Category Archives: Neuroscience

The Appeal of Scientific Heroism – The New Yorker

In 2008, the journalist Jonah Lehrer paid a visit to a lab in Lausanne, Switzerland, to profile Henry Markram, a world-renowned neuroscientist. Markram, a South African, had trained at a series of lite institutions in Israel, the United States, and Germany; in the nineties, he published foundational papers on neural connections and synaptic activity. Markrams work in the laboratory, which involved piercing neural membranes with what Lehrer described as an invisibly sharp glass pipette, was known for its painstaking precision. Lehrers visit, however, had been occasioned not by Markrams incremental contributions to the fieldits not easy to sell a colorful profile on the basis of such publications as The neural code between neocortical pyramidal neurons depends on neurotransmitter release probabilitybut by Markrams pivot, in the early two-thousands, to brain simulation.

Neuroscience, Markram declaimed to Lehrer, had reached an impasse. Researchers had generated an enormous wealth of fine-grained data, but the marginal returns had begun to diminish. If there was to be real progress in understanding what exactly was going on in our heads, a more enterprising approach would be required. With the help of supercomputers descended from I.B.M.s Deep Blue, he planned to construct a full-scale model of the brain from the ground up: each individual neuron would have a digital analogue. A by-product of this computational strategy would be a solution to the mystery of consciousness. Of his effort, Lehrer wrote in the sadly long-defunct Seed magazine, Markram hopes that it represents a whole new kind of neuroscience. As Markram put it to Lehrer, You need to look at the history of physics. He continued, From Copernicus to Einstein, the big breakthroughs always came from conceptual models.

Such unapologetic self-mythologizing on the part of a subject is difficult for a journalist to resist, and Lehrer was patently captivated by Markram, who had an aquiline nose and a lustrous mop of dirty blond hair that he likes to run his hands through when contemplating a difficult problem. Though his eyes were bloodshot from lack of sleep, Lehrer comments, Markram could pass for a European playboy. Lehrer was primed to believe Markram, and, when treated to a theatrical visualization of one of the teams preliminary achievements, of a simulated portion of a mouse brains neocortex, he was not disappointed. One of Markrams scientists told Lehrer that their study of neurons in silicothat is, on a chipwas more propitious than the in-vivo and in-vitro processes used by actual experimenters: they enjoyed access to much cleaner data than their error-prone human colleagues did. Lehrer wrote, The model, in other words, has exceeded its own inputs. The virtual neurons are more real than reality.

At the time, Noah Hutton was studying neuroscience as an undergraduate at Wesleyan University. Hutton was an aspiring filmmakerhis first documentary, Crude Independence, which he shot in a North Dakota boomtown between his junior and senior years, premiered at SXSW before he graduated from college. Hutton had encountered Markrams seminal early work in a class on mammalian cortical circuits, but, as with Lehrer, it was the brain-simulation effortthe attempt to construct the legendary brain in a vat, with all of the philosophical issues it entailedthat took hold of his imagination. In 2009, when Hutton was in his final year of college, Markram delivered a viral TED talk in which he claimed that he could simulate a human brain within ten years.

I was fully awe-inspired, Hutton told me recently. Markram was a hero of mine, and I thought, I need to get in on the ground floor of this. Lehrers profile had ended with the usual backside-covering caveatsto be sure, Markram might not succeed, etc.but Hutton wanted the entire glorious arc. He e-mailed Markram a few times but received no response. Hutton had recently shot a music video for a band called the Amygdaloids, a side project of the N.Y.U. neuroscientist Joseph LeDoux, and LeDoux offered to vouch for Hutton. With LeDouxs endorsement, Hutton secured an invitation to Lausanne to make his pitch. There were other documentarians circling the program, which was called the Blue Brain Project, but, if Markram was committed to seeing the whole thing through in ten years, Hutton said, he was prepared to make the same investment. Hutton was twenty-two. There was no one else crazy enough to commit to that timeline, Hutton told me, and Markram was won over by an ambition that seemed commensurate with his own. Hutton was taken to a screening room to experience an updated version of the fly-through that the team had shown Lehrer, and he shared Lehrers fervor. I was just awestruck by the visuals. I was an acolyte, and we immediately had a kind of teacher-student relationship. I had not a shred of critical energy.

For the next decade, Hutton made an annual pilgrimage to Lausanne to check in on the project and interview Markram. The first eight visits were self-fundedHutton was supporting himself as a commercial editor in New Yorkand all of them were solo; Hutton had no one to help schlep his equipment around or set up his shots. His final product, the excellent In Silico, had its streaming dbut in September. Hutton is a talented filmmakerLapsis, a low-budget sci-fi movie that he wrote and directed himself, appeared last year, and portends a career in the conceptual mode of someone like Alex Garlandbut few documentary projects extend for more than a year or two, and in most instances their trajectories are rigged up to fit an arbitrary ending. Had Hutton encountered his subject over the standard documentary interval, he almost inevitably would have come away with a version of the story that Lehrer told: a familiar tale of a bold, charismatic visionary destined to triumph over the forces of cautious bureaucracy, opening up expansive new vistas of inquiry. As it turned out, however, Hutton found himself narrating a much more complicated storyone in which his own personal hopes for the project would be implicated.

An early montage sets us up for what seems like the first version of the story: a series of neuroscientists at prestigious institutions explain that we dont know nearly enough about the brains intricacies to permit wholesale simulation, and that it might be a century or more before we have such knowledge. In his TED talk, Markram explains that hell have nothing to do with such prognoses of impossibility, and in his year-one interview with Hutton he goes even further: as he sees it, the epistemic modesty of the neuroscience community is an alibi for timidity and self-preservation. A full-brain simulation, in his view, is the necessary basis we need to solve such problems as Alzheimers and severe autism; his son is autistic, which gives his work a particular personal urgency. As a scientist, you want to sit back and say, O.K., its enough for me to study my microcircuit, and Im happy, he tells Hutton, shuffling papers in front of himself with feigned dismissiveness, as he nods in imitation of scientific paper shufflers. I dont think thats enough. And thats what keeps me going.

If Markram succeeds, Hutton explains, in voice-over, brain researchers will neither need to experiment with animals anymore, nor run up against the limits of invasive procedures on human subjects. Markram goes on, Well have an intelligence. Youll be able to dial down a molecule and see that you dropped the I.Q., dial up a molecule, see that you raised the I.Q. I believe that we will understand the brain before we finish building it. With nave admiration, Hutton asks Markram what keeps him going, and Markram responds to the softball with a gentle head pat of a smile. Well, I want to see this built. In ten years, as I said, its going to be built. Hutton is ushered into a screening room and shown a fly-through of a portion of simulated mouse brain; the Blue Danube waltz plays, and stunning visuals unfurl before his eyes. Hutton says, Though it was just a tiny piece of the whole, this was the first rendering of the most detailed brain simulation ever attempted. He told me, I thought, Holy shit! No one else has ever seen thisIm seeing inside of a brain! I had a few years of that feeling.

