Publisher Health

One in three young people say their mental health and wellbeing improved during COVID-19 lockdown measures, with potential contributing factors including feeling less lonely, avoiding bullying and getting more sleep and exercise, according to researchers at the universities of Cambridge and Oxford.
As the COVID-19 pandemic swept the world, many countries imposed strict lockdown measures, with workplaces and businesses closing and people forced to remain at home. Measures also included school closures, with exceptions for young people whose parents were classified as essential workers and those considered ‘vulnerable’, for example children under the care of social services and those in families or social situations deemed by schools to be of concern.
Several studies have reported that the lockdown had a negative impact on the mental health and wellbeing of young people, but this effect has not been uniformly reported, with a number of studies suggesting that some young people may have benefited from lockdown.
Emma Soneson, a PhD student and Gates Scholar at the Department of Psychiatry, University of Cambridge, said: “The common narrative that the pandemic has had overwhelmingly negative effects on the lives of children and young people might not tell the full story. In fact, it seems as though a sizeable number of children and young people may have experienced what they felt was improved wellbeing during the first national lockdown of 2020.
“After hearing from patients in our clinical practice and informally from several parents and young people that they thought the lockdown was beneficial for their or their child’s mental health, we decided to look at this trend.”
Ms Soneson and colleagues explored this issue using the OxWell Student Survey, a large, school-based survey of students aged eight to 18 years living in England. More than 17,000 students took part in the June/July 2020 survey, during the tail end of the first national lockdown, answering questions about their experiences of the pandemic, school, home life, and relationships, among others. The results of their research have been published in European Child and Adolescent Psychiatry.

Focusing on what’s important — this is one of the main tasks of our brain. After all, countless amounts of information are constantly flooding our senses. But how do we manage to separate the important from the unimportant? It has long been known that oscillatory neural activity is a key factor for this attentional selection in the mammalian brain. Scientists from the German Primate Center in Göttingen and the University of Melbourne have now investigated how this works. They found that coupling lower frequencies of oscillations with higher ones allows fine-tuning the brain and is thus the basis for higher cognitive functions, such as selective attention (Trends in Neurosciences).
Contrary to our intuition, the precision with which we perceive the real world is not stable in time, rather it rhythmically fluctuates between high precision and low precision states several times per second. These fluctuations follow rhythmic electrical activities in the brain. Electrical rhythms of the brain range across different frequencies, from 1 to 250 hertz. Using these different frequencies the brain regulates how relevant information is transmitted between different brain regions. A group of neuroscientists from the German Primate Centre, Goettingen, Germany and the University of Melbourne, Australia has critically reviewed the evidence on this subject and shows how these frequencies may determine fundamental perceptual processes in the brain.
Cross-frequency coupling enables selective attention
One basic phenomenon observed throughout brain areas is that slower rhythms (approx. 4 to 8 hertz) modulate the strength of a faster rhythm (approx. 40 to 80 hertz). This is known as cross-frequency coupling. The pair of frequencies coupled to each other varies, based upon the cortical area and its function for behavior. In some instances, attention may cause nerve cells to become de-synchronized, allowing them to carry different information, like when one string instrument plays a different melody from the rest of the orchestra. In others, attention may lead to the activation of large numbers of neurons to maximize their impact. “These two different functions may be organized in the brain through cross frequency coupling,” says Moein Esghaei, one of the authors.
Distinguishing between different types of information
The simultaneous existence of different frequency bands in the brain also helps tagging different modalities of information arriving at the same brain region. For example colour and direction of a hang glider flying in the sky. “Our brain routes information about color and motion through different frequencies to higher order brain areas, just like telecommunication systems transmitting different types of information to the same receiver,” says Moein Esghaei.
Understanding neurological diseases
“The rhythmic activity of neuronal networks plays a critical role for visual perception in humans and other primates,” summarizes Stefan Treue, head of the Cognitive Neuroscience Laboratory at the German Primate Center as a co-author. “Understanding how exactly these activity patterns interact and are controlled, not only helps us to better understand the neural basis of perception, but also may help to elucidate some of the perceptual deficits in neurological conditions, such as dyslexia, ADHD, and schizophrenia.”
