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<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News</span></td>
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<td><a href="https://www.psypost.org/dysfunction-within-the-sensory-processing-cortex-of-the-brain-is-associated-with-insomnia-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Dysfunction within the sensory processing cortex of the brain is associated with insomnia, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 9th 2025, 10:00</div>
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<p><p>A neuroimaging study comparing individuals with insomnia to healthy adults found disrupted connectivity in the sensory processing cortex and subcortical nuclei of the brain among those with insomnia. This dysfunction likely contributes to the imbalance in their sleep-wake cycles. The findings were published in <a href="https://doi.org/10.1007/s11682-024-00958-8"><em>Brain Imaging and Behavior</em></a>.</p>
<p>Insomnia is a common sleep disorder that makes it difficult to fall asleep, stay asleep, or return to sleep after waking up too early. It can be short-term (acute) or long-term (chronic), lasting from a few days to several months or more. People with insomnia often feel tired during the day, which can negatively affect concentration, mood, and performance.</p>
<p>Many factors can contribute to insomnia, including stress, anxiety, depression, poor sleep habits, and medical conditions. Lifestyle factors such as caffeine intake, screen use before bed, and irregular sleep schedules can also play a role. Treatment typically involves improving sleep hygiene, undergoing cognitive behavioral therapy, or using medication in some cases. Although insomnia can occur at any age, it is more common among older adults and women.</p>
<p>Lead author Hui Wang and colleagues aimed to explore how insomnia develops and identify neural changes that may underlie the disorder using neuroimaging techniques. To do this, they examined a measure called dynamic degree centrality. This metric captures how often and how strongly a specific brain region connects with other regions over time. Unlike static measures, dynamic degree centrality reflects moment-to-moment changes in a region’s connectivity, indicating its shifting importance within brain networks during different mental states or tasks.</p>
<p>The study involved 29 individuals diagnosed with insomnia and 28 healthy control participants. The control group was matched to the insomnia group by gender, age, and education level. All participants underwent magnetic resonance imaging of the brain. The researchers then calculated both static and dynamic degree centrality values from the imaging data. Participants also completed assessments of sleep quality using the Pittsburgh Sleep Quality Index and levels of depression using the Hamilton Depression Scale.</p>
<p>The results revealed that individuals with insomnia had higher static degree centrality in brain areas associated with sensory processing, such as the occipital gyrus, inferior temporal gyrus, and supramarginal gyrus. Conversely, they showed lower static degree centrality in regions including the parahippocampal gyrus, amygdala, insula, and thalamus—areas involved in emotional processing, memory, and sensory integration.</p>
<p>The researchers also observed group differences in dynamic degree centrality in several regions, including the parahippocampal gyrus, anterior cingulate cortex, medial superior frontal gyrus, inferior parietal gyrus, and precuneus. Notably, higher dynamic degree centrality in the inferior parietal gyrus was associated with better sleep quality. On the other hand, higher static degree centrality in the inferior temporal gyrus correlated with more severe depressive symptoms.</p>
<p>“These findings suggest that dysfunction in centrality within the sensory processing cortex and subcortical nuclei may be associated with the sleep–wake imbalance in individuals with insomnia disorder, contributing to our understanding of hyperarousal mechanisms in insomnia,” the study authors wrote.</p>
<p>The study adds to the scientific knowledge about neural correlates of sleep disorders. However, it should be noted that the design of the study does not allow any causal inferences to be derived from the results. Additionally, the study was conducted on a very small group of participants. Results on larger groups of participants might not be identical.</p>
<p>The paper, “<a href="https://doi.org/10.1007/s11682-024-00958-8">Abnormal sensory processing cortex in insomnia disorder: a degree centrality study,</a>” was authored by Hui Wang, Haining Li, Ziyi Liu, Chiyin Li, Zhaoyao Luo, Wei Chen, Meiling Shang, Huiping Liu, Fatemeh Naderi Nejad, Yuanping Zhou, Ming Zhang, and Yingxiang Sun.</p></p>
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<td><a href="https://www.psypost.org/prenatal-exposure-to-forever-chemicals-linked-to-autistic-traits-in-children-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Prenatal exposure to “forever chemicals” linked to autistic traits in children, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 9th 2025, 08:00</div>