When Hutton returns for another visit, in 2011, the team has made what they describe as a significant leap: they have seen, for the first time, glimmers of brain activity that they hadnt themselves programmed, a sign that the simulated brain has begun to exhibit emergent properties. Hutton lingers on a shot of their computer displays, where a wave of color washes over the digital neurons. Their promotional apparatus has also been upgraded, and Hutton notes the introduction of giant touch screens. One of Markrams lieutenants shows him a bottle of champagne theyve locked in a desk drawer for future celebrations of breakthroughs they feel certain are imminent.

That year, Hutton read a new book by the neuroscientist Sebastian Seung, then at M.I.T., that described his skepticism of Markrams brain-simulation project. In an interview, Seung, who is just as good-looking, charismatic, and camera-ready as Markram, seems unable to take Markrams venture seriously: If we dont have detailed knowledge about the connections in neural networks that we can really depend on, I think that the endeavor of simulating them is really bound to fail. Seung explains that the fundamental problem with Blue Brain is that there are no intermediate benchmarks. Absent some connection to the real, experimental world of rats in mazes or humans in MRI machines, Seung explains, theres no way to know whether Markrams team is simulating something like actual brain activity or merely producing cool graphics. Hutton cuts back and forth between his interviews with Seung, who calls brain simulation highly unrealistic and a waste of time, and Markram, who calmly explains that his efforts have been severely distorted by his critics, who are hopelessly limited by the old, plodding ways of doing things. Markram seems to pity them in their attachment to a superannuated model, as if they were still hard at work refining inquiries into the Ptolemaic spheres; as he puts it to Hutton, Were dealing with a cultural change.

Hutton, for the most part, gives Markram the final word; after all, he had hitched his own ten-year project to Markrams. Privately, however, Hutton was less sure. He told me, I thought, Do I need to jump over and follow Sebastian now? Have I picked the right vessel for the film? But I felt I had to stay with it. Hutton felt malleable, tossed in two directions. When he met with Markrams critics, he found their storythat Markram represented the conquest of traditional neuroscience by computational colonistspersuasive, but, when he relayed versions of these opinions to Markram, he was once again convinced that Markram was misunderstood, a maverick visionary. Hutton realized that his own role in the documentary had to change. He told me, Id made two documentaries before, and I wasnt in those films at allthey were vrit-style. Id thought this film would be the same. But then I thought: whos the narrator? It wasnt Henry, because at that point I couldnt place him at the center of the film. I had to step in, which meant I had to figure out my own point of view. Before Hutton returned to Lausanne for the third year, a short portion of his work in progress, including his interview with Seung, was published by the Scientific American. When he arrived for the next shoot, he was steered aside by one of Markrams subordinates; in the future, they told him, they wanted to know who else he was talking to. Hutton put the warning into the film.

On a superficial level, the rest of In Silico is about Markrams rise and fall: through the brute force of his salesmanship, he brings together hundreds of researchers from as many institutions to win a flagship billion-dollar grant from the European Commission, and his efforts at Blue Brain become the centerpiece of whats known as the Human Brain Project. Hutton is swept up in the renewed enthusiasm for a far-reaching effort now described as akin to the Human Genome Project, or to CERN, the European Organization for Nuclear Research; at one point, he appeared on MSNBC to announce that he had updated his own timeline to fifteen years, to track Markrams, and he was partway through what was now a fifteen-year documentary. Markrams imperial stewardship of the Human Brain Project was, however, short-lived: eight hundred neuroscientists signed an open letter of protest, arguing that the neuroscientific community had been sold a bill of goods, and that participants had been enlisted against their better judgment in what was no longer a cordinated effort to study the brain but a monumental boondoggle and an egregious squandering of scientific resources on expensive information technology. Markram was pushed out of the Human Brain Project, and resumed his old position at Blue Brain, which was supported by the Swiss government.

By year seven, Markram has begun to fully turn inward; he tells Hutton that hes tired of fighting for his position in the media, and that hes decided that this is his silent year, that hes going into hibernation. His science, he believes, will speak for itself. He removes his microphone, ending the interview early. In voice-over, Hutton explains the way hes been buffeted back and forth between the outside critics and Blue Brains spellbinding visuals. (Huttons own animated sequences, by the wonderful illustrator Andrew Khosravani, are, by deliberate contrast, decidedly anti-realistic; cartoonishly florid and surreal, they bring to mind the interstitial scenes from Monty Python.) Now, Huttons narration continues, something else was starting to creep in, a sense of multiplying touch screens, curved screens, headsets, but a lack of meaning to anything and anyone outside this glass-and-steel building in Geneva. Markram now suggests, against all evidence, that the ten-year timeline was never supposed to be taken literally, he insists that his team remains on track to complete the construction of a digital mouse brain; he produces as confirmation the fact that their simulations are growing larger and more theatrically vivid with the passage of time. Where Jonah Lehrer, the journalist, had to conclude with boilerplate about how Markram might very well fail, Hutton has put himself in the opposite position: Markram, he grants, might be vindicated in the end. But, even if that never proves to be the case, Hutton goes on, the story of scientific progress is as much a story of mistakes as it is one of successes. He allows that theres a certain grandeur in Markrams ability to make mistakes on such a tremendous scale, and with such tremendous initiative.

All of this is, of course, true enough, but Huttons more profound point is that there remains an important difference between being wrong and being not even wrong. The danger isnt that Markram has made mistakes, but that the mistakes hes making arent productiveor are only productive on a meta level, insofar as they suggest that science is only on rare occasion the proper realm for Nietzschean heroism, and that layers of bureaucratic oversight tend to exist for good reason. The portrait of Markram that ultimately emerges is of a lordly sovereign stalking the halls of an island mansion, an autumn of the scientific patriarch. Perhaps Lehrer was caught in the usual short-term trapthat, had he had Huttons longitudinal Sitzfleisch, he would have discovered that the whole thing was a castle in the air. (As the blogger Scott Alexander recently put it, just as economists have predicted ten of the last two recessions, so science journalists have predicted ten of the last two paradigm shifts.) But there were clues available to Lehrer even thenones that made their way, unexamined, into his own article. Markram had compared himself to Copernicus, suggesting that his own conceptual breakthrough would be of the same order. But Copernicus did not begin with a new conceptual framework. Copernicus began with the sense that there was something about our astronomical measurements that didn't quite add up. It may have been a conceptual breakthrough that solved the problem, but it was the painstaking incremental workwhat Thomas Kuhn called the practice of normal sciencethat demonstrated that there was in fact a problem to be solved.

Go here to see the original:
The Appeal of Scientific Heroism - The New Yorker

Timely Interventions for Depression Might Lower the Future Risk of Dementia – Neuroscience News

Summary: Symptomatic depression increases the risk of developing dementia by 51%, but those being treated for depression had a significantly lower risk of being diagnosed with depression later in life.

Source: Elsevier

Depression has long been associated with an increased risk of dementia, and now anew studyprovides evidence that timely treatment of depression could lower the risk of dementia in specific groups of patients.

Over 55 million people worldwide live with dementia, a disabling neurocognitive condition that mainly affects older adults. No effective treatment for dementia exists but identifying ways to help minimize or prevent dementia would help to lessen the burden of the disease.