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Autism spectrum disorder (ASD) is associated with an increased focus on one’s internal experiences along with a reduction in responsiveness to external social surroundings. Now, a new study investigates the dynamics of brain connectivity between brain networks associated with internal experiences, external attention, and switching between internal versus external states. The study appears in Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, published by Elsevier.
The researchers used functional magnetic resonance imaging (fMRI) data from the Autism Brain Imaging Data Exchange (ABIDE) to compare 325 individuals with ASD with 356 people in a typically developing control group. They measured connectivity dynamics between three key brain networks: the default-mode network (DMN), the frontoparietal network (FPN), and the salience network across time.
“The role of each of these intrinsic brain networks has been investigated individually in people with ASD,” said Tae-Ho Lee, PhD, co-senior investigator at Virginia Tech, Blacksburg, VA, USA, “but our study is the first to examine how these three networks interacted dynamically at the large-scale brain-systems level, rather than focusing on a single network or static connection.”
The authors’ analysis determined that the salience network excessively activates the DMN — which is associated with mind-wandering and introspective thoughts — while inhibiting the FPN over time in those with ASD. On the contrary, in the typically developing group, the salience network deactivates the DMN and activates the FPN, which directs attention to the external surroundings spontaneously and momentarily, and leads them to regularly monitor (and be more responsive to) possible environmental changes.
“Our study provides a potential mechanistic explanation of why ASD is associated with more internally-focused cognition, including mind-wandering and prospection, and less of a focus on external environmental cues,” added co-senior author Hyungwook Yim, PhD, Hanyang University, Seoul, Republic of Korea.
The work might provide a better understanding of the interplay between brain networks in other situations, as well. “For example, older adults are more likely to fail to ignore unnecessary information from their surroundings,” said Dr. Lee. “According to previous studies, the salience network in older adults excessively activates the FPN while inhibiting the DMN — just the opposite of ASD interactions. Future research might find that children with ADHD have a pattern of connectivity dynamics that is opposite to that of those with ASD,” he speculated.
Cameron Carter, MD, Editor of Biological Psychiatry: Cognitive Neuroscience and Neuroimaging, said of the work, “This important study shows how new approaches to analyzing the dynamic patterns of interactions between brain systems over time can help us understand the neural basis of disabling symptoms such as increased lapses of attention in autism, and identify important new targets for invention to improve cognitive functioning in children and adults who are on the autism spectrum.”
“Our study provides a mechanistic explanation of why ASD individuals are less attentive to their surroundings and show more internally focused cognition such as mind-wandering and prospection. This new knowledge could be potentially useful for improving diagnosing ASD, or aid in informing therapeutic strategies for improving the wellbeing of those with ASD,” said Dr. Lee.
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New research indicates that for some individuals — even those who have steered clear of becoming infected with SARS-CoV-2 — societal and lifestyle disruptions during the COVID-19 pandemic may have triggered inflammation in the brain that can affect mental health. The study, which was conducted by a team led by investigators at Massachusetts General Hospital (MGH), is published in Brain, Behavior, and Immunity.
Beyond causing a staggering number of infections and deaths, the COVID-19 pandemic has led to significant social and economic disruptions that have impacted the lives of a large swath of the world’s population in multiple ways. Also, since the start of the pandemic, the severity and prevalence of symptoms of psychological distress, fatigue, brain fog, and other conditions have increased considerably in the United States, including among people not infected with SARS-CoV-2.
To obtain a better understanding of the effects of the pandemic on brain and mental health, researchers analyzed brain imaging data, conducted behavioral tests, and collected blood samples from multiple uninfected volunteers — 57 before and 15 after lockdown/stay-at-home measures were implemented to limit the pandemic’s spread.
After lockdowns, the study participants demonstrated elevated brain levels of two markers of neuroinflammation — translocator protein (measured using positron emission tomography) and myoinositol (measured using magnetic resonance spectroscopy) — compared with pre-lockdown participants. Blood levels of two inflammatory markers — interleukin-16 and monocyte chemoattractant protein-1 — were also elevated in post-lockdown participants, although to a lesser extent.
Participants who reported a higher burden of symptoms related to mood and mental and physical fatigue showed higher levels of translocator protein in certain brain regions, compared with those reporting little or no symptoms. Also, higher post-lockdown translocator protein levels correlated with the expression of several genes involved in immune functions.