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<p><p>New research suggests that exposure to certain synthetic chemicals during early pregnancy may be linked to a higher likelihood of autistic traits in children. The study found that children whose mothers had higher levels of a chemical called perfluorooctanoic acid (PFOA) in their blood during early pregnancy were more likely to show signs of social and communication difficulties by age four. Additionally, another chemical, perfluorohexane sulfonate (PFHxS), was more strongly associated with autistic traits in children who had a higher inherited risk for autism.</p>
<p>Per- and polyfluoroalkyl substances, or PFAS, are a large group of human-made chemicals used in a wide variety of consumer and industrial products, including non-stick cookware, stain-resistant fabrics, firefighting foams, and food packaging. Because they do not easily break down in the environment or in the human body, PFAS are often referred to as “forever chemicals.” These compounds can persist in the body for years and have been linked to various health risks. Due to their persistence and potential harm, some PFAS have been banned or restricted in many countries. Still, production and exposure remain widespread, especially in developing countries such as China.</p>
<p>In the United States, PFAS have become a growing focus of environmental and public health regulation. In April 2024, the Environmental Protection Agency under the Biden administration finalized the first legally enforceable national limits for six PFAS compounds in drinking water, including strict limits of 4 parts per trillion for PFOA. However, in May 2025, the Trump administration rolled back these standards by delaying enforcement for PFOA and repealing limits for four other PFAS.</p>
<p>Previous research has raised concerns that exposure to PFAS during pregnancy could interfere with a child’s brain development. Animal studies and limited human research have shown that PFAS may alter hormone levels, disrupt neurotransmitters, and interfere with normal signaling in the brain. Yet the human evidence linking PFAS exposure to autism-related traits has been inconsistent. Some studies suggest a connection, while others do not. Many of these earlier studies were conducted in populations where PFAS exposure was relatively low due to stricter regulations.</p>
<p>The new study, published in the <em><a href="https://doi.org/10.1016/j.jhazmat.2024.135857" target="_blank" rel="noopener">Journal of Hazardous Materials</a></em>, sought to fill some of the gaps in current understanding by analyzing a large sample of mother-child pairs in China, where PFAS levels are typically higher. The researchers focused on whether prenatal exposure to these chemicals might increase the likelihood of autism-related behaviors in children, and whether a child’s genetic makeup influenced the effect of this exposure.</p>
<p>The study used data from 1,610 mother-child pairs in the Shanghai Birth Cohort, a long-term study that follows children from early pregnancy through childhood. Blood samples were collected from mothers during the first trimester of pregnancy, and concentrations of ten different PFAS were measured. These included PFOA, PFHxS, and several other commonly detected compounds. When the children reached age four, their social and communication skills were assessed using a parent-completed questionnaire called the Social Responsiveness Scale (short form), which measures behaviors often associated with autism.</p>
<p>The researchers also calculated a polygenic risk score for autism, based on the presence of specific genetic variants known to be linked to autism. This score allowed the researchers to assess how a child’s genetic risk for autism might interact with environmental exposures like PFAS.</p>
<p>After adjusting for other factors that could influence child development—such as maternal age, education level, and body mass index—the researchers found that higher levels of PFOA during early pregnancy were associated with a three-fold increase in the odds of a child scoring in the range associated with autistic traits. However, among mothers who reported taking folic acid supplements before pregnancy, the association between PFOA and autistic traits appeared to be weaker.</p>
<p>In addition, the study found a potential interaction between PFHxS and genetic risk. Children with both higher prenatal exposure to PFHxS and a higher polygenic risk score were more likely to show signs of autistic traits. This interaction suggests that children who are already genetically more susceptible to autism may be more vulnerable to environmental exposures like PFAS.</p>
<p>When the researchers analyzed the effects of the entire PFAS mixture as a group, they did not find a clear association with autistic traits. This suggests that the risks may be driven by specific compounds like PFOA and PFHxS, rather than PFAS exposure in general.</p>