The study, led by Jin-Tai Yu, MD, PhD, Huashan Hospital, Shanghai Medical College, Fudan University, and Wei Cheng, PhD, Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, China, appears inBiological Psychiatry.

Professor Yu and Professor Cheng used data collected by the UK Biobank, a population-based cohort of over 500,000 participants. The current study included more than 350,000 participants, including 46,280 participants with depression. During the course of the study, 725 of the depressed patients developed dementia.

Previous studies examining whether depression therapies such as pharmacotherapy and psychotherapy could lower the risk for dementia produced mixed results, leaving the question unresolved.

Older individuals appear to experience different depression patterns over time, said Professor Yu.

Therefore, intra-individual variability in symptoms might confer different risk of dementia as well as heterogeneity in effectiveness of depression treatment in relation to dementia prevention.

To address that heterogeneity, the researchers then categorized participants into one of four courses of depression: increasing course, in which mild initial symptoms steadily increase; decreasing course, starting with moderate- or high-severity symptoms but subsequently decreasing; chronically high course of ongoing severe depressive symptoms; and chronically low course, where mild or moderate depressive symptoms are consistently maintained.

As expected, the study found that depression elevated the risk of dementia by a striking 51% compared to non-depressed participants. However, the degree of risk depended on the course of depression; those with increasing, chronically high, or chronically low course depression were more vulnerable to dementia, whereas those with decreasing course faced no greater risk than participants without depression.

The researchers most wanted to know whether the increased risk for dementia could be lowered by receiving depression treatment. Overall, depressed participants who received treatment had reduced risk of dementia compared to untreated participants by about 30%.

When the researchers separated the participants by depression course, they saw that those with increasing and chronically low courses of depression saw lower risk of dementia with treatment, but those with a chronically high course saw no benefit of treatment in terms of dementia risk.

Once again, the course of ineffectively treated depression carries significant medical risk, saidBiological Psychiatryeditor John Krystal, MD. He notes that, in this case, symptomatic depression increases dementia risk by 51%, whereas treatment was associated with a significant reduction in this risk.

This indicates that timely treatment of depression is needed among those with late-life depression, added Professor Cheng. Providing depression treatment for those with late-life depression might not only remit affective symptoms but also postpone the onset of dementia.

The new findings shed some light on previous work as well, said Professor Cheng. The differences of effectiveness across depression courses might explain the discrepancy between previous studies.

Author: Eileen LeahySource: ElsevierContact: Eileen Leahy ElsevierImage: The image is in the public domain

Original Research: Closed access.Depression, Depression Treatments, and Risk of Incident Dementia: A Prospective Cohort Study of 354,313 Participants by Wei Cheng et al. Biological Psychiatry

Abstract

Depression, Depression Treatments, and Risk of Incident Dementia: A Prospective Cohort Study of 354,313 Participants

To investigate the associations between courses of depression, the application of depression treatment, and the risk of incident dementia.

In this prospective cohort study, 354,313 participants aged 50 to 70 years were recruited from the UK Biobank between 2006 and 2010, and were followed-up until 2020, with a total of 4,212,929 person-years. We initially studied the effect of depression on dementia incidence across four subgroups characterized by courses of depressive symptoms. Then, 46,820 participants with depression diagnose were further categorized into the treated and untreated groups. We compared the risks of dementia among different depression treatments groups in all participants that depressed as well as four courses of depressive symptoms by performing survival analyses.

Depression was associated with a 51% higher risk of dementia, among which the increasing, chronically high and chronically low courses were associated with increased dementia risk while no association was found in the decreasing course. Compare to those who were depressed but untreated, receiving depression treatments corresponded to a hazard ratio of 0.7 (95% confidence interval= 0.62-0.77). Among the three detrimental courses, treatments for increasing and chronically low symptoms of depression were associated with a 42% and 29% lower risk of dementia while the reduction effect for chronically high symptoms was insignificant.

The negative association between depression treatment and incident dementia was significant in the increasing and chronically low course, highlighting the necessity of timely interventional strategies before depression progress to a chronically severe state.

Visit link:
Timely Interventions for Depression Might Lower the Future Risk of Dementia - Neuroscience News

Dr. Xiaokui Zhang to Present Aspen Neuroscience, Inc. at 2022 Cell & Gene Meeting on the Mesa – PR Newswire

SAN DIEGO, Oct. 11, 2022 /PRNewswire/ -- This week Xiaokui Zhang, Ph.D., Chief Scientific Officer of Aspen Neuroscience, Inc. will present at the 2022 Cell & Gene Meeting on the Mesa Conference in Carlsbad, Calif. including presenting a live corporate update and participating in a panel session to highlight new developments in the induced pluripotent stem cell (iPSC) field.

Dr. Xiaokui Zhang to Present Aspen Neuroscience at 2022 Cell & Gene Meeting on the Mesa

This morning Dr. Zhang will present "Transforming Cell Therapy: Autologous in the Neuroscience Space," taking place at 9:15 a.m. in the Oxford Biomedica Ballroom. Dr. Zhang will provide the latest updates in a corporate overview of Aspen Neuroscience, which is developing the first iPSC-derived autologous neuron replacement treatment for Parkinson's disease (PD).

This Thursday, Dr. Zhang will serve as panel member for the discussion, "New Developments and Advancements in the World of PSCs," which will highlight the latest advances in the field, taking place at 9:45 a.m. in the UBC Ballroom.

Headquartered in San Diego, Aspen Neuroscience, Inc. is a development stage, private biotechnology company focused on personalized autologous cell therapies. The company is developing iPSCs to address diseases with high unmet medical need, beginning with autologous neuron replacement for both sporadic and genetic forms of Parkinson's disease, and extending across the brain and affected organs.

A leading iPSC company, Aspen combines stem cell biology with the latest artificial intelligence and genomic approaches to investigate patient-specific restorative treatments.

The company has developed a best-in-class platform to create and characterize pluripotent-derived cell medicines, which includes in-house bioinformatics, manufacturing and QC. Aspen's platform consistently produces high quality iPSCs and autologous dopaminergic neurons and has broad potential with multiple opportunities to expand the current pipeline.

For more information and important updates, please visitaspenneuroscience.com.

SOURCE Aspen Neuroscience , Inc.

Follow this link:
Dr. Xiaokui Zhang to Present Aspen Neuroscience, Inc. at 2022 Cell & Gene Meeting on the Mesa - PR Newswire

Faculty, Staff Honored as Good Stewards – University of California, Davis

Chancellor Gary S. May, center, is flanked by Faculty and Staff Stewardship Award recipients Kimberley McAllister, left, and Tammy Ainsley, right. Also pictured are Shaun Keister, vice chancellor, Development and Alumni Relations, and Cecelia Sullivan, chair of the UC Davis Foundation. Not pictured: Marcie Kirk Holland. (Samuel Sellers/UC Davis)

UC Davis last week presented its annual Faculty and Staff Stewardship Awards, honoring three individuals considered exceptionally dedicated to building the strong relationships that are critical to the universitys fundraising efforts.

