Category Archives: Neuroscience

Neuroscience

New Research Explores the Appeal of Dangerous Men – Neuroscience News

Summary: For short-term relationships, most women are more attracted to risk-taking men, a new study reports. Women who are in better health or have greater access to quality healthcare are more likely to be attracted to risk-taking men than women from other socioeconomic or health backgrounds.

Source: University of Western Australia

A new study led by The University of Western Australia has probed the age-old question of whether women prefer risk-taking men over their more careful cousins and come up with some surprising results.

The study, published today inEvolutionary Psychological Science, used anevolutionary perspectiveto shed light on the topic and found that relationship context and the health status ofwomenwere critical factors.

More than 1,300 women from 47 countries were surveyed for the study.

Lead researcher Dr. Cyril Grueter, from UWAs School of Human Sciences, said the findings clearly showed that risk-taking men were more attractive for short-term flings than long-term relationships.

For casual sexual liaisons, women prefer courageous cads with a good genetic constitutionrisk-takers seem to fit this bill, Dr. Grueter said.

For more serious long-term relationships, women place agreater valueon committed men.

Interestingly, the study found that women in better health and with better access to health care were more attracted to risk-takers than women from other socioeconomic backgrounds.

Women in healthier countries may have greater control over whether they become pregnant in a short-term relationshipthrough contraceptives and abortionand therefore can afford to choose a risk-prone male partner, Dr. Goodman said.

The study also showed thatbisexual womenand so-called adrenaline junkies were more into risk-takers thanheterosexual womenand risk-avoiders.

Bisexual women may have less conservative perceptions about relationships, and the pairing of similar-minded couples may bring greater relationship satisfaction, Dr. Grueter said.

Author: Press OfficeSource: University of Western AustraliaContact: Press Office University of Western AustraliaImage: The image is in the public domain

Original Research: Open access.Preference for Male Risk Takers Varies with Relationship Context and Health Status but not COVID Risk by Cyril C. Grueter et al. Evolutionary Psychological Science

Abstract

Preference for Male Risk Takers Varies with Relationship Context and Health Status but not COVID Risk

Risk taking is more commonly shown by males than females and has a signalling function, serving to advertise ones intrinsic quality to prospective mates.

Previous research has established that male risk takers are judged as more attractive for short-term flings than long-term relationships, but the environmental and socioeconomic context surrounding female preferences for male risk takers has been overlooked.

Using a survey instrument, we examined female preferences for male risk takers across 1304 females from 47 countries.

We found preferences for physical risk takers to be more pronounced in females with a bisexual orientation and females who scored high on risk proneness. Self-reported health was positively associated with preferences for high risk takers as short-term mates, but the effect was moderated by country-level health, i.e. the association was stronger in countries with poorer health.

The security provided by better health and access to health care may allow females to capitalise on the genetic quality afforded by selecting a risk-prone male whilst concurrently buffering the potential costs associated with the risk takers lower paternal investment.

The risk of contracting COVID-19 did not predict avoidance of risk takers, perhaps because this environmental cue is too novel to have moulded our behavioural preferences.

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New Research Explores the Appeal of Dangerous Men - Neuroscience News

Neuroscience

Pill for Skin Disease Also Curbs Excessive Drinking – Neuroscience News

Summary: Apremilast, an FDA-approved drug for the treatment of skin conditions including psoriasis and psoriatic arthritis, triggers increased activity in the nucleus accumbens, a brain area associated with regulating alcohol intake. Apremilast reduced drinking behaviors in mouse models with a genetic risk of alcohol use disorder.

Source: Oregon Health and Science University

Researchers from Oregon Health & Science University and institutions across the country have identified a pill used to treat a common skin disease as an incredibly promising treatment for alcohol use disorder.

The study was recentlypublished in theJournal of Clinical Investigation.

On average, the people who received the medication, called apremilast, reduced their alcohol intake by more than half from five drinks per day to two.

Ive never seen anything like that before, said co-senior authorAngela Ozburn, Ph.D., associate professor of behavioral neuroscience in the OHSU School of Medicine and a research biologist with the Portland VA Health Care System.

The lead author isKolter Grigsby, Ph.D., a postdoctoral fellow in the Ozburn laboratory at OHSU.

Beginning in 2015, Ozburn and collaborators searched a genetic database looking for compounds likely to counteract the expression of genes known to be linked to heavy alcohol use. Apremilast, an FDA-approved anti-inflammatory medication used to treatpsoriasis and psoriatic arthritis, appeared to be a promising candidate.