<p>The study also included a number of additional analyses to test the reliability of the results. These included separating the sample by child sex and by whether mothers took folic acid supplements. Interestingly, the researchers found that some PFAS appeared to have different associations with autistic traits in boys versus girls. For example, one chemical, PFDoA, was associated with fewer autistic traits in boys but not in girls. Another compound, PFBS, was linked to increased risk in boys but reduced risk in girls. These findings point to possible sex-specific effects that need more investigation.</p>
<p>The authors note that the study has several strengths, including a relatively large sample size, prospective design, and the ability to account for both genetic and environmental factors. However, they also caution that there are important limitations.</p>
<p>One limitation is that the measure of autistic traits relied on parent reports, which can be influenced by subjective perceptions. Also, only 24 children in the sample had scores in the range that suggested possible autism-related traits, which may limit the ability to detect small effects or to generalize the findings. In addition, the genetic risk score was based on data from mostly European populations, which may not perfectly reflect the genetic architecture of autism in a Chinese population. Differences in how genetic variants are inherited across populations could affect how well the polygenic risk score captures true genetic susceptibility.</p>
<p>Another limitation is that the PFAS levels in this study were relatively high compared to studies in Western countries. For example, median PFOA levels in this Shanghai sample were roughly three times higher than those reported in the United States. This means that the findings may not apply to populations with lower exposure levels. Also, the researchers could not rule out the influence of other environmental chemicals, such as heavy metals or plasticizers, although these are not strongly correlated with PFAS.</p>
<p>The study also raises new questions about the potential protective role of folic acid supplementation. While the researchers observed that pre-pregnancy supplementation appeared to lessen the association between PFOA and autistic traits, the biological reasons for this are not yet understood. Folic acid plays an important role in brain development, and previous studies have linked adequate folate intake to reduced risk of developmental disorders. It is possible that folic acid helps counteract some of the negative effects of PFAS on fetal brain development, but more research is needed to clarify the mechanisms involved.</p>
<p>Overall, the findings contribute to a growing body of evidence suggesting that early-life exposure to environmental chemicals like PFAS may have lasting effects on child development. The study highlights the importance of considering both environmental and genetic factors in understanding neurodevelopmental outcomes. While the results do not prove that PFAS cause autism or autistic traits, they suggest that certain exposures during pregnancy may increase the risk, particularly in children who are genetically more susceptible.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.jhazmat.2024.135857" target="_blank" rel="noopener">Prenatal exposure to per- and polyfluoroalkyl substances, genetic factors, and autistic traits: Evidence from the Shanghai birth cohort</a>,” was authored by Yun Huang, Weiran Chen, Yuexin Gan, Xin Liu, Ying Tian, Jun Zhang, and Fei Li.</p></p>
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<td><a href="https://www.psypost.org/ketamine-repairs-reward-circuitry-to-reverse-stress-induced-anhedonia/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Ketamine repairs reward circuitry to reverse stress-induced anhedonia</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 9th 2025, 06:00</div>
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<p><p>A single low dose of the anesthetic ketamine restored the ability to enjoy sweet treats and social contact in mice that had been made apathetic by long-term stress, according to new research published in <em><a href="https://doi.org/10.1016/j.neuron.2025.02.021" target="_blank" rel="noopener">Neuron</a></em>. The same injection also repaired weakened connections onto a specific group of reward-related brain cells. When those repaired connections were blocked, the animals’ recovery disappeared—suggesting the synaptic fix is a key part of ketamine’s sustained antidepressant effects.</p>
<p>Originally developed as an anesthetic in the 1960s, ketamine has more recently drawn attention for its fast-acting antidepressant properties. Over the past two decades, clinicians have found that sub-anesthetic doses can lift mood within hours in many people with major depression who do not respond to conventional medications. That rapid action stands in contrast to commonly prescribed drugs like selective serotonin reuptake inhibitors, which often take weeks to alleviate symptoms.</p>