This years recipients are recognized as leaders in a variety of fields on the Davis and Sacramento campuses:

These faculty and staff go the extra mile in their commitment to philanthropy at UC Davis, inspiring donors and those around them, said Shaun Keister, vice chancellor of Development and Alumni Relations and president of the UC Davis Foundation, who joined in presenting the awards during an Oct. 7 luncheon. The passion they have for their work and for building strong relationships has a transformational impact on our campus.

Chancellor Gary S. May and UC Davis Foundation Chair Cecelia Sullivan 83 also participated in the awards presentation.

Kimberley McAllister is passionate for neuroscience research and training, and dedicated to the Center for Neuroscience, or CNS, with which she has been affiliated for 23 years, bolstering its research, contributing to its success and inspiring the support of many donors.

Since becoming the director in 2016, McAllister has led several initiatives to strengthen the center, including launching the CNS Directors Circle, a recognition society aimed at engaging generous donors with the centers research, faculty and trainees through several popular annual events.

McAllister also leads the centers annual Brain Awareness Week event, NeuroFest, to bring the community together to learn about neuroscience at UC Davis. With her support, the event continues to grow each year.

A personal touch is key to McAllisters stewardship. She has traveled throughout California and beyond, visiting many donors, giving presentations, writing handwritten thank-you notes and providing follow-up information about the impact of philanthropy. She cares deeply about each of the centers donors and is dedicated to making sure that the impact of their investments is maximized in every way possible.

Tammy Ainsley has been with UC Davis Health for more than 20 years, building strong relationships within her department and with patients, including those who are donors.

She inspires her team in their commitment to patient care. Ainsleys priority is always ensuring every patient and family at the UC Davis Medical Center has the best experience possible during their stays.

She led the development and launch of a guest relations team to better guide and support patients and their loved ones as they arrive at the medical center.

Receiving medical services is often a stressful experience, but Ainsley offers wonderful customer care and establishes trust to serve those in need in a timely manner with compassion and kindness.

Ainsley believes that donor stewardship is good for patient and family health and healing, and she leads the way to make it happen. She ensures her team is a compassionate and collaborative partner to development, and that they do their part to help advance philanthropy at UC Davis.

Marcie Kirk Holland is a longtime advocate of helping students find success in their post-graduation careers and has been a key player in growing and initiating career prep programs across campus.

A UC Davis employee of 30 years, she has served as executive director of the Internship and Career Center since 2014. Her many years of service on campus are fueled by her love of helping students find paths that are meaningful to them.

She is the co-champion for Aggie Launch, the UC Davis initiative to provide comprehensive career preparation resources for all students. Kirk Hollands leadership was essential to growing the program into a major campus priority, and in inspiring greater giving and engagement from individuals, corporations and foundations.

Always focusing on people and follow-through, Kirk Holland fosters strong relationships with donors and makes herself available to anyone who is interested in supporting Aggie Launch programs.

She frequently speaks at receptions for parents and students and is always looking for new ways to serve the university while providing resources and assistance to others.

Clmentine Sicard is a communications specialist in the Office of Development and Alumni Relations.

View post:
Faculty, Staff Honored as Good Stewards - University of California, Davis

Birth Weights Below the 25th Percentile Linked to Later Developmental Concerns – Neuroscience News

Summary: Babies born below the 25th percentile for birth weight are at higher risk for developmental concerns than children born between the 25-75th percentiles, with the smallest babies carrying the most risk.

Source: PLOS

Being born below the 25th percentile for birthweight may put a child at risk for developmental difficulties, according to a new study by Abiodun Adanikin of Coventry University, U.K., and colleagues, publishing October 11 in the open access journalPLOS Medicine.

Babies that are too big or too small are believed to be at risk of poor birth outcomes and problems related tochildhood development, but little is known about this relationship across the entire range of birthweights for non-prematurebabies. To fill this gap, researchers studied the development of more than 600,000 infants born after 37 weeks of gestation in Scotland.

At around two or three years of age, the children underwent evaluation forsocial developmentand for fine motor, gross motor and communication skills. The researchers looked for associations betweenbirthweightandearly childhooddevelopmental concerns, taking into account complicating factors, such as the childs sex and gestational age at delivery, as well as the health, ethnicity and socio-economic status of the mother.

The study showed that babies born below the 25th percentile for birthweight had a higher risk of developmental concerns compared to babies born between the 25th and 75th percentiles, with the smallest babies carrying the greatest risk.

Babies born above the 75th percentile of weights did not have a substantially increased risk of developmental concerns compared to babies born in the middle range.

The researchers conclude that having a low birthweight is an unrecognized and potentially important contributor to the prevalence of issues related to childhood development.

Traditionally, babies below the 10th percentile were believed to be at risk for developmental concerns. But the new study found a greater number of babies within the 10th to 24th percentile range of birthweights with these issues, simply because there are a larger number of babies within that population.

The researchers suggest that better birthweight surveillance, counseling for the parents and increased support during childhood may help reduce the risks associated with babies born with lower birthweights.

Coauthor Abiodun Adanikin adds, Though it is mostly unrecognized, babies who are mild-to-moderately small at birth are key contributors to the burden of childhood developmental concerns. They may need closer monitoring and increased support to reduce the risk of developmental concerns.

Author: Press OfficeSource: PLOSContact: Press Office PLOSImage: The image is in the public domain

Original Research: Open access.Association of birthweight centiles and early childhood development of singleton infants born from 37 weeks of gestation in Scotland: A population-based cohort study by Abiodun Adanikin et al. PLOS Medicine

Abstract

Association of birthweight centiles and early childhood development of singleton infants born from 37 weeks of gestation in Scotland: A population-based cohort study

Birthweight centiles beyond the traditional thresholds for small or large babies are associated with adverse perinatal outcomes but there is a paucity of data about the relationship between birthweight centiles and childhood development among children born from 37 weeks of gestation. This study aims to establish the association between birthweight centiles across the whole distribution and early childhood development among children born from 37 weeks of gestation.

This is a population-based cohort study of 686,284 singleton infants born from 37 weeks of gestation. The cohort was generated by linking pregnancy and delivery data from the Scottish Morbidity Records (2003 to 2015) and the child developmental assessment at age 2 to 3.5 years. The main outcomes were childs fine motor, gross motor, communication, and social developmental concerns measured with the Ages and Stages Questionnaires3 (ASQ-3) and Ages and Stages Questionnaire: Social & Emotional2 (ASQ:SE-2), and for a subset of children with additional specialist tools such as the Modified Checklist for Autism in Toddlers (M-CHAT) if the ASQ3/SE indicate these are necessary. The ASQ score for each domain was categorised as concern and no concern.

We used multivariate cubic regression splines to model the associations between birthweight centiles and early childhood developmental concerns. We used multivariate Poisson regression models, with cluster robust errors, to estimate the relative risks (RRs) of developmental concerns below and above the established thresholds. We adjusted for maternal age, early pregnancy body mass index (BMI), parity, year of delivery, gestational age at delivery, smoking history, substance misuse in pregnancy, alcohol intake, ethnicity, residential area deprivation index, maternal clinical conditions in pregnancy (such as diabetes and pre-eclampsia), induction of labour, and childs sex.

