detection and treatment for AF, which, according to the British Heart Foundation, affects more than 1.5 million people in the UK. 

    But the findings reveal significant health inequalities, showing that the most socioeconomically deprived patients were 22% more likely to die from AF-related conditions than people from the most affluent group. 

    Additionally, patients are now more likely to be diagnosed with coexisting health conditions such as diabetes, cancer and chronic kidney disease, which have greater health implications for them than AF. 

    Senior author Chris Gale, Professor of Cardiovascular Medicine, Honorary Consultant Cardiologist, and Co-Director of the Leeds Institute for Data Analytics at the University of Leeds said: “Atrial fibrillation is a common and often undetected heart rhythm disorder that increases the risk of stroke. Advances in health care have now reduced the chance of having a stroke related to AF, and from dying as result of it, if AF is detected and treated. 

    “However, our study also reveals important disparities in care associated with deprivation and the co-existence of other illnesses. Proactively diagnosing and treating AF in these groups will likely further reduce death and disability from cardiovascular disease. Equally, for many people, AF is a marker of co-existent disease – identifying and treating these additional disease states could further improve outcome for people with AF.” 

    The team is now calling for randomised clinical trials to determine whether the earlier identification and treatment of AF and associated co-morbidities could effectively improve cardiovascular health. 

    Data analysis 

    The research examined data from electronic health records of 72,412 patients from a representative sample of the UK population, who had been diagnosed with AF between 2001 and 2017. The team assessed the health outcomes in patients in the first year after their AF diagnosis, and analysed changes in cause-specific mortality and hospitalisation over time and by sex, age, socioeconomic status and diagnostic care setting. 

    The average patient was aged 75.6. Some 48.2% of patients were women, and 61.8% had three or more comorbidities. 

    Over the study period, coexisting health concerns became more common, with almost 70% of newly diagnosed AF patients also having at least three comorbidities. 

    Mortality rates at one year post diagnosis were investigated, as well as the number of hospital admissions with an overnight stay within 1 year of diagnosis. 

    Over the study period, 20% of patients died from any cause within a year of being diagnosed with AF – but this declined over time. 

    However the researchers found that deaths due to cardiovascular and cerebrovascular events (strokes) more than halved over the study period. Cardiovascular deaths declined from 7.3% in 2001/02 to 3% in 2016/2017, while cerebrovascular deaths declined from 2.6% to 1.1%. 

    The researchers say that the lower rates of cardiovascular deaths among AF patients in the study may be partly explained by improvements in strategies to prevent heart disease, and by changes in clinical practice that could lead to people being diagnosed earlier. 

    By contrast, there was an increase in mortality rates from mental and neurological disorders, from 2.5% in 2001/02 to 10.1% in 2016/17. Of these deaths, 87.2% were caused by dementia, Alzheimer’s disease and Parkinson’s disease. The research team say that while this could be partly due to greater awareness 

    of dementia, it also strengthens the evidence that the relationship between AF and dementia is a pressing research priority. 

    Other findings include: 

    • Hospitalisation is common within a year of AF diagnosis, with almost two further admissions experienced by patients 

    • Hospitalisation rates have increased by 17% due to increasing admissions from non-cardio/cerebrovascular causes, especially in older patients 

    • Hospitalisation for cardiovascular and cerebrovascular causes have decreased by 38% and 28%, respectively, but for non-cardio/cerebrovascular causes hospitalisation has increased by 42% 

    • Older people have experienced the greatest rise in hospitalisation, with those aged 80 years or more experiencing a 39% rise in hospitalisation within a year of AF diagnosis 

    Health inequalities 

    Professor Gale said: “Patients diagnosed in hospital or from the most deprived group had worse outcomes compared with those diagnosed in the community or from the most affluent group. 

    “Although increased burden of comorbidities might partly explain the increased frequency of death in these groups, the persisting difference after full adjustment for these factors suggests other social and health-care factors might also contribute. 

    “Our previous research showed that the most deprived individuals in the UK experience an AF diagnosis at a younger age than the most affluent individuals. This discrepancy in outcomes warrants targeted strategies and healthcare resource planning.” 

    Lead author Jianhua Wu, Professor of Biostatistics and Health Data Science in the Queen Mary University of London’s Wolfson Institute of Population Health said: “AF is one of the most prevalent heart conditions in the UK and as such it is crucial that we understand whether or not the current management of the condition is successful. Our findings provide vital evidence about the effectiveness of treatments for this condition, while also showing that other conditions are becoming more prevalent among AF patients – potentially providing avenues for exploration of more targeted treatments.” 

    University of Leeds

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  • Impact of Psychedelic Drugs on Rat Brain Functions Explored

    Impact of Psychedelic Drugs on Rat Brain Functions Explored

    Newswise — Researchers at Lund University have developed a technique for simultaneously measuring electrical signals from 128 areas of the brain in awake rats. They have then used the information to measure what happens to the neurons when the rats are given psychedelic drugs. The results show an unexpected and simultaneous synchronisation among neurons in several regions of the brain.