They then tested it in two unique animal models that have a genetic of risk for excessive drinking, as well as in other strains of mice at laboratories across the country. In each case, apremilast reduced drinking among a variety of models predisposed to mild to heavy alcohol use. They found that apremilast triggered an increase in activity in the nucleus accumbens, the region of the brain involved in controlling alcohol intake.

Researchers at the Scripps Research Institute in La Jolla, California, then tested apremilast in people.

The Scripps team conducted a double-blind, placebo-controlled clinical proof-of-concept study involving 51 people who were assessed over 11 days of treatment.

Apremilasts large effect size on reducing drinking, combined with its good tolerability in our participants, suggests it is an excellent candidate for further evaluation as a novel treatment for people with alcohol use disorder, said co-senior authorBarbara Mason, Ph.D., Pearson Family professor in the Department of Molecular Medicine at Scripps.

The clinical study involved people with alcohol use disorder who werent seeking any form of treatment, and Mason predicts that apremilast may be even more effective among people who are motivated to reduce their alcohol consumption.

Its imperative for more clinical trials to be done on people seeking treatment, Ozburn said. In this study, we saw that apremilast worked in mice. It worked in different labs, and it worked in people. This is incredibly promising for treatment of addiction in general.

An estimated 95,000 people in the United Statesdie every year from alcohol-related deaths, according to the National Institute on Alcohol Abuse and Alcoholism.

Currently, there are three medications approved foralcohol use disorderin the United States: Antabuse, which produces an acute sensitivity akin to a hangover when alcohol is consumed; acamprosate, a medication thought to stabilize chemical signaling in the brain that is associated with relapse; and naltrexone, a medication that blocks the euphoric effects of both alcohol and opioids.

Funding: The research reported here was supported by the National Institutes of Health awards AA016651, AA013519, AA010760, AA07468, AA027692, U01 AA013498, DA013429, P60AA06420 and U01AA025476; the U.S. Department of Veterans Affairs awards BX000313, BX004699 and IK2 BX002488; and a gift from the John R. Andrews Family. The content is solely the responsibility of the researchers and does not necessarily represent the official views of the NIH or the U.S. Department of Veterans Affairs.

Author: Erik RobinsonSource: Oregon Health and Science UniversityContact; Erik Robinson Oregon Health and Science UniversityImage: The image is in the public domain

Original Research: Open access.Pre-clinical and clinical evidence for suppression of alcohol intake by apremilast by Angela Ozburn et al. Journal of Clinical Investigation

Abstract

Pre-clinical and clinical evidence for suppression of alcohol intake by apremilast

Treatment options for Alcohol Use Disorders (AUD) have minimally advanced since 2004, while the annual deaths and economic toll have increased alarmingly. Phosphodiesterase type 4 (PDE4) is associated with alcohol and nicotine dependence. PDE4 inhibitors were identified as a potential AUD treatment using a novel bioinformatics approach.

We prioritized a newer PDE4 inhibitor, apremilast, as ideal for repurposing, (i.e. FDA approved for psoriasis, low incidence of adverse events, excellent safety profile), and tested it using multiple animal strains and models, as well as in a human Phase IIa study.

We found that apremilast reduced binge-like alcohol intake and behavioral measures of alcohol motivation in mouse models of genetic risk for drinking to intoxication. Apremilast also reduced excessive alcohol drinking in models for stress-facilitated drinking and alcohol dependence.

Using site-directed drug infusions and electrophysiology, we uncovered that apremilast may act to lessen drinking in mice by increasing neural activity in the nucleus accumbens, a key brain region in the regulation of alcohol intake. Importantly, apremilast (90 mg/d) reduced excessive drinking in non-treatment seeking individuals with AUD in a double blind, placebo-controlled study.

These results demonstrate that apremilast suppresses excessive alcohol drinking across the spectrum of AUD severity.

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Pill for Skin Disease Also Curbs Excessive Drinking - Neuroscience News

Neuroscience

Protein Biomarkers Identified in Women Who Developed Perinatal … – Neuroscience News

Summary: Study reveals women who develop anxiety and mood disorders such as perinatal depression during pregnancy have specific altered proteins circulating in their bloodstream during the third trimester.

Source: Cedars Sinai Medical Center

Cedars-Sinai investigators found that women who developed mood and anxiety disorders associated with pregnancy and childbirth had specific altered proteins circulating in their bloodstream in the third trimester.

The study is published in theAmerican Journal of Obstetrics & Gynecology.