Babies born from 37 weeks of gestation with birthweight below the 25th centile, compared to those between the 25th and 74th centile, were at higher risk of developmental concerns. Those born between the 10th and 24th centile had an RR of 1.07 (95% CI: 1.03 to 1.12,p< 0.001), between the 3rd and 9th centile had an RR: 1.18 (95% CI: 1.12 to 1.25,p< 0.001), and <3rd centile had an RR of 1.37 (95% CI: 1.24 to 1.50,p< 0.001). There was no substantial increase in the risk of early childhood developmental concerns for larger birthweight categories of 75th to 89th (RR: 1.01; 95% CI: 0.97 to 1.05;p= 0.56), 90th to 96th (RR: 0.99; 95% CI: 0.94 to 1.05;p= 0.86), and 97th centiles (RR: 1.04; 95% CI: 0.97 to 1.12;p= 0.27), referent to birthweight between 25th and 74th centile.

The percentage of developmental concerns attributable to birthweight between the 10th and 24th centile was more than that of birthweight <3rd centile (p= 0.023) because this group includes more of the population. Approximately 2.50% (95% CI: 1.26 to 3.61) of social skills concerns and 3.00% (95% CI: 1.33 to 4.67) of fine motor developmental concerns were attributable to birthweight between the 10th and 24th centile compared to 0.90% (95% CI: 0.48 to 1.26) and 2.30% (95% CI: 1.73 to 2.67) respectively for birthweight <3rd centile. We acknowledge the limitation of ASQ as a screening tool, the subjective nature of developmental assessments (particularly for speech) among young children, and inability to control for early childhood illness and upbringing factors may have an impact on our findings.

We observed that from 37 weeks of gestation birthweight below the 25th centile was associated with child developmental concerns, with an association apparent at higher centiles above the conventional threshold defining small for gestational age (SGA, 3rd or 10th centile). Mild to moderate SGA is an unrecognised potentially important contributor to the prevalence of developmental concerns. Closer surveillance, appropriate parental counselling, and increased support during childhood may reduce the risks associated with lower birthweight centiles.

Here is the original post:
Birth Weights Below the 25th Percentile Linked to Later Developmental Concerns - Neuroscience News

Ask Me Anything: Neuroscience with Andrew Huberman – Scope

Ever wonder what science says you should do to quell daily anxiety? What about how to fall back asleep when you wake in the middle of the night?

In our latest #AskMeAnything on Stanford Medicine's Instagram account, neuroscientist and podcaster Andrew Huberman, PhD, untangled those and other complicated questions about human behavior, and shared the latest on what's brewing in his lab.

During a live conversation with our senior manager of media relations, Lisa Kim, Huberman explored, among other things, how to get a good night's sleep, the importance of exercise and quality nutrition, building resilience against stress, and why we need sunlight in our day-to-day lives.

Parts of the conversation are represented in the following Q&A, which has been condensed and edited for clarity.

Light sets your circadian rhythm for wakefulness, and it helps you feel better throughout the day. It's what we call a slow integration system. Going outside first thing in the morning and looking into sunlight for five to 30 minutes, depending on how bright it is outside, taps into hormone systems and neurotransmitter systems in the brain and body that kick in over the course of minutes to hours.

That ends up feeling like a slow increase in your overall energy and mood. Every 24 hours, we release a hormone called cortisol. A lot of people think cortisol is bad, but it's important for your immune system and for energy, provided it's not too high or too frequent. A cortisol release needs to arrive early in the day to get the most out of it.

But work from my Stanford Medicine colleague David Spiegel and others has shown that if you don't get sunlight early in the day, that cortisol release starts shifting later, which creates issues with insomnia and anxiety and even some low-level depression later in the day. Now, that does not mean that if you miss getting sunlight one day that you're going to get depressed. It's a slow, integrated mechanism.

It's effective in that it can shift your circadian clock. But I am a strong believer in avoiding taking exogenous melatonin. First of all, it's been well documented that many of the supplements that contain melatonin have far too much -- 3 to 6 milligrams is a massive dose. Typically, the body makes very little melatonin.

The other issue is that not all supplements contain what they say they contain. This is especially true for melatonin -- even supposedly reliable brands can contain 15% to 155% of the dosage that's listed on the bottle.

There are healthier alternatives, but I want to really emphasize -- and I'll probably go into my grave saying this -- use behavioral tools first. Get morning sunlight, avoid too much light late at night, then look to quality of nutrition and eating habits. Being too hungry or eating too close to bedtime can both inhibit sleep. Get quality exercise, and don't drink caffeine after 2 or 3 o'clock in the afternoon. Before you start thinking about supplements or prescription drugs for sleep, it's really important to have all the other things right. And the nice thing about all those is that they are all zero cost.

For day-to-day anxiety as opposed to an anxiety disorder -- which should be taken seriously and addressed with the help of a medical professional -- there are real-time tools to push back on anxiety and stress and raise our threshold for stress. We are collaborating with our associate chair of psychiatry, David Spiegel, on a study that harnesses a natural pattern of breathing that we do in sleep. It's called the physiological sigh, which was discovered by physiologists in the 1930s and is very effective at reducing anxiety practices while we're awake.

During sleep, carbon dioxide in your bloodstream sometimes gets too high and your levels of oxygen will get too low, so you're actually becoming asphyxiated but don't realize it because you're asleep. Under those conditions, your body will do a double inhale through your nose and then a long exhale through your mouth.

To use this technique to address anxiety, take a really deep inhale through the nose and, when you feel your lungs are full, make every effort to sneak in a little bit more air. Then slowly release all the air through the mouth.

What does the physiological sigh do to the brain and body?

When you are stressed, you tend to under-breathe, which can elevate the level of carbon dioxide in your bloodstream. This makes the little sacs, or alveoli, that increase the surface of your lungs collapse. They don't easily re-inflate, which is why we sneak that air in at the end. Then do a long exhale to get rid of all the carbon dioxide that's built up in your system and is causing your body stress.

When someone is trying to help you de-stress and they tell you to take a deep breath, what they really should tell you is take a long exhale. This type of sigh can also be great if you are having a hard time falling asleep or back to sleep. Try doing a few physiological sighs, really extending that exhale, and you'll notice your core, your diaphragm region, will start to relax. This feeds back to the nervous system, then to the brain, which then feeds back to the body to relax it.

What about being mentally strong? How do you build mental resilience?

We hear about grit, resilience and mental toughness. How do you cope better? The best way to cope is to not get stressed in the first place. But the next best thing is to get comfortable with certain levels of stress -- with having a spike of adrenaline in your body.

Many people are not familiar with the feeling of their heart racing, which can happen in a social setting: Maybe you're preparing for a presentation at work or for a tough conversation, or you're afraid of going to the doctor. These situations can increase adrenaline, and people start to get nervous. So, here's the key: David Spiegel says there's something very powerful about self-inducing a state. The stress isn't created from the outside; you're creating that sense of stress deliberately.

There are a couple ways to do this. You need to increase the adrenaline but you need to do it in a healthy way. What can you do? You could take a cold shower and learn to stay calm or calm yourself with the inevitable increase in adrenaline. Remember, adrenaline is non-negotiable. What matters is how you navigate the choppy waters of adrenaline in your system. You can train that by taking a cold shower for a minute to three minutes, and you will get better at tolerating stress.That shot of adrenaline will become a familiar place.