    The idea that electrical oscillations in the brain could be used to teach us more about our experiences was conceived several years ago. Pär Halje and the research team was studying rats with Parkinson’s disease that had problems with involuntary movements. The researchers discovered a tone – an oscillation or wave in the electrical fields – of 80 hertz in the brains of the rats with Parkinson’s disease. It turned out that the wave was closely connected to the involuntary movements. 

    “A Polish researcher had observed similar waves after giving rats the anaesthetic ketamine. The ketamine was given at a low dose so that the rats were conscious, and the equivalent dose in a human causes psychedelic experiences. The waves they saw were in more cognitive regions of the brain than in the rats with Parkinson’s, and the frequency was higher, but that still made us consider whether there were links between the two phenomena. Perhaps excessive brain waves in the motor regions of the brain cause motor symptoms, while excessive waves in cognitive regions give cognitive symptoms,” says Pär Halje, researcher in neurophysiology at Lund University.

    The research team that Pär Halje belongs to has developed a method that uses electrodes to simultaneously measure oscillations from 128 separate areas of the brain in awake rats. The electrical waves are caused by the cumulative activity in thousands of neurons, but the researchers also succeeded in isolating signals from individual neurons.

    “For several of these areas, it is the first time anyone has successfully shown how individual neurons are affected by LSD in awake animals. When we gave the rats the psychedelic substances LSD and ketamine, the waves were clearly registered.”

    Collective wave patterns 

    Despite ketamine and LSD affecting different receptors in the brain – they have completely different ways into the nervous system – they resulted in the same wave patterns even if the signals from individual cells differed. When the rats were given LSD, researchers saw that their neurons were inhibited – they signalled less – in all parts of the brain. Ketamine seemed to have a similar effect on the large neurons – pyramidal cells – which saw their expression inhibited, while interneurons, which are smaller neurons that are only collected locally in tissue, increased their signalling. 

    Pär Halje interprets the results seen in the study, which is published in Communication Biology, to mean that the wave phenomenon is connected to the psychedelic experience. 

    “Activity in the individual neurons caused by ketamine and LSD looks quite different, and as such cannot be directly linked to the psychedelic experience. Instead, it seems to be this distinctive wave phenomenon – how the neurons behave collectively – that is most strongly linked to the psychedelic experience.”

    Research model for psychoses

    Even if what is happening in individual cells is interesting, Pär Halje argues that the whole is bigger and more exciting than the individual parts.

    “The oscillations behave in a strange way. One might think that a strong wave starts somewhere, which then spreads to other parts of the brain. But instead, we see that the neurons’ activity synchronises itself in a special way – the waves in the brain go up and down essentially simultaneously in all parts of the brain where we are able to take measurements. This suggests that there are other ways in which the waves are communicated than through chemical synapses, which are relatively slow.” 

    Pär Halje emphasises that it is difficult to know whether the waves cause hallucinations or are merely an indication of them. But, he argues, it opens up the possibility that this could be used as a research model for psychoses, where no good models exist today.

    “Given how drastically a psychosis manifests itself, there ought to be a common pattern that we can measure. So far, we have not had that, but we now see a very specific oscillation pattern in rats that we are able to measure.”

    Can the waves reveal more about consciousness?

    There is also a dream – that the model will help us in the hunt for the mechanisms behind consciousness and that the measurements may be a way to study how consciousness is shaped. 

    “In light of the development of AI, it is becoming increasingly important to clarify what we mean by intelligence and what we mean by consciousness. Can self-awareness occur spontaneously, or is it something that needs to be built in? We do not know this today, because we do not know what the required ingredients for consciousness in our brains are. This is where it is exciting, the synchronised pattern we see, and whether this can help us to track down the neural foundations of consciousness,” says Pär Halje.

    Lund University

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  • Free energy principle predicts self-organized learning in neurons

    Free energy principle predicts self-organized learning in neurons

    Newswise — An international collaboration between researchers at the RIKEN Center for Brain Science (CBS) in Japan, the University of Tokyo, and University College London has demonstrated that self-organization of neurons as they “learn” follows a mathematical theory called the free energy principle. The principle accurately predicted how real neural networks spontaneously reorganize to distinguish incoming information, as well as how altering neural excitability can disrupt the process. The findings thus have implications for building animal-like artificial intelligences and for understanding cases of impaired learning. The study was published August 7 in Nature Communications.

    When we learn to tell the difference between voices, faces, or smells, networks of neurons in our brains automatically organize themselves so that they can distinguish between the different sources of incoming information. This process involves changing the strength of connections between neurons, and is the basis of all learning in the brain. Takuya Isomura from RIKEN CBS and his international colleagues recently predicted that this type of network self-organization follows the mathematical rules that define the free energy principle. In the new study, they put this hypothesis to the test in neurons taken from the brains of rat embryos and grown in a culture dish on top of a grid of tiny electrodes.