In thispilot study, we found that participants with perinatal mood and anxiety disorder (PMAD) symptoms had a unique and distinct prenatal plasma protein signature that regulated certain brain signaling activity and pro-inflammatory pathways, said Eynav Accortt, Ph.D., director of the Reproductive Psychology Program at Cedars-Sinai and corresponding author of the study.

The controlled pilot study included 34 women at risk for developing PMAD and 18 controls. Mental health screening was conducted in the third trimester and again three months after giving birth. Investigators used a highly sensitive tool called slow off-rate modified aptamers (SOMA) scan technology to detect plasma biomarkers correlated with specific disorders, such as anxiety, depression and post-traumatic stress.

According to the Centers for Disease Control and Prevention, about 1 in 8 women experience significant symptoms of perinatal mood and anxiety disorders that can interfere with overall health, daily activities andfamily life.

The critical first step in prevention of any disease is knowing if you are at risk. The process of discovering adiagnostic testfor perinatal mood andanxiety disorders, through biomarker research like this, is our holy grail, said Accortt, a clinical psychologist.

It can be incredibly challenging for a woman who is distressed to identify her need for intervention. Family members and friends can look for red flags but may not know how to help. If we had an early blood test, like the test all women take for gestational diabetes, she and her family would know that she is at higher risk and begin to get education and consider treatment options much earlier, said Accortt.

A previous study led by Accortt and published in theAmerican Journal of Reproductive Immunologyfound that women with prolongedmental health problemsup to three years after childbirth may be suffering from chronic irregularities in their immune system.

Larger validation studies are needed to determine whether biomarkers identified in this pilot study can be used with traditional risk factorssuch as a previous history of depression or medical complications during pregnancy or childbirthto develop protocols for early detection.

The financial and societal costs for untreated maternal mental illness are enormous. One study published in theAmerican Journal of Public Healthestimated the national cost in 2017 to be $14 billion.

In addition to the financial costs of mood disorders associated with pregnancy and childbirth, including reduced economic productivity and more preterm births, children and the family structure can be deeply affected.

We need research-based diagnostics developed so we can help women find a pathway to wellness and be able to emerge out of the shadow of debilitating mood disorders that harm their health and thehealthof their families, said Sarah Kilpatrick, MD, Ph.D., chair of the Department of Obstetrics and Gynecology at Cedars-Sinai and study co-author.

Author: Press OfficeSource: Cedars Sinai Medical CenterContact: Press Office Cedars Sinai Medical CenterImage: The image is in the public domain

Original Research: Closed access.Perinatal mood and anxiety disorders: biomarker discovery using plasma proteomics by Eynav Accortt et al. American Journal of Obstetrics and Gynecology

Abstract

Perinatal mood and anxiety disorders: biomarker discovery using plasma proteomics

Perinatal mood and anxiety disorders encompass a range of mental health disorders that occur during pregnancy and up to 1 year postpartum, affecting approximately 20% of women. Traditional risk factors, such as a history of depression and pregnancy complications including preeclampsia, are known. Their predictive utility, however, is not specific or sensitive enough to inform clinical decision-making or prevention strategies for perinatal mood and anxiety disorders. Better diagnostic and prognostic models are needed for early identification and referral to treatment.

This study aimed to determine if a panel of novel third-trimester plasma protein biomarkers in pregnant women can be used to identify those who have a high predisposed risk for perinatal mood and anxiety disorders within 3 months postpartum.

We studied 52 women (n=34 with a risk for perinatal mood and anxiety disorders and n=18 controls) among whom mental health screening was conducted at 2 time points, namely in the third trimester and again at 3 months postdelivery. An elevated perinatal mood and anxiety disorder risk was identified by screening individuals with above-validated cutoffs for depression (Edinburgh Postnatal Depression Scale 12), anxiety (Overall Anxiety Severity and Impairment Scale 7), and/or posttraumatic stress disorder (Impact of Events Scale >26) at both time points. Plasma samples collected in the third trimester were screened using the aptamer-based SomaLogic SomaScan proteomic assay technology to evaluate perinatal mood and anxiety disorderassociated changes in the expression of 1305 protein analytes. Ingenuity Pathway Analysis was conducted to highlight pathophysiological relationships between perinatal mood and anxiety disorderspecific proteins found to be significantly up- or down-regulated in all subjects with perinatal mood and anxiety disorder and in those with perinatal mood and anxiety disorders and no preeclampsia.