Another way is called cyclic hyperventilation, or self-directing adrenaline increases by deliberately hyperventilating. I would suggest that people who have anxiety not do this when they're in an anxious state and to ease into it over time, because it will very quickly liberate adrenaline in your body.

It's essentially breathing rapidly in through the nose and out through the mouth repeatedly, then exhaling all your air, waiting 10 or 15 second and trying again. But be very careful: If you're somebody who is prone to panic attacks, you might throw yourself into one.

But if you're somebody who suffers from moderate levels of anxiety and you want to build resilience, try five breaths every few days, then maybe 10 breaths for few rounds. What you'll notice over time is that your threshold for adrenaline starts to go up.

Can you talk about the power of cognition in health?

I'm always a proponent of changing behaviors first. But wouldn't it be beautiful if there was something that we could do just with our mind, with our thinking, to enhance our health and well-being? Well, that tool exists. It's a script, of sorts, that my lab has been working on called non-sleep deep rest, or NSDR. It can help us rewire our thinking and our ability to heal and deal with psychological and/or physical problems better.

NSDR involves bringing your nervous system into a state of deep relaxation, and it has been shown to have a handful of major positive effects. It can lead to replenished levels of dopamine, which is a molecule responsible for motivation, among other things. There is also early data showing improvements in cognitive function for people who do this regularly. It can also help replace some of the sleep that you may have missed. If you're not getting enough sleep, you can do this when you wake up in the morning.

For more information on Andrew Huberman's research, visit the Huberman Lab website. For more #AskMeAnything content, visit the Stanford Medicine Instagram page or related Scope stories.

Photo courtesy of Andrew Huberman

Continue reading here:
Ask Me Anything: Neuroscience with Andrew Huberman - Scope

Beautiful brain: exhibit illuminates the human connections behind neuroscience – University of Alberta

It can be hard to get your head around the scope of neuroscience. The never-ending and complex interactions between all of the neurons that drive our nervous systems and our brains are almost unfathomable. Just a small malfunction can lead to disease, yet research to find potential repairs so far just scratches the surface of what there is to know and understand.

This is why pharmacology professor Simonetta Sipione an expert in the causes of neurodegeneration in Huntingtons disease and member of the Neuroscience and Mental Health Institute reached out to experts from other disciplines to give others insight into neuroscience research.

The result is Connections: Bringing Neuroscience and Art Together, a luminous art exhibit of 70 multimedia pieces and a few poems that has been on display at the Friends of University Hospitals McMullen Gallery over the summer and is now available online and as a book.

The exhibit depicts the beauty of the brain, its fragility, and the hope that connects everyone touched by the field of neuroscience from patients to family members, scientists and clinicians. The institute conceived and sponsored the cross-faculty collaboration between the Faculty of Medicine & Dentistry and the Faculty of Arts.

As scientists, we had this desire to share with the general public our excitement for the beauty of the brain, for the way the brain works, things that are revealed on a daily basis during our research work at the institute, says Sipione.

But they also wanted to connect directly on an emotional level with people living with brain diseases and mental health problems.

We wanted to send the message that we hear them, we see them, and we really work hard as scientists and as clinicians to clarify the mysteries of the brain and understand what goes wrong in diseases and develop treatments, Sipione says.

The images on their own and as a collection are striking. A fractured photo collage depicts the nonlinear thought of a person with dementia. A painted face with flesh dripping off one side to reveal the skull illustrates the experience of chronic migraines. A sculpture of wool, silk, wire and wood shows a female figure bent over with the anguish of isolation during the COVID-19 pandemic.

Social anxiety, stress, stroke, autism, benign brain tumour, depression, borderline personality disorder, attention deficit hyperactivity disorder all are explored in submissions sent in by U of A students, neuroscience researchers, professional artists, and community members with lived experience who make art to heal.

The materials used are just as varied as the artists: paint, beads, glass, metal, even sticky notes. Some are actual medical images, such as the live photo of a larval zebrafishs eye submitted by neuroscience post-doctoral fellow Chinmayee Das. Her piece, An angle of observation, captures the moment when the fish perceives a threat and calcium rushes into its eye cells to trigger a fight-or-flight response.

A masters student in the Neuroscience and Mental Health Institute graduate program, An Bui studies recovery after stroke, but she also works as a freelance artist and illustrator. Her print, A beautiful mind, shows a doctor peering into the eye of a patient, with flowers and leaves of gold depicting what the doctor sees inside her mind.

There are so many ways connections are made in neuroscience, between different parts of the brain, between the brain and the rest of the body systems, and most importantly, between humans and humans, Bui says.

Master of fine arts candidate Emily Legleitners woodcut on mulberry paper, entitled I will nestle myself within your hunger for the ground, depicts her personal struggle with anxiety. Legleitner says sharing her own experiences helps others feel safe to share stories of their own mental health.

Art can be a very powerful tool in this way: it opens doors and asks us to grapple with difficult questions, Legleitner says.

Sipione collaborated with assistant professor of art Marilne Oliver, assistant professor in design studies Gillian Harvey, and professor of French and media studies Daniel Laforest. The trio had previously worked together on Dyscorpia, an exhibition exploring the impact of technology on the human body.

They considered the title Disconnections, since that is often what happens in disease, but instead settled on Connections as a better description of the goals of the project. A class ofHarveys visual communication design students designed concepts for the visualidentity, which Harvey applied to the design of the catalogue, website and exhibition. Laforest wrote an essay on the overarching theme of the exhibition and introductions to the three parts of the collection.

The purpose of our efforts is to display the beautiful connections that exist among our brain cells; to weave together the threads that bridge neuroscience research, clinical care, and recovery from brain diseases and mental health disorders; to amplify the warm, inspiring, healing power of art; and most importantly, to highlight our human connection, he wrote on the projects website.

Laforest is struck by how the artists reveal their own stories through their art.

It reaches very deep for a lot of these artists, showing experiences that are sometimes heartbreaking, sometimes awesome, but every time there's a lot of personal emotion tied to both being ill and to healing, he says.

For Oliver, the exhibit is like a conversation between the artworks and the artists, illuminating connections between people, between art and science, and between illness and health.

Its only when we're surrounded by the pieces that we realize there are very few images that have depth of field, and the surfaces are often kind of fragmented or fractured, Oliver notes.

Harvey agrees, pointing out that the layering in each piece is almost like a symbolic representation of psychosis or brain dysfunction.

For Sipione, she hopes the exhibit will help people understand the importance of scientific research on disease mechanisms and treatments, and that her neuroscience colleagues and students will find a powerful emotional stimulus for their work from the exhibit.

The art and the contributions of all these many artists help us remember why we do what we do.

Read the original here:
Beautiful brain: exhibit illuminates the human connections behind neuroscience - University of Alberta

A New Function of the Cerebellum – Neuroscience News

Summary: The cerebellum plays a key role in the storage of both positive and negative memories of emotional events.

Source: University of Basel

The cerebellum is known primarily for the regulation of movement. Researchers at the University of Basel have now discovered that the cerebellum also plays an important role in remembering emotional experiences.