“While COVID-19 research has seen an explosion in the literature, the impact of pandemic-related societal and lifestyle disruptions on brain health among the uninfected has remained under-explored,” says lead author Ludovica Brusaferri, PhD, a postdoctoral research fellow at MGH and Harvard Medical School. “Our study demonstrates an example of how the pandemic has impacted human health beyond the effects directly caused by the virus itself.”
Senior author Marco L. Loggia, PhD, co-director of the Center for Integrative Pain NeuroImaging at MGH and Harvard Medical School notes that acknowledging a role of neuroinflammation in the symptoms experienced by many during the pandemic might point to possible strategies to reduce them. “For instance, behavioral or pharmacological interventions that are thought to reduce inflammation — such as exercise and certain medications — might turn out to be helpful as a means of reducing these vexing symptoms.”
Loggia adds that the findings also provide further support to the notion that stressful events might be accompanied by brain inflammation. “This could have important implication for developing interventions for a broad number of stress-related disorders,” he says.
Study co-authors include Zeynab Alshelh, Daniel Martins, Minhae Kim, Akila Weerasekera, Hope Housman, Erin J. Morrissey, Paulina C. Knight, Kelly A. Castro-Blanco, Daniel S. Albrecht, Chieh-En Tseng, Nicole R. Zürcher, Eva-Maria Ratai, Oluwaseun Akeju, Meena M. Makary, Ciprian Catana, Nathaniel D. Mercaldo, Nouchine Hadjikhani, Mattia Veronese, Federico Turkheimer, Bruce R. Rosen, and Jacob M. Hooker.
The study was supported by the National Institutes of Health and The Landreth Family Foundation.

Scientists think they may have uncovered a whole new approach to fighting antibiotic-resistant bacteria, which, if successful, would help address a health crisis responsible for more deaths every year than either AIDS or malaria.
A team of researchers led by Despoina Mavridou of The University of Texas at Austin found a new way to impair antibiotic resistance in bacteria that cause human disease, including E. coli, K. pneumoniae and P. aeruginosa, which are responsible for the majority of harm caused by resistant infections. The team made the bacteria vulnerable again to antibiotics by inhibiting a particular protein that drives the formation of resistance capabilities within the bacteria.
“It’s a completely new way of thinking about targeting resistance,” said Mavridou, an assistant professor of molecular biosciences.
Bacteria are becoming increasingly resistant to existing antibiotics, and researchers have struggled to identify new bacteria-fighting drugs, leaving the world vulnerable to deadly superbugs. A January study in The Lancet by another team found antimicrobial resistance to be the direct cause of at least 1.27 million deaths globally in 2019, making antibiotic resistance one of the world’s leading causes of death.
Antibiotic resistant bacteria have a host of different proteins in their arsenals that neutralize antibiotics. To function properly, these resistance proteins must be folded into the right shapes. The researchers discovered that yet another protein, called DsbA, helps fold resistance proteins into those shapes.
For their proof-of-concept study, which was recently published in the journal eLife, Mavridou and her fellow scientists inhibited DsbA using chemicals that cannot be used directly in human patients. The team plans now to work on developing inhibitors that can achieve the same outcome and be safely used in humans.

We’re always hearing that we should eat more fiber. It’s known to be vitally important for a healthy digestive system and also has cardiovascular benefits like reduced cholesterol. Now, evidence is emerging that fiber is also important for a healthy brain. In a new study published this month in the journal Nutritional Neuroscience, researchers in Japan have shown that a high-fiber diet is associated with a reduced risk of developing dementia.
“Dementia is a devastating disease that usually requires long-term care,” says lead author of the study Professor Kazumasa Yamagishi. “We were interested in some recent research which suggested that dietary fiber may play a preventative role. We investigated this using data that were collected from thousands of adults in Japan for a large study that started in the 1980s.”
Participants completed surveys that assessed their dietary intake between 1985 and 1999. They were generally healthy and aged between 40 and 64 years. They were then followed up from 1999 until 2020, and it was noted whether they developed dementia that required care.
The researchers split the data, from a total of 3739 adults, into four groups according to the amount of fiber in their diets. They found that the groups who ate higher levels of fiber had a lower risk of developing dementia.