From a panel of 53 significant perinatal mood and anxiety disorderassociated proteins, a unique 20-protein signature differentiated perinatal mood and anxiety disorder cases from controls in a principal component analysis (P<.05). This protein signature included NCAM1, NRCAM, and NTRK3 that converge around neuronal signaling pathways regulating axonal guidance, astrocyte differentiation, and maintenance of GABAergic neurons. Interestingly, when we restricted the analysis to subjects without preeclampsia, a 30-protein signature differentiated perinatal mood and anxiety disorder cases from all controls without overlap on the principal component analysis (P<.001). In the nonpreeclamptic perinatal mood and anxiety disorder group, we observed increased expression of proteins, such as CXCL11, CXCL6, MIC-B, and B2MG, which regulate leucocyte migration, inflammation, and immune function.

Participants with perinatal mood and anxiety disorders had a unique and distinct plasma protein signature that regulated a variety of neuronal signaling and proinflammatory pathways. Additional validation studies with larger sample sizes are needed to determine whether some of these molecules can be used in conjunction with traditional risk factors for the early detection of perinatal mood and anxiety disorders.

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Protein Biomarkers Identified in Women Who Developed Perinatal ... - Neuroscience News

Neuroscience

Department of Neuroscience School of Medicine and Public Health UW …

Neuroscience, which has had a longstanding tradition of excellence at the University of Wisconsin-Madison, has now entered an exciting new era by the creation of a Department of Neuroscience in the School of Medicine and Public Health. This department brings together research and teaching in wide ranging areas of neuroscience including the study of ion channels, synaptic transmission, neural development, sensory and cognitive physiology and neural circuits. The recent move of the department to a new research building, the second wing of the Wisconsin Institutes for Medical Research (WIMR) has further strengthened collaboration and innovation through shared interests, techniques, equipment and facilities. Proximity of WIMR to the Waisman Center and University Hospitals has also promoted collaborative efforts to apply the findings of basic research in neuroscience to the study and treatment of human disease.

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Department of Neuroscience School of Medicine and Public Health UW ...

Neuroscience

Empyrean Neuroscience Launches with $22M Series A and Genetic Engineering Platform to Advance Pipeline of Neuroactive Compounds Targeting CNS…

NEW YORK & CAMBRIDGE, England--(BUSINESS WIRE)--Empyrean Neuroscience, Inc., a leading genetic engineering company dedicated to developing neuroactive compounds to treat neuropsychiatric and neurologic disorders, today announced that it has launched with a $22 million Series A financing and a genetic engineering platform to advance a pipeline of neuroactive compounds targeting disorders of the central nervous system (CNS). The company is founded on a proprietary platform designed to genetically engineer small molecule therapeutics from fungi and plants. Veteran biotech executives Usman Oz Azam, M.D., Chief Executive Officer, and Fred Grossman, D.O., FAPA, Chief Medical Officer, lead the company.

Through precision targeting and engineering of the fungal and plant genomes, Empyrean is working to enhance and modulate neuroactive compounds produced by these kingdoms. The platform is being used to identify therapeutic fungal alkaloids, cannabinoids, and other small molecules that may exhibit enhanced efficacy and safety. In addition, the platform is designed to discover novel small molecules that may exhibit a therapeutic benefit.

There is an enormous medical need for safe and effective therapeutics that treat neuropsychiatric and neurologic disorders and we believe genetic engineering provides the answer, said Dr. Azam, Empyreans Chief Executive Officer. By applying our genetic engineering platform to make precise modifications to the genomes of fungi and plants, we can change the amount and kind of neuroactive small molecules they produce, with the goal of developing safe and effective treatments for difficult-to-treat diseases of the CNS.

The companys developmental pipeline includes fungal alkaloids, cannabinoids, and other neuroactive compounds, such as N,N-Dimethyltryptamine (DMT), for the potential treatment of major depressive disorder (MDD), post-traumatic stress disorder (PTSD), neurologic disorders, substance abuse and dependence, and chronic pain. Investigational New Drug (IND) enabling studies of the companys first genetically engineered encapsulated mushroom drug product are currently underway, and the company aims to enter the clinic for MDD in 2023.

Fungal alkaloids and cannabinoids have shown promise in treating depression, PTSD, anxiety, and other neuropsychiatric and neurologic disorders, said Dr. Grossman, Empyreans Chief Medical Officer. We believe our approach of genetically engineering fungi and plants can improve their safety and efficacy and will ultimately help to address the substantial unmet medical need in patients who suffer from these diseases.

As part of its genetic engineering platform, the company has licensed CRISPR/Cas9 technology from ERS Genomics for genetic engineering applications related to its therapeutic pipeline.