The study appears in the journalPNAS.

Both positive and negative emotional experiences are stored particularly well in memory. This phenomenon is important to our survival, since we need to remember dangerous situations in order to avoid them in the future.

Previous studies have shown that a brain structure called the amygdala, which is important in the processing of emotions, plays a central role in this phenomenon.

Emotions activate the amygdala, which in turn facilitates the storage of information in various areas of the cerebrum.

The current research, led by Professor Dominique de Quervain and Professor Andreas Papassotiropoulos at the University of Basel, investigates the role of the cerebellum in storing emotional experiences. In a large-scale study, the researchers showed 1,418 participants emotional and neutral images and recorded the subjects brain activity using magnetic resonance imaging.

In a memory test conducted later, the positive and negative images were remembered by the participants much better than the neutral images. The improved storage of emotional images was linked with an increase in brain activity in the areas of the cerebrum already known to play a part.

However, the team also identified increased activity in the cerebellum.

The cerebellum in communication with the cerebrum

The researchers were also able to demonstrate that the cerebellum shows stronger communication with various areas of the cerebrum during the process of enhanced storage of the emotional images. It receives information from the cingulate gyrus a region of the brain that is important in the perception and evaluation of feelings.

Furthermore, the cerebellum sends out signals to various regions of the brain, including the amygdala and hippocampus. The latter plays a central role in memory storage.

These results indicate that the cerebellum is an integral component of a network that is responsible for the improved storage of emotional information, says de Quervain.

Although an improved memory for emotional events is a crucial mechanism for survival, it does have its downsides: in the case of very negative experiences, it can lead to recurring anxiety.

This means that the findings, which have now been released, may also be relevant in understanding psychiatric conditions such as post-traumatic stress disorder.

Basel research on emotions and memory

The current study forms part of a large-scale research project conducted by the Research Platform Molecular and Cognitive Neurosciences (MCN) at the University of Basel and the University Psychiatric Clinics (UPK) Basel.

The aim of this project is to gain a better understanding of emotional and cognitive processes and to transfer results from basic research to clinical projects.

Author: Angelika JacobsSource: University of BaselContact: Angelika Jacobs University of BaselImage: The image is credited to MCN, University of Basel

Original Research: Open access.Human cerebellum and corticocerebellar connections involved in emotional memory enhancement by Dominique de Quervain et al. PNAS

Abstract

Human cerebellum and corticocerebellar connections involved in emotional memory enhancement

Emotional information is better remembered than neutral information. Extensive evidence indicates that the amygdala and its interactions with other cerebral regions play an important role in the memory-enhancing effect of emotional arousal.

While the cerebellum has been found to be involved in fear conditioning, its role in emotional enhancement of episodic memory is less clear.

To address this issue, we used a whole-brain functional MRI approach in 1,418 healthy participants. First, we identified clusters significantly activated during enhanced memory encoding of negative and positive emotional pictures. In addition to the well-known emotional memoryrelated cerebral regions, we identified a cluster in the cerebellum.

We then used dynamic causal modeling and identified several cerebellar connections with increased connection strength corresponding to enhanced emotional memory, including one to a cluster covering the amygdala and hippocampus, and bidirectional connections with a cluster covering the anterior cingulate cortex.

The present findings indicate that the cerebellum is an integral part of a network involved in emotional enhancement of episodic memory.

View post:
A New Function of the Cerebellum - Neuroscience News

New Study Undermines the Theory That Depressed People Are Just More Realistic – Neuroscience News

Summary: Depressive realism, a theory that has been touted since the late 1970s, states those with depression are more realistic in how they judge the control they have over their lives. A new study says the evidence is not there to sustain this old theory.

Source: UC Berkeley

Are depressed people simply more realistic in judging how much they control their lives, while others view the world through rose-colored lenses, living under the illusion that they have more control than they do?

Thats the general idea behind depressive realism, a theory that has held sway in science and popular culture for more than four decades.

The problem is, its just not true, new research finds.

Its an idea that exerts enough appeal that lots of people seem to believe it, but the evidence just isnt there to sustain it, says Professor Don Moore, the Lorraine Tyson Mitchell Chair in Leadership and Communication at UC Berkeleys Haas School of Business and co-author of the study in the journalCollabra:Psychology. The good news is you dont have to be depressed to understand how much control you have.

Depressive realism

The concept of depressive realism stems from a 1979 study ofcollege studentsexamining whether they could predict how much control they had over whether a light turned green when they pushed a button.

The original research concluded that the depressed students were better at identifying when they had no control over the lights, while those who werent depressed tended to overestimate their level of control.

Moore and his colleagues set out to try to replicate those findings as part of a broader effort to restore trust inscientific research, much of which is woven into the fabric of the scientific community and wider culture. Researchers are revisiting bedrock studies to shore up the most basic of scientific principles: Can the researchand its conclusionsbe replicated?

Why test the theory of depressive realism in particular? Its decades-long infusion into science, culture, and even potential mental health treatment policy makes it important, Moore says. The original study, for instance, was cited more than 2,000 times in subsequent studies or research, according to Google Scholar.

At the top of the list of reasons why we ought to revisit this particular article is its widespread acceptance in both the scholarly and popular literature, says Moore, who studies overconfidence, confidence, and decision-making. That means a lot of people are building theories or policies premised on this effect being true. If its not, its really important to establish that.

Replicating the original study

Moore co-authored the study with University of California Berkeley psychology professor Sheri Johnson and former undergraduate student researcher Karin Garrett, BA 21, along with University of Miami doctoral student Amelia Dev, BA 17.

The authors studied two groups of participants, whom they screened for depression via a questionnaire. The first group of 248 participants came from Amazons Mechanical Turk, an online service that provides paid survey-takers and study participants from a range of backgrounds, in this case all over 18 years old. The second group was made up of 134 college students who participated in return for college credit.

The researchers added or used more modern and robust measurements for the study. For example, they added a mechanism to measure bias, and experimentally varied the amount of control participants actually had.

Participants performed a task similar to that in the 1979 study. In 40 rounds, each chose whether to press a button, after which a lightbulb or a black box appeared. Each was told to figure out whether pushing (or not pushing) the button impacted whether the light came on. After the rounds, each reported how much control they had over the light.

Both the online groups and college student groups were split into three experimental conditions. Each condition experienced different relationships between the button and the light during the 40 rounds.

The participants in the first two conditions had no actual control over the lights appearance, yet saw it illuminate one-quarter or three-quarters of the time, respectively. Participants in the third condition had some control, seeing the light three-quarters of the time after pushing the button.

The researchers were unable to replicate the original studys results. In fact, people in the online group with a higher level of depression overestimated their controla direct contradiction to the original study. That finding may be driven by anxiety rather than depression, the researchers note, an observation Moore says merits further study.

In the college student group, depression levels had little impact on their view of their control, the authors found.

Researchers also tested for overconfidence. Study participants were asked to estimate their scores on an intelligence test. Depression had no impact there, either.

Results undermine the theory

The results, Moore says, undermined his belief in depressive realism.