<p>One symptom of depression that appears to respond especially well to ketamine is anhedonia—the loss of pleasure in normally rewarding experiences. Yet it remains unclear which brain circuits are responsible for the drug’s lasting effects on mood and motivation. The new study set out to identify those changes down to the level of individual synapses.</p>
<p>“Depression is a leading cause of morbidity and mortality worldwide, and it is projected to become the second leading cause of disability by 2030,” said study author <a href="https://www.pignatellilab.org/" target="_blank" rel="noopener">Marco Pignatelli</a>, an assistant professor of psychiatry at <a href="https://psychiatry.wustl.edu/people/marco-pignatelli/" target="_blank" rel="noopener">Washington University School of Medicine in St. Louis</a>.</p>
<p>“Despite the urgent need to address depression as a public health priority, current pharmacotherapies require prolonged administration—weeks, if not months—for clinical improvement, and are often associated with high non-response rates. In contrast, a single sub-anesthetic dose of ketamine induces a rapid antidepressant effect in about 70% of treatment-resistant patients.”</p>
<p>“Importantly, this improvement often occurs within the context of anhedonia,” he added. “Conventional antidepressants do poorly in relieving anhedonia, which is one of the two core symptoms used to diagnose major depression. That makes ketamine a promising and unique pharmacological option. However, without understanding the circuits and synapses that support this effect, our ability to design safer, more targeted medications is limited.”</p>
<p>To model anhedonia in mice, the researchers implanted slow-release corticosterone pellets under the animals’ skin to mimic chronic stress. Over three weeks, the hormone reduced the animals’ interest in sweetened water, decreased time spent with other mice, and lowered their willingness to work for rewards in a progressive ratio task where nose-pokes earned sugar pellets.</p>
<p>Twenty-four hours before each test, half the stressed mice received a single injection of ketamine at 10 milligrams per kilogram—a dose well below what’s used for anesthesia. The rest received saline, as did a group of unstressed control mice. Ketamine restored reward-seeking behavior across all tasks, while saline had no effect. The drug did not increase overall activity levels, ruling out general stimulation as an explanation.</p>
<p>To uncover what had changed in the brain, the researchers prepared thin slices from another group of similarly treated mice and recorded electrical activity in the nucleus accumbens, a key hub for processing reward. They focused on medium spiny neurons that express dopamine receptor type 1, a subtype linked to motivation and approach behavior.</p>
<p>Chronic stress reduced the strength and frequency of excitatory inputs to these neurons, but ketamine reversed this effect within a day—possibly as soon as one hour after injection. These changes were not observed in neighboring neurons that express dopamine receptor type 2, highlighting the cell-type specificity of the effect.</p>
<p>To test whether these restored synapses were necessary for ketamine’s behavioral benefits, the researchers used a molecular technique to block them. They introduced a HaloTag protein into dopamine receptor type 1 neurons, allowing them to tether a glutamate receptor blocker to just those cells. Delivering the blocker into the nucleus accumbens 24 hours after ketamine erased the previously observed improvements in sugar preference, sociability, and motivation. Blocking the same receptors on dopamine receptor type 2 neurons had no effect, pinpointing the importance of the type 1 cells.</p>
<p>The team then asked whether strengthening the same synapses—without ketamine—would be enough to reverse anhedonia. They inserted a light-sensitive version of Rac1, a protein that clusters glutamate receptors, into the dopamine receptor type 1 neurons. Mice exposed to blue light showed restored motivation and sociability, while exposure to red light had no effect. The findings suggest that targeted synaptic enhancement alone can substitute for ketamine in relieving anhedonia.</p>
<p>To identify where the restored signals were coming from, the researchers injected a light-activated protein into several brain areas that send input to the nucleus accumbens. They found that chronic stress weakened glutamatergic connections from the medial prefrontal cortex and ventral hippocampus—regions involved in decision-making and memory. Ketamine restored both pathways but did not affect inputs from the amygdala, thalamus, or ventral tegmental area.</p>
<p>Further analysis revealed distinct mechanisms for each pathway. The prefrontal input gained stronger unitary synaptic responses, while the hippocampal input showed both stronger responses and increased release events. These changes indicate different modes of adaptation at the two inputs.</p>