    Once you can distinguish two sensations, like voices, you will find that some of your neurons respond to one of the voices, while other neurons respond to the other voice. This is the result of neural network reorganization, which we call learning. In their culture experiment, the researchers mimicked this process by using the grid of electrodes beneath the neural network to stimulate the neurons in a specific pattern that mixed two separate hidden sources. After 100 training sessions, the neurons automatically became selective—some responding very strongly to source #1 and very weakly to source #2, and others responding in the reverse. Drugs that either raise or lower neuron excitability disrupted the learning process when added to the culture beforehand. This shows that the cultured neurons do just what neurons are thought to do in the working brain.

    The free energy principle states that this type of self-organization will follow a pattern that always minimizes the free energy in the system. To determine whether this principle is the guiding force behind neural network learning, the team used the real neural data to reverse engineer a predictive model based on it. Then, they fed the data from the first 10 electrode training sessions into the model and used it to make predictions about the next 90 sessions. At each step, the model accurately predicted the responses of neurons and the strength of connectivity between neurons. This means that simply knowing the initial state of the neurons is enough to determine how the network would change over time as learning occurred.

    “Our results suggest that the free-energy principle is the self-organizing principle of biological neural networks,” says Isomura. “It predicted how learning occurred upon receiving particular sensory inputs and how it was disrupted by alterations in network excitability induced by drugs.”

    “Although it will take some time, ultimately, our technique will allow modelling the circuit mechanisms of psychiatric disorders and the effects of drugs such as anxiolytics and psychedelics,” says Isomura. “Generic mechanisms for acquiring the predictive models can also be used to create next-generation artificial intelligences that learn as real neural networks do.”

    RIKEN

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  • Understanding the Brain’s Circuit for Socially Subjective Reward Valuation

    Understanding the Brain’s Circuit for Socially Subjective Reward Valuation

    Newswise — Okazaki, Japan – Although you might never have consciously considered it, it’s very likely that when you receive a reward, part of the value that you place on it depends on what other people have received as similar rewards. In a recent study published in Nature Communications, Japanese researchers have identified an important brain circuit for this specific process.
    Although researchers have identified the brain regions that are important for deciding the value of a reward in relation to those of others (a process the authors termed ‘socially subjective reward valuation’), the connections between these regions have never been tested experimentally. The research team from the National Institute for Physiological Sciences (NIPS) decided to create a temporary disconnect between the medial prefrontal cortex, which is part of the social brain network, and the lateral hypothalamus, which is involved in social reward valuation.
    “We used a relatively new technique that is commonly known as DREADD, or ‘designer receptor exclusively activated by designer drug’, in macaque monkeys,” says senior author of the study Masaki Isoda. “This method allowed us to temporarily block most of the connections from the brain’s medial prefrontal cortex to the lateral hypothalamus.”

    To test the effects of functionally disconnecting two regions of the monkeys’ brains responsible for socially subjective reward valuation, the researchers used an existing experimental setup. Two monkeys were sat together and shown pictures on a screen. After seeing each picture, only one of the monkeys (or sometimes neither of the monkeys) received water as a reward. By varying the probability of reward for each monkey over a series of tests, the researchers were able to see what happened when the monkeys expected a reward for themselves (they made many licking motions with their tongues) versus a reward for the other monkey (they made fewer licking motions).

    “Using this test, we were able to see the effects of disconnecting the medial prefrontal cortex from the lateral hypothalamus on the monkeys’ expectations of rewards,” says Isoda. “We were excited to see that, with this disconnect, the monkeys were much less susceptible to the prospect of others receiving rewards, but that their own expectations of a reward did not change, suggesting that this pathway is a key circuit in socially subjective reward valuation only.”

    Together with recent research suggesting that the medial prefrontal cortex/lateral hypothalamus circuit is crucial for social rank information in mice, these results indicate that this circuit underlies many important social behaviors. A better understanding of this pathway will aid in the clinical diagnosis and treatment of injuries or alterations to the medial prefrontal cortex and lateral hypothalamus.

    ###
    The article, “Chemogenetic dissection of a prefrontal-hypothalamic circuit for socially subjective reward valuation in macaques,” was published in Nature Communications at DOI: 10.1038/s41467-023-40143-x.

     

    National Institutes of Natural Sciences (NINS)

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  • Researchers Challenge Experiments Denying Free Will Validity

    Researchers Challenge Experiments Denying Free Will Validity

    Newswise — The dispute about how much free will people have in making their decisions has been going for decades. Neuroscientists have joined this discussion thanks to the electroencephalographic (EEG) experiments of Benjamin Libet. In the 1970-1980s, he showed that 0.5–1.5 seconds before conscious awareness of the intention to perform a movement, subjects emit EEG activity that predicts this movement. It turns out that the brain makes a decision and sends readiness potential before a person realises it, and our actions are nothing more than the result of an unconscious physiological process in the brain.