The team also examined whether there were differences for the two main types of fiber: soluble and insoluble fibers. Soluble fibers, found in foods such as oats and legumes, are important for the beneficial bacteria that live in the gut as well as providing other health benefits. Insoluble fibers, found in whole grains, vegetables, and some other foods, are known to be important for bowel health. The researchers found that the link between fiber intake and dementia was more pronounced for soluble fibers.
The team has some ideas as to what might underlie the link between dietary fiber and the risk of dementia.
“The mechanisms are currently unknown but might involve the interactions that take place between the gut and the brain,” says Professor Yamagishi. “One possibility is that soluble fiber regulates the composition of gut bacteria. This composition may affect neuroinflammation, which plays a role in the onset of dementia. It’s also possible that dietary fiber may reduce other risk factors for dementia, such as body weight, blood pressure, lipids, and glucose levels. The work is still at an early stage, and it’s important to confirm the association in other populations.”
In many countries today, such as the US and Australia, many people consume less fiber than is recommended by nutritionists. By encouraging healthy eating habits with high dietary fiber, it might be possible to reduce the incidence of dementia.
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Little has been known to date about how the immune system’s natural killer (NK) cells detect which cells have been infected with SARS-CoV-2. An international team of scientists led by researchers from Karolinska Institutet in Sweden now shows that NK cells respond to a certain peptide on the surface of infected cells. The study, which is published in Cell Reports, is an important piece of the puzzle in our understanding of how the immune system reacts to COVID-19.
NK cells are white blood cells that are part of the innate immune system. Unlike cells in the adaptive immune defence, they are able to recognise and kill cancer cells and virus-infected cells immediately without having encountered them before. This ability is controlled by a balance between the NK cells’ activating and inhibiting receptors, which can react to different molecules on the surface of other cells.
The virus is revealed by a peptide
A new study shows why certain NK cells are activated when encountering a cell infected with SARS-CoV-2. The infected cells contain a peptide from the virus that triggers a reaction in NK cells that carry a particular receptor, NKG2A, able to detect the peptide.
“Our study shows that SARS-CoV-2 contains a peptide that is displayed by molecules on the cell surface,” says Quirin Hammer, researcher at the Center for Infectious Medicine (CIM), Karolinska Institutet. “The activation of NK cells is a complex reaction, and here the peptide blocks the inhibition of the NK cells, which allows them to be activated. This new knowledge is an important piece of the puzzle in our understanding of how our immune system reacts in the presence of this viral infection.”
The study was a major collaboration between Karolinska Institutet, Karolinska University Hospital and research laboratories and universities in Italy, Germany, Norway and the USA. The first phase was to test their hypothesis using computer simulations that were then confirmed in the laboratory. The decisive phase was the infection of human lung cells with SARS-CoV-2 in a controlled environment, whereupon the researchers could show that NK cells with the receptor in question are activated to a greater degree than the NK cells without it.
Monitoring new virus variants
“These findings are important to our understanding of how immune cells recognise cells infected with SARS-CoV-2,” says Dr Hammer. “This may become significant when monitoring new virus variants with the aim to determine how well the immune system responds to them.”
The study is now being followed up with the help of a biobank at Karolinska University Hospital and Karolinska Institutet containing blood samples from over 300 people treated for COVID-19 during the first wave of the pandemic.
“We’ll be examining if the composition of NK cells a person has contributes to how severe their symptoms are when infected with SARS-CoV-2,” he continues.
The study was financed by the EU, Deutsche Forschungsgemeinschaft (DFG), the Karolinska Institutet Foundation for Virus Research, the Petrus and Augusta Hedlund Foundation, the Clas Groschinsky Memorial Foundation, the Lars Hierta Memorial Foundation, the Tornspiran Foundation, the Swedish Cancer Society, the Norwegian Research Council, the Swedish Research Council, the Knut and Alice Wallenberg Foundation and Nordstjernan AB. Co-author Hans-Gustaf Ljunggren is a member of the board of XNK Therapeutics AB and Vycellix Inc. Karl-Johan Malmberg is scientific advisor for and has a research grant from Fate Therapeutics, and is a member of Vycellix Inc’s scientific advisory board.
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Researchers at Indiana University School of Medicine Department of Microbiology and Immunology have made an important new discovery about how a particular molecule could improve lung function for people with asthma and food allergies.