<p>To confirm that both inputs were required for ketamine’s effects, the team used a two-virus strategy to express a designer inhibitory receptor specifically in either the prefrontal or hippocampal projection to the nucleus accumbens. Administering a drug that silenced the targeted neurons before ketamine blocked the behavioral rescue.</p>
<p>Interestingly, the type of failure depended on which pathway was silenced. Turning off the ventral hippocampal input delayed the animals’ first approach to a social partner and the first attempt to obtain a reward. In contrast, silencing the prefrontal input did not affect initiation, but reduced overall engagement. These results suggest that hippocampal input helps trigger reward-seeking, while prefrontal input helps sustain it.</p>
<p>“We’ve uncovered a brain mechanism through which ketamine restores reward-related behavior after chronic stress in mice, and we believe these mechanisms are likely conserved across species,” Pignatelli said. “That makes this discovery relevant for clinical applications.”</p>
<p>But, as with all research, there are limitations. “It is always important to highlight that our mechanistic studies are taking place by using murine animal models,” Pignatelli noted. “In general, the findings of a study in mice may not directly translate to humans or other species, but they offer valuable insights into biological processes within that model.”</p>
<p>Future studies could use brain imaging to examine whether similar changes occur in patients who recover from anhedonia after ketamine treatment. Identifying specific synapses that support antidepressant effects may eventually allow researchers to design drugs that improve motivation without the dissociative side effects associated with ketamine.</p>
<p>“I hope that results from this body of work will have a sustained impact on the field by propelling the rational design of more targeted treatments, thereby facilitating more effective and safer therapies aiming at alleviating anhedonia,” Pignatelli said.</p>
<p>The study, “<a href="https://www.cell.com/neuron/fulltext/S0896-6273(25)00139-4" target="_blank" rel="noopener">Ketamine rescues anhedonia by cell-type- and input-specific adaptations in the nucleus accumbens</a>,” was authored by Federica Lucantonio, Jacob Roeglin, Shuwen Li, Jaden Lu, Aleesha Shi, Katherine Czerpaniak, Francesca R. Fiocchi, Leonardo Bontempi, Brenda C. Shields ,Carlos A. Zarate, Jr., Michael R. Tadross, and Marco Pignatelli.</p></p>
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<td><a href="https://www.psypost.org/neuroscientists-decode-how-people-juggle-multiple-items-in-working-memory/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Neuroscientists decode how people juggle multiple items in working memory</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 8th 2025, 18:00</div>
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<p><p>When we try to remember more than one thing at a time, our brains don’t treat each item equally. New research published in <em><a href="https://www.science.org/doi/10.1126/sciadv.adr8015" target="_blank" rel="noopener">Science Advances</a></em> shows that the brain dynamically adjusts how much effort it devotes to each item based on its importance. By tracking brain activity while people remembered two locations on a screen, scientists discovered that two brain regions—the visual cortex and the frontal cortex—work together to allocate more resources to items deemed more important. This results in sharper, more precise memory for high-priority items, while low-priority ones are remembered with less clarity.</p>
<p>The research team, led by Hsin-Hung Li at The Ohio State University, wanted to understand how the brain deals with the fact that working memory is limited. Working memory helps us temporarily store information we need for things like making decisions, solving problems, or navigating the world. But it can only hold a small amount of information at a time. Past studies have shown that people can improve their memory for important items by prioritizing them. But scientists did not know how the brain manages this internally or what parts of the brain make those decisions.</p>
<p>To answer this, the researchers developed a method to measure how the brain represents multiple items held in memory at once and how it adjusts those representations based on priority. They combined functional MRI brain scans with a sophisticated computational model that could decode what participants were remembering—and how precisely they were remembering it.</p>
<p>The experiment involved 11 participants who each took part in several scanning sessions. While lying in an MRI scanner, participants looked at a screen where two colored lines appeared briefly—each in a different half of the screen. Before the lines appeared, a cue indicated which side of the screen was more likely to be tested later, marking one of the items as high-priority and the other as low-priority. After the lines disappeared, participants had to wait 12 seconds while trying to remember their locations. Then, they were prompted to look with their eyes at the location of one of the items, using a quick eye movement known as a saccade.</p>