    The results of Libet’s experiments have generated a lot of controversy about free will, and some neurophysiologists have even concluded that it does not exist. Moreover, Libet’s experiment has been repeated using functional magnetic resonance imaging, and it turns out that the decision of the subject can be predicted even 6-10 seconds before their conscious awareness of it.

    The staff of the HSE Institute for Cognitive Neuroscience questioned this experimental paradigm and in their new study confirmed that the time of intention awareness in Libet’s experiments was determined incorrectly. In addition, EEG activity, or the brain signal indicating the readiness of a decision, which was recorded by Benjamin Libet before the decision was made, actually has no direct link to this decision.

    In the Libet’s original experiment, the subjects were asked to occasionally bend their wrists and at the same time remember the moment when they felt ready to perform this action. The time of intention awareness was recorded from the words of the subjects themselves: they observed a point that moved along the screen-dial, similar to a clock hand, and indicated the position of the point when they felt the desire to bend their hand. The moment of the final decision was determined by the exact reading of the sensor attached to the wrist of the subjects.

    The HSE neuroscientists repeated the experiment with two groups of subjects, adding small changes to the task in one of the groups. Using behavioral reports and hypersensitive EEG techniques, the scientists investigated the correlation between the time of intention awareness and the time of final decision. It turned out that the time of awareness can be influenced by experimental procedures: for example, without certain training, the subjects are barely able to determine their intentions, and the traditional Libet paradigm pushes them to the feeling that they can determine the moment of decision-making and intention. Apparently, the instruction itself in the Libet task makes the participants feel that the intention should emerge long before the final decision is made.

    In addition, the study confirmed that there is no direct link between the activity of the brain preceding the action and the intention to perform the action. The sense of intention emerged in the subjects at different points in time, whereas the readiness potential was always registered at about the same time. Thus, the readiness potential may reflect the general dynamics of the decision-making process about making a move, but it does not mean that the intention to act has already been generated.

    “Our study highlights the ambiguity of Libet’s research and proves the absence of a direct correlation between the brain signal and decision-making. It appears that the classical Libet paradigm is not suitable for answering the question of whether we have free will while making decisions. We need to come up with a new approach to this extremely interesting scientific puzzle,” says Dmitry Bredikhin, author of the research, Junior Research Fellow at the Centre for Cognition & Decision Making.

    “Neuroscience tries to answer key questions in our life, including questions of free will and responsibility for our actions. We need to be especially precise in order to draw conclusions that affect our outlook and attitude to life. Therefore, we tried to understand the predetermination of our decisions and confirmed a number of shortcomings in the famous experiments of Benjamin Libet. This does not mean that we have closed this issue of the illusory nature of our free will, but rather emphasizes that the discussion continues. This might be one of the most interesting questions in modern science, to which we have yet to give a definitive answer,” comments Vasily Klucharev, Project coordinator, Leading Research Fellow of the Institute for Cognitive Neuroscience.

    National Research University – Higher School of Economics (HSE)

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  • Advanced Virtual Reality Technology Enables Brain Activity Measurement

    Advanced Virtual Reality Technology Enables Brain Activity Measurement

    Newswise — Researchers have modified a commercial virtual reality headset, giving it the ability to measure brain activity and examine how we react to hints, stressors and other outside forces.

    The research team at The University of Texas at Austin created a noninvasive electroencephalogram (EEG) sensor that they installed in a Meta VR headset that can be worn comfortably for long periods. The EEG measures the brain’s electrical activity during the immersive VR interactions.

    The device could be used in many ways, from helping people with anxiety, to measuring the attention or mental stress of aviators using a flight simulator, to giving a human the chance to see through the eyes of a robot.

    “Virtual reality is so much more immersive than just doing something on a big screen,” said Nanshu Lu, a professor in the Cockrell School of Engineering’s Department of Aerospace Engineering and Engineering Mechanics who led the research. “It gives the user a more realistic experience, and our technology enables us to get better measurements of how the brain is reacting to that environment.”

    The research is published in Soft Science.

    The pairing of VR and EEG sensors has made its way into the commercial sphere already. However, the devices that exist today are costly, and the researchers say their electrodes are more comfortable for the user, extending the potential wearing time and opening up additional applications.

    The best EEG devices today consist of a cap covered in electrodes, but that does not work well with the VR headset. And individual electrodes struggle to get a strong reading because our hair blocks them from connecting with the scalp. The most popular electrodes are rigid and comb-shaped, inserting through the hairs to connect with the skin, an uncomfortable experience for the user.

    “All of these mainstream options have significant flaws that we tried to overcome with our system,” said Hongbian Li, a research associate in Lu’s lab.