“Millions of children and adults in the United States have asthma, which results from allergen-induced inflammation in the lungs,” said Mark Kaplan, PhD, chair of the Department of Microbiology and Immunology and the senior author of the study. “The ability of cells to communicate with each other is critical in the development of inflammation and occurs through the release of molecules called cytokines.
One of these cytokines, interleukin-9 (IL-9), has been found in patients with asthma and food allergy, but how IL-9 promotes inflammation has been unclear. In the study published recently in Science Immunology, researchers define one of the cell types, called the lung macrophage, as a major target of IL-9.
They found allergic lung inflammation decreased when the receptor for IL-9 was missing and the macrophage is critical for IL-9 function in the allergic lung. They also defined downstream effectors of IL-9 in the macrophage, identifying enzymes and additional cytokines that are required for the development of allergic inflammation, and found a correlation between IL-9 and the downstream effectors with the diagnosis of asthma in patients.
“This work is a significant advancement in our study of allergic lung inflammation,” Kaplan said. “We can use this information to further study the macrophage populations and determine how it could be a potential therapeutic approach for treatment of asthma and other types of lung inflammation.”
The study was led by Yongyao Fu, PhD, MS, a former graduate student and now an adjunct assistant scientist in microbiology and immunology at IU School of Medicine and a scientist at Genentech in California. Read the full publication in Science Immunology.
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Materials provided by Indiana University School of Medicine. Original written by Christina Griffiths. Note: Content may be edited for style and length.

New research from Penn State found that children with positive, early interactions with their care givers — characterized by warmth, responsiveness, and a sitmulating home environment — were at reduced risk of childhood obesity.
“A lot of the discussion around childhood obesity and other health risks focuses on identifying and studying the exposure to risk,” said Brandi Rollins, assistant research professor of biobehavioral health. “We took a strength-based approach in our analysis. We found that a supportive family and environment early in a child’s life may outweigh some of the cumulative risk factors that children can face.”
The study, “Family Psychosocial Assets, Child Behavioral Regulation, and Obesity,” recently appeared in the journal Pediatrics. In the article, Rollins and Lori Francis, associate professor of biobehavioral health, analyzed data from over 1,000 mother-child pairs and found that children’s early exposures to family psychosocial assets — including a quality home environment, emotional warmth from the mother, and a child’s ability to self-regulate — reduced the risk of developing childhood obesity.
Encouragingly, these factors were protective even when children faced familial risks for obesity, including poverty, maternal depression, or residence in a single-parent home.
“Research on parenting has shown that these types of family assets influence children’s behavior, academic success, career, and — not surprisingly — health,” Rollins said. “It is significant that these factors also protect against childhood obesity because the family assets we studied are not food or diet-specific at all. It is heartening to know that, by providing a loving, safe environment, we can reduce the risk that children will develop obesity.”
Severe obesity
Children are deemed to have obesity when their body mass indices (BMIs) are greater than 95% of other children their age and gender. There is a great deal of variance, however, in the BMIs of children who exceed the obesity threshold. Children whose BMI is 20% higher than the obesity threshold are considered to have severe obesity.

Gene regulation is an important process that controls the activity of genes in cells.Incorrect gene regulation can contribute to the onset of many diseases, including cancer.
The DNA of the human genome contains genes that code for proteins, which in turn give muscle cells their strength and brain cells their ability to process information. DNA also contains gene regulatory elements that determine when and where genes are expressed — so that muscle genes are expressed in muscles and brain genes in the brain.
However, the regulatory code that determines gene activity remains poorly understood. Even though the human genome comprises almost three billion base pairs, it is too short for learning the gene regulatory code from the genomic sequence alone. The problem is similar to that faced by a linguist who tries to understand a forgotten language on the basis of a few short texts.
A research group of Professor Jussi Taipale that belongs to the Academy of Finland’s Centre of Excellence in Tumour Genetics Research, has now found a way around this problem to solve the regulatory code.
The new study was recently published in the Nature Genetics journal.
“We measured the gene regulatory activity from a collection of DNA sequences that together are 100 times larger than the entire human genome,” says Academy of Finland Research Fellow Biswajyoti Sahu, the first author of the study.