<p>In most trials, the high-priority item was the one tested, but in a smaller number of trials, the low-priority item was selected instead. Eye-tracking data allowed researchers to measure how accurate each memory was, depending on whether it was high or low in priority.</p>
<p>The researchers found that participants were consistently better at remembering the high-priority item. Their eye movements landed closer to the correct location, and they responded more quickly when recalling high-priority information. These results confirmed that people can adjust their memory performance based on what they think will matter most.</p>
<p>What made this study unique was its ability to decode brain activity related to each memory item—separately and in real time. Using a model rooted in a theory called probabilistic population coding, the team translated patterns of brain activity in the visual cortex into predictions about what the participant was remembering and how certain their brain was about it. They showed that high-priority items were encoded with more “gain,” meaning the brain devoted more neural resources to representing them. These representations were not only stronger but also more precise.</p>
<p>By analyzing data from both the visual and frontal areas of the brain, the researchers were able to go a step further. They found that activity in the frontal cortex predicted how much emphasis was placed on the high-priority item. The frontal cortex didn’t store the memory itself, but it seemed to decide which item deserved more attention. Once that decision was made, it influenced how the visual cortex represented each item. This suggests a kind of top-down control: the frontal cortex acts like a manager, telling the visual system how to distribute limited memory resources.</p>
<p>In trials where the high-priority item received more gain in the visual cortex, participants made fewer mistakes when recalling it. The researchers also showed that when the brain was less certain about an item—reflected by more “noisy” neural activity—participants took longer to respond and were more likely to make errors. This indicated a strong link between the brain’s internal sense of certainty and actual behavior.</p>
<p>The study also identified a specific part of the frontal cortex, the superior precentral sulcus, as playing a key role in prioritization. Activity in this region increased when participants were allocating more memory resources to the high-priority item. Its activity also predicted quicker response times, especially when participants felt more certain about the remembered location. In addition, the researchers found involvement from parts of the parietal cortex and a region in the temporal lobe called the posterior inferior temporal cortex—areas that are known to participate in attention and visual processing.</p>
<p>While the results help clarify how different brain regions coordinate to prioritize memories, the study had some limitations. The sample size was relatively small, with only 11 participants, which may limit how generalizable the findings are. The tasks were also highly controlled and may not reflect how working memory operates in everyday settings where people remember many types of information at once, not just spatial locations.</p>
<p>Another limitation is that although the researchers could estimate how much “gain” was assigned to each item, they could not directly measure how this translated into specific neural firing rates at the level of individual neurons. Future studies might combine brain imaging with methods that can capture more detailed neural activity to get a fuller picture of how memory prioritization works.</p>
<p>Even with these caveats, the study offers a new way to look at working memory. It suggests that rather than being a fixed bucket that can only hold a few items, working memory is a flexible system that can shift resources from one item to another depending on its relevance. The frontal cortex helps manage this process by signaling which memories deserve more attention, while the visual cortex adjusts how clearly those memories are encoded.</p>
<p>Lead author Hsin-Hung Li noted that this is one of the first studies to decode the brain’s memory for two different items on a single trial. He believes this technique could be useful for exploring many situations where people try to hold multiple thoughts in their minds at once. “There are so many situations in which people are trying to hold multiple thoughts in their minds and it is very useful to be able decode more than one,” he said.</p>
<p>The study, “<a href="https://doi.org/10.1126/sciadv.adr8015" target="_blank" rel="noopener">Neural mechanisms of resource allocation in working memory</a>,” Hsin- Hung Li, Thomas C. Sprague, Aspen H. Yoo, Wei Ji Ma, and Clayton E. Curtis.</p></p>