    For this project, the researchers created a spongy electrode made of soft, conductive materials that overcome those issues, an effort led by Li. The modified headset features electrodes across the top strap and forehead pad, a flexible circuit with conductive traces similar to Lu’s electronic tattoos, and an EEG recording device attached to the back of the headset.

    This technology will play into another major research project at UT Austin: A new robot delivery network that will also serve as the largest study to date on human-robot interactions.

    Lu is a part of that project, and the VR headsets will be used by people either traveling with robots or in a remote “observatory.” They will be able to watch along from the robot’s perspective, and the device will also measure the mental load of this observation for long periods.

    “If you can see through the eyes of the robot, it paints a clearer picture of how people are reacting to it and lets operators monitor their safety in case of potential accidents,” said Luis Sentis, a professor in the Department of Aerospace Engineering and Engineering Mechanics who is co-leading the robot delivery project and is a co-author on the VR EEG paper.

    To test the viability of the VR EEG headset, the researchers created a game. They worked with José del R. Millán, a faculty member in the Chandra Family Department of Electrical and Computer Engineering and the Dell Medical School and an expert in brain-machine interfaces, to develop a driving simulation that has the user press a button to react to turn commands.

    The EEG measures the brain activity of the users as they make driving decisions. In this case, it shows how closely the subjects are paying attention.

    The researchers have filed preliminary patent paperwork for the EEG, and they’re open to partner with VR companies to create a built-in version of the technology.

    Other members of the research team include Hyonyoung Shin, Minsu Zhang, Nicholas Riveira and Susmita Gangopadahyay of the Chandra Family Department of Electrical and Computer Engineering; Andrew Yu, Heeyong Huh, Zhengjie Li, and Yifan Rao from the Department of Aerospace Engineering and Engineering Mechanics; Sangjun Kim from the Walker Department of Mechanical Engineering, Jessie Peng of the Department of Biomedical Engineering; and Gubeum Kwon of Artue Associates Inc. in South Korea.

    University of Texas at Austin (UT Austin)

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  • Barry Arnason, first Chair of Neurology at UChicago, 1933-2023

    Barry Arnason, first Chair of Neurology at UChicago, 1933-2023

    Newswise — Barry Arnason, MD, the founding Chair of the Department of Neurology at the University of Chicago, died on July 17, 2023. He was 89 years old.

    Arnason joined the faculty at UChicago in 1976 and led the department until 1996, establishing it as a nationally prominent program for both research and patient care. As a physician-scientist, he is considered to be one of the founders of the field of neuro-immunology, which focuses on understanding how the immune system and the nervous system communicate with each other and maintain the body’s overall health.

    Arnason was an author on more than 400 scientific papers on the underlying causes of autoimmunity, neurological diseases, and the development of therapeutic interventions. He was an investigator on more than 70 clinical trials, including studies that led to the approval of interferon-β1b (Betaseron) as the first therapy for relapsing multiple sclerosis (MS). He played a pivotal role in discovering how dysfunctional T cells affect the development of multiple sclerosis, which led him to breakthrough studies that influenced drug management therapies, ultimately affecting how people with MS manage the disease. He also studied what happens—or does not happen—during MS attacks to further advance therapies that may not involve T cells at all. He earned numerous prizes over his long career, including the prestigious John Dystel Prize in MS Research from the American Academic of Neurology and the National MS Society (2014) and election to the American Society of Clinical Investigation in 1974.

    Former colleagues and trainees remember Arnason as a polymath who spoke multiple languages, lectured on six different continents, and knew incredible amounts of history and culture in addition to his professional work. He was gifted at making connections and offering insights for colleagues, even outside his field of expertise, and made an indelible impact on their work.

    “He read over everyone’s grant proposals and added incredibly insightful comments, no matter what the topic,” said Anthony Reder, MD, Professor of Neurology, who joined the department under Arnason in 1982. “I would be working on a proposal about MS and no one else I talked to could add content; but then I’d talk to Barry and he would double what I had done. He was so good at connecting ideas.”

    Arnason was a mentor for scores of clinicians, scientists, residents, and fellows, so numerous that a former trainee of his has presided at the Department of Neurology’s annual Arnason Resident Research Symposium for the past 20 years. Jack Antel, MD, Professor of Neurology and Neurosurgery at McGill University in Montreal, was part of the first cohort of faculty Arnason recruited to UChicago, working with him for 10 years. He called Arnason a true original thinker, equally capable at patient care, clinical research, and basic investigations in animal model systems, who also fostered a collaborative atmosphere in the department.

    “If you had something to say, his door was always open,” Antel said. “He treated the faculty like one big family. We were a very cohesive group, like a series of atoms working together as a molecule. He pushed everyone, but he shared his ideas and wanted everyone to do well.”