Dr. Azam was previously President and Chief Executive Officer of Tmunity Therapeutics, a biotech developing genetically engineered cell therapies for applications in cancer. Before Tmunity, he was Global Head of Cell & Gene Therapies at Novartis, where he was responsible for commercial operations, business development licensing, new product commercialization, clinical development, regulatory affairs, and other aspects of the global cell and gene therapies business. He was Chief Executive Officer of Novaccel Therapeutics, Chief Medical Officer of Aspreva Pharmaceuticals, and earlier in his career, held positions at Johnson & Johnson, GSK, and Pfizer. Dr. Azam received his M.D. from the University of Liverpool School of Medicine and is board certified in obstetrics and gynecology in the United Kingdom.

Before joining Empyrean, Dr. Grossman was Chief Medical Officer of Mesoblast Ltd. and President and Chief Medical Officer of Glenmark Pharmaceuticals. He has held executive leadership positions in large pharmaceutical companies, including Eli Lilly, Johnson & Johnson, Bristol Myers Squibb, and Sunovion. He has been responsible for leading the development, approval, and supporting the launch of numerous global medications addressing significant unmet medical needs across therapeutic areas, particularly in the CNS. He has held academic appointments and has authored numerous scientific publications. He was trained in psychiatry at Hahnemann University in Philadelphia and at the National Institute of Mental Health in Bethesda, Maryland and completed a Fellowship in the Section on Clinical Pharmacology at the National Institutes of Health. Dr. Grossman is a board-certified psychiatrist and Fellow of the American Psychiatric Association.

About Empyrean Neuroscience

Empyrean Neuroscience is a genetic engineering company developing a pipeline of neuroactive therapeutics to treat a range of neuropsychiatric and neurologic disorders. Through precision genetic modification, transformation, and regeneration of fungi and plants, the platform allows for the creation of small molecule therapeutics. In addition, the platform enables the discovery of novel small molecules that may exhibit therapeutic properties. The company is based in New York City and Cambridge, UK.

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Empyrean Neuroscience Launches with $22M Series A and Genetic Engineering Platform to Advance Pipeline of Neuroactive Compounds Targeting CNS...

Neuroscience

A New Protein That May Contribute to Alzheimers Disease Identified – Neuroscience News

Summary: The GM2A protein reduces neural firing and induces a loss of neurite integrity.

Source: Brigham and Womens Hospital

Alzheimers disease (AD) currently has no cure and is predicted to affect over 100 million people worldwide by 2050.

Ongoing research is focused on two key neurotoxic proteins: amyloid beta (A) and tau. While these proteins have been shown to be associated with AD, for some people with the disease, the levels of A and tau do not consistently explain or correlate with the severity of cognitive decline.

To identify other proteins that may be directly involved with fundamental aspects of AD, like synaptic loss and neurodegeneration, investigators at Brigham and Womens Hospital, a founding member of the Mass General Brigham healthcare system, exposed laboratory neurons to human brain extracts from about 40 people who either had AD, were protected from AD despite having high A and tau levels, or were protected from AD with little or no A and tau in their brains.

The researchers identified and validated ganglioside GM2 activator (GM2A) as a protein able to reduce neuronal firing and induce a loss of neurite integrity. These protein characteristics may contribute to the cause of AD, progression of the disease, or both.

Our data helps identify a new and potentially important protein that may be associated with the pathogenesis of Alzheimers disease, said senior author Tracy Young-Pearse, PhD, from the Department of Neurology.

Interestingly, GM2A has been previously implicated as a causative agent in a lysosomal storage disorder very similar to Tay-Sachs disease, another condition like AD that destroys neurons.

Author: Haley BridgerSource: Brigham and Womens HospitalContact: Haley Bridger Brigham and Womens HospitalImage: The image is in the public domain

Original Research: Open access,Elevated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity by Tracy Young-Pearse et al. Molecular Neurodegeneration

Abstract

Elevated ganglioside GM2 activator (GM2A) in human brain tissue reduces neurite integrity and spontaneous neuronal activity

Alzheimers Disease (AD) affects millions globally, but therapy development is lagging. New experimental systems that monitor neuronal functions in conditions approximating the AD brain may be beneficial for identifying new therapeutic strategies.

We expose cultured neurons to aqueous-soluble human brain extract from 43 individuals across a spectrum of AD pathology. Multi-electrode arrays (MEAs) and live-cell imaging were used to assess neuronal firing and neurite integrity (NI), respectively, following treatments of rat cortical neurons (MEA) and human iPSC-derived neurons (iN) with human brain extracts.