The study does not suggest that there are benefits to being depressed, so no one should seek depression as a cure to their cognitive biases, Moore says.

Imagine, for example, a manager hiring someone who is depressed because they believebased on the original studythat the person is less likely to be overconfident and will have better judgment. That would be a mistake, Moore says.

While depression may not improve judgment, the issue of how to accurately gauge our level of control in various situations has broader implications throughout life, Moore says.

We live with a great deal of uncertainty about how much control we haveover our careers, our health, our body weight, our friendships, or our happiness, says Moore. What actions can we take that really matter? If we want to make good choices in life, its very helpful to know what we control and what we dont.

Author: Press OfficeSource: UC BerkeleyContact: Press Office UC BerkeleyImage: The image is in the public domain

Original Research: Closed access.Sadder Wiser: Depressive Realism is not Robust to Replication by Amelia Shepley Dev et al. Collabra:Psychology

Abstract

Sadder Wiser: Depressive Realism is not Robust to Replication

The theory of depressive realism holds that depressed individuals are less prone to optimistic bias, and are thus more realistic, in assessing their control or performance.

Since the theory was proposed 40 years ago, many innovations have been validated for testing cognitive accuracy, including improved measures of bias in perceived control and performance.

We incorporate several of those innovations in a well-powered, pre-registered study designed to identify depressive realism. Amazon MTurk workers (N = 246) and undergraduate students (N = 134) completed a classic contingency task, an overconfidence task, and measures of mental health constructs, including depression and anxiety.

We measured perceived control throughout the contingency task, allowing us to compare control estimates at the trial-level to estimates assessed at task conclusion. We found no evidence that depressive symptoms relate to illusory control or to overconfidence.

Our results suggest that despite its popular acceptance, depressive realism is not replicable.

Link:
New Study Undermines the Theory That Depressed People Are Just More Realistic - Neuroscience News

The Effect of the Color Red on Brain Waves – Neuroscience News

Summary: The color red is not particularly strong in terms of the strength of gamma oscillations it generates in the brain.

Source: ESI

Red traffic lights make drivers stop. The color red produces a signaling and warning effect. But is this also reflected in the brain?

Researchers at the Ernst Strngmann Institute (ESI) for Neuroscience have now investigated this question. They wanted to know whether red triggers brain waves more strongly than other colors.

The study, titled Human visual gamma for color stimuli, is published in the journaleLife.

The research of Benjamin J. Stauch, Alina Peter, Isabelle Ehrlich, Zora Nolte, and ESI director Pascal Fries focuses on the early visual cortex, also known as V1. It is the largest visual area in the brain and the first to receive input from the retina.

When this area is stimulated by strong and spatially homogeneous images, brain waves (oscillations) arise at a specific frequency called thegammaband (3080 Hz). But not all images generate this effect to the same extent.

Color is hard to define

Recently, a lot of research has attempted to explore which specific input drives gamma waves, explains Benjamin J. Stauch, first author of the study. One visual input seems to be colored surfaces. Especially if they are red. Researchers interpreted this to mean that red is evolutionarily special to the visual system because, for example, fruits are often red.

But how can the effect of color be scientifically proven? Or refuted? After all, it is difficult to define a color objectively, and it is equally difficult to compare colors between different studies.

Every computer monitor reproduces a color differently, so red on one screen is not the same as on another. In addition, there are a variety of ways to define colors: based on a single monitor, perceptual judgments, or based on what their input does to thehuman retina.

Colors activate photoreceptor cells

Humans perceive color when photoreceptor cells, the so-called cones, are activated in the retina. They respond to light stimuli by converting them into electrical signals, which are then transmitted to the brain.

To recognize colors, we need several types of cones. Each type is particularly receptive to a specific range of wavelengths: red (L cones), green (M cones), or blue (S cones). The brain then compares how strongly the respective cones have reacted and deduces a color impression.

It works similarly for all human beings. It would therefore be possible to define colors objectively by measuring how strongly they activate the different retinal cones. Scientific studies with macaques have shown that the early primate visual system has two color axes based on these cones: the L-M axis compares red to green, and the S(L+M) axis is yellow to violet.

We believe that a color coordinate system based on these two axes is the right one to define colors when researchers want to explore the strength of gamma oscillations. It definescolorsaccording to how strongly and in what way they activate the earlyvisual system, Benjamin J. Stauch says.

He and his team wanted to measure a larger sample of individuals (N = 30) because previous work on color-related gamma oscillations has mostly been run withsmall samplesof a few primates or human participants, and the spectra of cone activation can vary genetically from individual to individual,

Red and green have an equal effect

In doing so, Benjamin J. Stauch and his team investigated whether the color red is special and whether this color causes stronger gamma oscillations than green of comparable color intensity (i.e., cone contrast).

They also explored a side question: Can color-induced gamma oscillations also be detected by magnetoencephalography (MEG), a method for measuring the magnetic activities of the brain?

They conclude that the color red is not particularly strong in terms of the strength of the gamma oscillations it induces. Rather, red and green produce equally strong gamma oscillations in the early visual cortex at the same absolute L-M cone contrast.

Moreover, color-induced gamma waves can be measured in human MEG when treated carefully, so future research could follow the 3R principles foranimal experiments(reduce, replace, refine) by using humans rather than nonhuman primates.

Colors that activate only the S-cone (blue) generally appear to elicit only weak neuronal responses in the early visual cortex. To some extent, this is to be expected, since the S-cone is less common in the primate retina, evolutionarily older, and more sluggish.

The results of this study led by ESI scientists contribute to understanding how the early human visual cortex encodes images and may one day be used to help develop visual prostheses. These prostheses may attempt to activate the visual cortex to induce vision-like perceptual effects in people with damaged retinas. However, this goal is still a long way off.

Much more needs to be understood about the specific responses of the visual cortex to visual input.

Author: Press OfficeSource: ESIContact: Press Office ESIImage: The image is credited to ESI/C. Kernberger

Original Research: Open access.Human visual gamma for color stimuli by Benjamin J Stauch et al. eLife

Abstract

Human visual gamma for color stimuli

Strong gamma-band oscillations in primate early visual cortex can be induced by homogeneous color surfaces (Peter et al., 2019; Shirhatti and Ray, 2018). Compared to other hues, particularly strong gamma oscillations have been reported for red stimuli.

However, precortical color processing and the resultant strength of input to V1 have often not been fully controlled for. Therefore, stronger responses to red might be due to differences in V1 input strength.

We presented stimuli that had equal luminance and cone contrast levels in a color coordinate system based on responses of the lateral geniculate nucleus, the main input source for area V1. With these stimuli, we recorded magnetoencephalography in 30 human participants.

We found gamma oscillations in early visual cortex which, contrary to previous reports, did not differ between red and green stimuli of equal L-M cone contrast.

Notably, blue stimuli with contrast exclusively on the S-cone axis induced very weak gamma responses, as well as smaller event-related fields and poorer change-detection performance.

The strength of human color gamma responses for stimuli on the L-M axis could be well explained by L-M cone contrast and did not show a clear red bias when L-M cone contrast was properly equalized.

Read the original:
The Effect of the Color Red on Brain Waves - Neuroscience News