    Born and raised in Canada, Arnason graduated from University of Manitoba Medical School before going to Massachusetts General Hospital in 1958 to complete his neurologic training and a fellowship in the laboratory of Byron Waksman. He served on the faculty at Harvard Medical School until he was recruited to UChicago. Following his tenure as Department Chair, he remained on the faculty until he retired in 2020, and actively continued MS immunology research until his death.

    Arnason was predeceased by his beloved wife Joan, who was a pillar of the university and Hyde Park community and actively helped young people. They are survived by their children Stephen, Jon, and Eva.

    University of Chicago Medical Center

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  • Five AANEM Members Will Race for a Cure in the TCS New York City Marathon

    Five AANEM Members Will Race for a Cure in the TCS New York City Marathon

    Newswise — Rochester, Minn. (July 26, 2023)- Five American Association of Neuromuscular Medicine (AANEM) members will race for a cure with American Neuromuscular Foundation (ANF)’s charity team in the 2023 TCS New York City Marathon on Nov. 5 to help raise awareness and funds for NM research and education.

    • Rebecca Dutton, MD: Physiatrist, team physician for the University of New Mexico Lobos, program director for the physical medicine and rehabilitation (PM&R) residency program, and acting division chief of PM&R at the University of New Mexico
    • Holli Horak, MD: NM specialist and director of the neurophysiology fellowship at the University of Arizona and former ANF president
    • Ileana Howard, MD: Medical co-director of the ALS Center of Excellence at the VA Puget Sound and associate professor of rehabilitation medicine at the University of Washington School of Medicine
    • Nadia Khalil, MD: Chief neurology resident at the University of South Florida and member of AANEM’s Young Leadership Council
    • Adeel Zubair, MD: Assistant professor of clinical neurology at Yale School of Medicine

    Each runner aims to raise $5,000, and all proceeds will directly fund critical research and education, ultimately improving the lives of those living with NM diseases. Don’t let them run alone – show your support by cheering them on from the sidelines and contributing to their fundraising campaigns. Visit ANF’s website at www.neuromuscularfoundation.org/marathon to donate, and follow along on social media @AmNmFoundation to learn more about the foundation and the five participating runners.

    About American Neuromuscular Foundation (ANF) Based in Rochester, MN, ANF is a nonprofit organization dedicated to strengthening the global effort to cure neuromuscular disease. As part of its mission to promote the advancement of scientific research and education, the ANF offers annual development grants and abstract and fellowship awards to launch research into muscle and nerve disorders by experts in the field. For more information about ANF, visit neurmuscularfoundation.org.

    American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM)

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  • How Breast Milk Boosts the Brain

    How Breast Milk Boosts the Brain

    Newswise — A new study by scientists at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University suggests that a micronutrient in human breast milk provides significant benefit to the developing brains of newborns, a finding that further illuminates the link between nutrition and brain health and could help improve infant formulas used in circumstances when breastfeeding isn’t possible.

    The study, published July 11 in the Proceedings of the National Academy of Sciences (PNAS),  also paves the way to study what role this micronutrient might play in the brain as we age.

    Researchers found that the micronutrient, a sugar molecule called myo-inositol, was most prominent in human breast milk during the first months of lactation, when neuronal connections termed synapses are forming rapidly in the infant brain. This was true regardless of the mother’s ethnicity or background; the researchers profiled and compared human milk samples collected across sites in Mexico City, Shanghai, and Cincinnati by the Global Exploration of Human Milk study, which included healthy mothers of term singleton infants.

    Further testing using rodent models as well as human neurons showed that myo-inositol increased both the size and number of synaptic connections between neurons in the developing brain, indicating stronger connectivity.

    “Forming and refining brain connectivity from birth is guided by genetic and environmental forces as well as by human experiences,” says Thomas Biederer, senior scientist on the Neuroscience and Aging Team at the HNRCA, senior author on the study, and faculty member at the Yale School of Medicine, where he leads a research group in the Department of Neurology.

    Diet is one of the environmental forces that offers many opportunities for study. In early infancy, the brain may be particularly sensitive to dietary factors because the blood-brain barrier is more permeable, and small molecules taken in as food can more easily pass from the blood to the brain.

    “As a neuroscientist, it’s intriguing to me how profound the effects of micronutrients are on the brain,” says Biederer. “It’s also amazing how complex and rich human breast milk is, and I now think it is conceivable that its composition is dynamically changing to support different stages of infant brain development.”

    Similar levels of myo-inositol across women in very different geographic locations point to its generally important role in human brain development, he observes.

    Research by others has shown that brain inositol levels decline over time as infants develop. In adults, lower than normal brain inositol levels have been found in patients with major depressive disorders and bipolar disease. Genetic alterations in myo-inositol transporters have been linked to schizophrenia. In contrast, in people with Down’s syndrome and patients with Alzheimer’s disease and Down’s syndrome, higher than normal accumulations of myo-inositol have been identified.