We observe associations between spontaneous activity and A42:40 levels, between neurite integrity and oligomeric A, and between neurite integrity and tau levels present in the brain extracts. However, these associations with A and tau do not fully account for the effects observed. Proteomic profiling of the brain extracts revealed additional candidates correlated with neuronal structure and activity. Neurotoxicity in MEA and NI assays was associated with proteins implicated in lysosomal storage disorders, while neuroprotection was associated with proteins of the WAVE regulatory complex controlling actin cytoskeleton dynamics. Elevated ganglioside GM2 activator (GM2A) associates with reductions in both NI and MEA activity, and cell-derived GM2A alone is sufficient to induce a loss of neurite integrity and a reduction in neuronal firing.

The techniques and data herein introduce a system for modeling neuronal vulnerability in response to factors in the human brain and provide insights into proteins potentially contributing to AD pathogenesis.

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A New Protein That May Contribute to Alzheimers Disease Identified - Neuroscience News

Neuroscience

NUCALM WILL UNLEASH THE POWER OF YOUR MENTAL STATE AT THE 2022 NEUROSCIENCE SUMMIT – PR Newswire

LOS ANGELES, Oct. 18, 2022 /PRNewswire/ -- NuCalm CEO Jim Poole will be this year's featured presenter at the 2022 Neuroscience Summit. The highly anticipated event will be broadcasting live, worldwide from October 20th to October 23rd, available on Roku TV and other streaming platforms. The brain health and wellness event features a stellar lineup of New York Times Bestselling authors, Harvard scientists and mental health experts. Complete details are on the event's website: http://www.nsciencesummit.com.

NuCalm research and their studies have led to a patented neuroscience technology unleashing the brain's unlimited potential. By participating in this year's summit, thousands of new users will have the chance see how they can take control of their lives and achieve their goals. NuCalm's unprecedented work in neuroscience gives individuals the power to improve memory, accelerate the learning process and most importantly the ability to harness calm. Calm, the absence of harmful emotions such as fear, nervousness, anxiety, panic or anger, can be leveraged to provide emotional intelligence to help leaders make the decisions necessary to achieve success.

NuCalm's CEO, Jim Poole, extols the impact that the 2022 Neuroscience Summit will have by saying, "This year's event will offer thousands of people a look into our neuroscience platform that changes the game for so many people. The abilities that NuCalm unlocks is the beginning of unleashing the full human potential." Poole said, "Through decades of research and development, we've made it possible to construct and consciously control the most complicated and powerful computing system, your brain. Drugs and stimulants are no longer necessary for one to leverage their brain wave frequencies to overcome obstacles and achieve their goals."

To date, millions of people across the globe have benefitted from regular use of NuCalm (www.NuCalm.com). This patented, clinically proven technology allows you to flip the switch from stress to rest and recovery within minutes, without drugs or side-effects. Since 2009, NuCalm has been used in over two million surgical procedures and used bysports teams, the military, the FBI, cancer patients, PTSD sufferers, pilots, busy executives and many others.

Contact for NuCalm:Alfred HoptonCapstone Communications Company[emailprotected]

Laurie D. MuslowIt's All Good Entertainment Inc.818-808-0868 Office Direct[emailprotected]

David PooleChief Business OfficerNuCalm617-259-0877[emailprotected]

For more info visit http://www.nucalm.comor call 800-810-1701 to speak to a representative.

SOURCE NuCalm

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NUCALM WILL UNLEASH THE POWER OF YOUR MENTAL STATE AT THE 2022 NEUROSCIENCE SUMMIT - PR Newswire

Neuroscience

Neuroscience Research Fellow Discovers the Power of Perseverance – St. Lawrence University Saints

Nadiana Acevedo 24 isnt afraid of a challenge. When she set out to investigate the effects of an anti-cancer drug this summer, she discovered that sometimes the best learning experiences can come from trial and error.

As part of the Collegiate Science and Technology Entry Program (CSTEP), Nadiana spent eight weeks conducting research alongside Professor of Biology and Psychology Ana Estevez. The scholar program is designed to increase the number of historically underrepresented and economically disadvantaged students in mathematics, science, technology, and health-related fields.

Nadiana shared what fueled her curiosity for research and how she defines success.

(Note: Responses have been edited for length.)

Major: Neuroscience

Hometown: Buffalo, New York

Project Title: "Observing Cell Viability of HT-22 Hippocampal Cells When Exposed to Anti-Cancer Dye MKT-077"

The focus of my research is looking at an anti-cancer dye, MKT-077. This dye is known to be selective to cancer cells meaning it only kills cancer cells. I am testing the drug on a mouse hippocampal neuronal cell line called HT-22 (brain cells) to observe the drug's effect on the cells' viability.

Cancer research is challenging and exciting because it is full of trial and error. I was interested in looking at how this drug would affect neuronal cells because there is a lack of data specific to neurons. I was intrigued that MKT-077 is selective to cancer cells because other drugs kill both healthy and cancerous cells.

The research process was difficult at times because my mentor and I did not know how the MKT-077 would affect the HT-22 cells. The data seemed off in the beginning. We weren't sure if there was an issue with fluorescence when the microplate reader was collecting data. We had to run a test to determine if the MKT-077 had its own fluorescence that would interfere with the dye we used to measure viability. The data showed no conflict between the MKT-077 and the CYQUANT dye we used to measure cell viability.

I did not get discouraged by the research outcomes and was able to complete my summer research and presented my findings.

Dr. Ana Estevez is an amazing advisor and mentor. I built a connection with her over the summer and learned many skills. She has helped me become a well-rounded researcher.

It is possible to succeed and gain knowledge regardless of the data outcome. There is always something to gain from every experience and there is always something new to discover.

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Neuroscience Research Fellow Discovers the Power of Perseverance - St. Lawrence University Saints

Neuroscience

COVID-19 Linked to Excessive Destruction of Connections Between Nerve Cells – Neuroscience News

Summary: COVID-19 infection causes microglia to excessively engulf synaptic structures and the upregulation of factors involved in phagocytosis.

Source: Karolinska Institute

Researchers at Karolinska Institutet have in a new study used cellular reprogramming to create human three-dimensional brain models and infected these models with SARS-CoV-2.

In infected models, the brain immune cells excessively eliminated synapses and acquired a gene expression pattern mimicking what has been observed in neurodegenerative disorders.

The findings could help to identify new treatments against persistent cognitive symptoms after a COVID-19 infection.

Multiple studies have reported persistent cognitive symptoms after a COVID-19 infection but the underlying mechanisms for this remains unknown.

The researchers behind the study, published as an Immediate Communication in the journalMolecular Psychiatry, have from human induced pluripotent stem (iPS) cells created three-dimensional models of the brain in a dishso-called brain organoids.

The model differs from previous organoid models as the researchers also included the brainimmune cellsmicrogliain the model.

In the infected models, microglia excessively engulfed synaptic structures and displayed upregulation of factors involved in phagocytosis. The developed model and the findings in the study could help to guide future efforts to target cognitive symptoms in the aftermath of COVID-19 and other neuroinvasive viral infections.

Cognitive deficits after the infection

Interestingly, our results to a large extent mimic what has recently been observed in mouse models infected with other neuroinvasive RNA viruses such as the West Nile virus. These viruses are also linked to residual cognitive deficits after the infection, and a persisting activation of microglia leading to an excessive engulfment of synapses, which has been suggested to drive these symptoms.

Multiple studies have now also reported remaining cognitive symptoms after a COVID-19 infection, as well as an increased risk of receiving a diagnosis of a disorder characterized by cognitive symptoms, says co-first author of the study Samudyata, postdoctoral fellow in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

Connections to Parkinsons and Alzheimers disease

Microglia are the resident immune cells of the brain but also carries out important regulatory functions of the neuronal circuitries in the developing and adultbrain. One of these crucial functions is to engulf unwanted synapses, a process that is believed to improve and maintain cognitive functions.

However, excessive engulfment of synapses has been linked to both neurodevelopmental disorders, such as schizophrenia, as well as to neurodegenerative disorders including Alzheimers disease.

By sequencing genes insingle cells, the authors could also study how different cell types in the model responded to the virus.

Microglia displayed a distinct gene signature largely characterized by an upregulation of interferon-responsive genes, and included pathways previously linked to neurodegenerative disorders such as Parkinsons and Alzheimers disease.

This signature was also observed at a later time-point when the virus load was minimal, says co-author of the study Susmita Malwade, doctoral student in Sellgren lab at the Department of Physiology and Pharmacology at Karolinska Institutet.

The researchers will now study how different pharmacological approaches can reverse the observed changes in the infected models.

Author: Press OfficeSource: Karolinska InstituteContact: Press Office Karolinska InstituteImage: The image is in the public domain

Original Research: Open access.SARS-CoV-2 promotes microglial synapse elimination in human brain organoids by Samudyata et al. Molecular Psychiatry

Abstract

SARS-CoV-2 promotes microglial synapse elimination in human brain organoids

Neuropsychiatric manifestations are common in both the acute and post-acute phase of SARS-CoV-2 infection, but the mechanisms of these effects are unknown.

In a newly established brain organoid model with innately developing microglia, we demonstrate that SARS-CoV-2 infection initiate neuronal cell death and cause a loss of post-synaptic termini.