    “The current research does indicate that for circumstances where breastfeeding is not possible, it may be beneficial to increase the levels of myo-inositol in infant formula,” Biederer says.

    However, Biederer says it is too soon to recommend that adults consume more myo-inositol, which can be found in significant quantities in certain grains, beans, bran, citrus fruits, and cantaloupe (but which is not present in great quantities in cow’s milk). “We don’t know why inositol levels are lower in adults with certain psychiatric conditions, or higher in those with certain other diseases,” he says.

    A host of research questions remain: Are lower inositol levels in people with depression or bipolar disease a cause of those diseases, or a side effect of drugs used to treat them? Do higher than normal levels in people with Down’s syndrome and Alzheimer’s disease suggest that too much myo-inositol is problematic? What is the “right” level of myo-inositol to have in one’s brain for optimal brain health at various stages of life?

    “My colleagues at the HNRCA and I are now pursuing research to test how micronutrients like myo-inositol may impact cells and connectivity in the aging brain,” says Biederer. “We hope this work leads to a better understanding of how dietary factors interplay with age-related brain aberrations.”

    This work was supported by Reckitt Benckiser / Mead Johnson Nutrition and a gift from the Robert and Margaret Patricelli Family Foundation. Complete information on authors, funders, methodology, and conflicts of interest is available in the published paper.

    The content is solely the responsibility of the authors and does not necessarily represent the official views of Reckitt Benckiser / Mead Johnson Nutrition or the Robert and Margaret Patricelli Family Foundation.

    Tufts University

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  • Structure of Opioid Receptors May Reveal How to Better Design Pain Relievers, Addiction Therapies

    Structure of Opioid Receptors May Reveal How to Better Design Pain Relievers, Addiction Therapies

    Newswise — Opioids remain the most potent and effective pain relievers in medicine, but they’re also among the most addictive drugs that can halt a person’s ability to breathe during an overdose — which can be deadly. Researchers have been racing to develop safer pain reliever drugs that target a specific opioid receptor, called the kappa opioid receptor, that is only found in the central nervous system and not elsewhere in the body, like other opioid receptors. Previous research suggests that such drugs may not lead to addiction or death due to overdose, but the currently known drugs that target these kappa opioid receptors have their own set of unacceptable side effects, including depression and psychosis.

    In one of the first steps towards eventually developing a new wave of kappa opioid receptor drugs without these side effects, researchers at the University of Maryland School of Medicine and Washington University have mapped the 3D structure of the central nervous system specific kappa opioid receptor and figured out how it differs from the other opioid receptors. In this new study, they discovered what instructs the kappa opioid receptor to change its shape, which uniquely binds to opioid drugs, akin to a lock fitting with a specific key.  

    They published their results in the May issue of Nature.

    Aside from relieving pain, opioid receptors are also involved in everything from sensing taste and smell to digestion and breathing, as well as responding to many of the body’s hormones. The way that opioid receptors can influence so many functions around the body is by acting with one of seven cell activity proteins, known as G-alpha proteins, that each help to specialize the function they suppress in the cell.

    “Knowing how these drugs interact with opioid receptors and having a clear view of this molecular snapshot is critical for allowing researchers to develop more effective pain-relieving drugs. This requires a drug that binds to the right type of opioid receptor, such as one in the central nervous system to reduce pain versus the ones that interact in the gut, causing side effects like constipation,” said study corresponding author Jonathan Fay, PhD, Assistant Professor of Biochemistry and Molecular Biology at UMSOM. “Additionally, these next generation medications will need to be designed with the appropriate kind of G-alpha protein in mind, as this will help to precisely target location and cell function by determining the specific shape of the opioid receptor — so the drug only reduces pain without affecting other body functions.”

    The known kappa opioid receptor drugs do not produce the same euphoria as traditional opioid drugs, making these kappa opioid receptor drugs less likely to be addictive.

    For the current study, the researchers used cryogenic electron microscopy in order to visualize the structure of the kappa opioid receptor. They first needed to flash freeze the receptors, which were bound to a hallucinogenic drug with one of two of the traditional G-alpha proteins. They then used a different drug to see how the kappa opioid receptor interacted with two other types of G-alpha proteins; one of these G-alpha proteins is found only in the central nervous system and the other is used to detect taste and smell.

    Dr. Fay described the G-protein as shaped like a chainsaw with a handle and a ripcord. Each G-protein had a slightly different position of its chainsaw handle when bound to the kappa opioid receptor. This change in position played an active role in determining the shape of the kappa opioid receptor and thus what drug bound the best to it. These findings ultimately could have implications for how new drugs will be designed.