Despite limited neurotropism and a decelerating viral replication, we observe a threefold increase in microglial engulfment of postsynaptic termini after SARS-CoV-2 exposure.

We define the microglial responses to SARS-CoV-2 infection by single cell transcriptomic profiling and observe an upregulation of interferon-responsive genes as well as genes promoting migration and synapse engulfment.

To a large extent, SARS-CoV-2 exposed microglia adopt a transcriptomic profile overlapping with neurodegenerative disorders that display an early synapse loss as well as an increased incident risk after a SARS-CoV-2 infection.

Our results reveal that brain organoids infected with SARS-CoV-2 display disruption in circuit integrity via microglia-mediated synapse elimination and identifies a potential novel mechanism contributing to cognitive impairments in patients recovering from COVID-19.

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COVID-19 Linked to Excessive Destruction of Connections Between Nerve Cells - Neuroscience News

Neuroscience

Patients With Clinical Depression Stopped Seeking Treatment During the COVID Waves – Neuroscience News

Summary: During the COVID-19 pandemic, the number of patients admitted to hospitals for clinical depression care dropped significantly. However, the number of people seeking outpatient care for depression increased.

Source: European College of Neuropsychopharmacology

In the first study of its kind, German researchers have shown that the COVID pandemic saw a huge drop in the number of patients being admitted to hospital for clinical depression.

Independently of these national statistics, the researchers found that the number of outpatients they dealt with increased over the same period in their department. As inpatient treatment offers more intensive levels of care, this implies that many patients did not receive care appropriate to their condition.

It is not yet known if this shift in treatment is also seen in other countries.

The researchers, from the University Hospital in Frankfurt, looked at German national databases. They found that during the first COVID wave new hospitalisations for first time clinical depression dropped by 57.5%, from 13457 in January 2020 down to 5723 in April 2020. In the same period, the number of patients being hospitalised for recurrent depression dropped by 56.3%, from 22188 down to 9698.

Lead researcher, Dr Mareike Aichholzer said We also saw a decrease in inpatient treatment of recurrent depression in our own hospital in Frankfurt. In addition to the stricter admission rules, this rather seemed to be due to a drop in demand from the patients themselves.

In contrast, the number of new outpatients being treated for clinical depression at the University Hospital in Frankfurt remained stable and the number of patients with recurrent depression showed a significant increase between 2019 and 2021.

However, Dr Aichholzer notesThis is data from a single center, so we need to wait to see what other centers say.

She continued, The results indicate that patients who have repeatedly suffered from depression during their lives were less likely to be admitted to hospital during the pandemic. However, these patients are often so severely affected by depression that outpatient treatment alone is not sufficient to bring about a satisfactory improvement in symptoms.

The result is that patients lose their quality of life in the long term. The actual reason for this observation is unclear. Although our study was not designed to identify the reasons for those changes, we however suspect that clinically depressed patients in particular withdraw more often from society/their friends/their family and that this behavior was more common during the times of the lock-down and the strict hygiene guidelines.

Moreover, we suspect, that clinically depressed patients avoided the hospital, because they were afraid of being infected with COVID-19 on the ward.

The data from our hospital in Frankfurt indicates that patients with clinical depression seem to have withdrawn themselves, rather than seeking adequate mental health help. To be prepared for the winter with potentially increasing COVID numbers, we have to provide easily accessible help and raise awareness for this topic.

Clinical depression, also known as Major Depressive Disorder (MDD) is a serious mental illness, affecting more than 6% of Europeans at any one time. The majority of sufferers can be treated with pharmaceuticals and/or counseling, although a minority of patients dont respond to treatment.

Commenting, Professor Brenda Penninx, Professor of psychiatric epidemiology at the Department of Psychiatry, University Medical Centre, Amsterdam, said:

The figures found by the Frankfurt team confirm a familiar pattern. We have recently found that quite a few countries are beginning to report a decreased pattern of mental health care use during the first pandemic years.

It is extremely important that in the next few years we follow whether postponed treatments may result in increased mental health problems.

This also illustrates that mental health care deserves adequate clinical attention during future pandemics.

This is an independent comment, Professor Penninx was not involved in this research.

Author: Tom ParkhillSource: European College of NeuropsychopharmacologyContact: Tom Parkhill European College of NeuropsychopharmacologyImage: The image is in the public domain

Original Research: The findings will be presented at the 35thEuropean College of Neuropsychopharmacology

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Patients With Clinical Depression Stopped Seeking Treatment During the COVID Waves - Neuroscience News