    UMSOM Dean Mark T. Gladwin, MD, Vice President for Medical Affairs, University of Maryland, Baltimore, and the John Z. and Akiko K. Bowers Distinguished Professor, said, “Researchers face an enormous challenge in developing safer pain-reliever drugs since they will need to target both the correct opioid receptor as well as the appropriate G-alpha protein. Studies like these reinforce the mission of our new Kahlert Institute for Addiction Medicine, which aims to help develop this next generation of engineered small molecule drugs that are less addictive.

    The research was supported by National Institutes of Health grants from the National Institute of General Medical Sciences (R35GM143061) and the National Institute of Neurological Disorders and Stroke (R01NS099341). The Titan X Pascal graphics card used for this research was donated by NVIDIA.

    About the University of Maryland School of Medicine

    Now in its third century, the University of Maryland School of Medicine was chartered in 1807 as the first public medical school in the United States. It continues today as one of the fastest growing, top-tier biomedical research enterprises in the world — with 46 academic departments, centers, institutes, and programs, and a faculty of more than 3,000 physicians, scientists, and allied health professionals, including members of the National Academy of Medicine and the National Academy of Sciences, and a distinguished two-time winner of the Albert E. Lasker Award in Medical Research. With an operating budget of more than $1.3 billion, the School of Medicine works closely in partnership with the University of Maryland Medical Center and Medical System to provide research-intensive, academic, and clinically based care for nearly 2 million patients each year. The School of Medicine has nearly $600 million in extramural funding, with most of its academic departments highly ranked among all medical schools in the nation in research funding. As one of the seven professional schools that make up the University of Maryland, Baltimore campus, the School of Medicine has a total population of nearly 9,000 faculty and staff, including 2,500 students, trainees, residents, and fellows. The combined School of Medicine and Medical System (“University of Maryland Medicine”) has an annual budget of over $6 billion and an economic impact of nearly $20 billion on the state and local community. The School of Medicine, which ranks as the 8th highest among public medical schools in research productivity (according to the Association of American Medical Colleges profile) is an innovator in translational medicine, with 606 active patents and 52 start-up companies. In the latest U.S. News & World Report ranking of the Best Medical Schools, published in 2021, the UM School of Medicine is ranked #9 among the 92 public medical schools in the U.S., and in the top 15 percent (#27) of all 192 public and private U.S. medical schools. The School of Medicine works locally, nationally, and globally, with research and treatment facilities in 36 countries around the world. Visit medschool.umaryland.edu

    University of Maryland School of Medicine

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  • Study: Hearing AIDS May Slow Cognitive Decline for at-Risk Adults

    Study: Hearing AIDS May Slow Cognitive Decline for at-Risk Adults

    Newswise — A new study published in the medical journal The Lancet found that hearing aids might slow cognitive decline for at-risk older adults with hearing loss.

    Sadie Braun, audiologist and clinical assistant professor in the Department of Speech and Hearing Science in the College of Applied Health Sciences at the University of Illinois, said she’ll incorporate these findings into her counseling with patients.

    “For people who have any sort of high risk for cognitive decline such as dementia (or) Alzheimer’s, this study tells us that those individuals should get hearing aids as soon as they need them,” Braun said. “The average person waits 5 to 7 years or more to get hearing aids once they know they have a hearing loss.”

    The study, co-led by Dr. Frank Lin of Johns Hopkins University School of Medicine and the Bloomberg School of Public Health, analyzed cognitive performance for groups of older adults (ages 70 to 84) with untreated hearing loss.

    Participants were randomly assigned to either the control group that received counseling on disease prevention, or to the intervention group, which received regular audiology treatment and hearing aids.

    Researchers followed up with participants every six months for three years. For participants at lower risk of cognitive decline, hearing aid interventions showed no significant effect on cognitive function. But for participants with high risk for dementia, cognitive decline slowed by 48 percent over the three-year period.

    “That’s a pretty amazing statistic to me,” Braun said. “We’ve known there was a correlation between hearing loss and cognitive decline, but there were a lot of unknowns regarding the exact nature of that correlation as well as whether hearing aids or other treatments could have a positive impact.”

    The connection between hearing loss and dementia is well-documented, but the “why” is still up for research inquiry, Braun said. Regardless, the finding adds to the growing list of reasons for adults to check their hearing sooner rather than later.

    Long-term speech understanding can improve the earlier a patient uses hearing aids, Braun said.

    “Cognitive health is something that people really care about,” Braun said. “I think this is going to cause more people to be more concerned about a mild or moderate hearing loss.”

    For at-risk adults and anyone interested in checking their hearing, Braun recommends a visit to an audiologist.

    The Audiology and Speech Language Pathology Clinic at 2001 S. Oak Street in Champaign is open to all patients, regardless of affiliation to the University of Illinois and accepts some insurance plans. It is operated by the College of Applied Health Sciences’ Department of Speech and Hearing Science.

    New patients are required to schedule an appointment by calling 217-333-2205 or emailing [email protected].

    College of Applied Health Sciences, University of Illinois Urbana-Champaign

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