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<td><a href="https://www.psypost.org/inside-the-bored-brain-unlocking-the-power-of-the-default-mode-network/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Inside the bored brain: Unlocking the power of the default mode network</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 8th 2025, 16:00</div>
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<p><p>We have all experienced boredom – that feeling of waning interest or decreased mental stimulation. Eventually we lose focus, we disengage. Time seems to pass slowly, and we may even start to feel restless. Whether it be watching a movie that disappoints, a child complaining that “there’s nothing to do”, or an adult zoning out during a meeting – boredom is a universal experience.</p>
<p>Generally defined as <a href="https://journals.sagepub.com/doi/full/10.1177/1745691612456044?casa_token=KmYQgUf470MAAAAA%3A0fH85E_WhFC3HrTkNZi4cOQHWweGawqp8WGxIAljCNyysjBeWgpKsuJqB2eKXbD-5TCk3pfaetzj1qE">difficulty maintaining attention or interest</a> in a current activity, boredom is commonly viewed as a negative state that we should try to avoid or prevent ourselves from experiencing.</p>
<p>But what if there’s another way to view boredom, as a positive state? Could learning to embrace boredom be of benefit?</p>
<h2>The brain on boredom</h2>
<p>The brain network is a system of interconnected regions that work together to support different functions. We can liken it to a city where suburbs (brain regions) are connected by roads (neural pathways), all working together to allow information to travel efficiently.</p>
<p>When we experience boredom – say, while watching a movie – our brain engages specific networks. The <a href="https://www.researchgate.net/profile/Steve-Petersen-2/publication/224823470_The_Attention_System_of_the_Human_Brain_20_Years_After/links/0c960521e148321d3c000000/The-Attention-System-of-the-Human-Brain-20-Years-After.pdf">attention network</a> prioritises relevant stimuli while filtering out distractions and is active when we commence the movie.</p>
<p>However, as our attention wanes, activity in the attention network decreases, reflecting our diminished ability to maintain focus on the unengaging content. Likewise, decreased activity occurs in <a href="https://onlinelibrary.wiley.com/doi/full/10.1002/hbm.22285?casa_token=G8fV_ZsDtlgAAAAA%3Az5aQfr8kCKuGvu8mQ6jk3e5PpzxTevK0TTqY_BLcjg2ElN6coX0H5F-QMTSmU9C-jiBKsbbEHcY4AvDO">the frontoparietal or executive control network</a> due to the struggle to maintain engagement with the unengaging movie.</p>
<p>Simultaneously, the <a href="https://www.sciencedirect.com/science/article/pii/S0896627323003082">default mode network</a> activates, shifting our attention toward internal thoughts and self-reflection. This is a core function of the default mode network, referred to as introspection, and suggestive of a strategy for coping with boredom.</p>
<p>This complex interplay of networks involves several key brain regions “working together” during the state of boredom. The <a href="https://www.sciencedirect.com/science/article/pii/S0149763422002251">insula</a> is a key hub for sensory and emotional processing. This region shows increased activity when detecting internal body signals – such as thoughts of boredom – indicating the movie is no longer engaging. This is often referred to as “<a href="https://www.boredomsociety.com/jbs/index.php/journal/article/view/23/49">interoception</a>”.</p>
<p>The <a href="https://www.christofflab.ca/wp-content/uploads/2017/10/Raffaelli2016-boredom.pdf">amygdala</a> can be likened to an internal alarm system. It processes emotional information and plays a role in forming emotional memories. During boredom, this region processes associated negative emotions, and the <a href="https://www.christofflab.ca/wp-content/uploads/2017/10/Raffaelli2016-boredom.pdf">ventral medial prefrontal cortex</a> motivates us to seek alternative stimulating activities.</p>
<h2>Boredom versus overstimulation</h2>
<p>We live in a society that subjects us to information overload and high stress. Relatedly, many of us have adopted a fast-paced lifestyle, constantly scheduling ourselves to keep busy. As adults we juggle work and family. If we have kids, the habit of filling the day with schooling and after-school activities allows us to work longer hours.</p>
<p>In between these activities, if we have time to pause, we may be on our screens constantly organising, updating, or scrolling to simply stay occupied. As a result, adults inadvertently model the need to be constantly “on” to younger generations.</p>
<p>This constant stimulation can be costly – <a href="https://dictionary.apa.org/autonomic-hyperactivity">particularly for our nervous system</a>. Our overscheduling can feed into overstimulation of the nervous system. The sympathetic nervous system which manages our fight-or-flight response is designed to deal with times of stress.</p>
<p>However, when we are constantly stressed by taking in new information and juggling different activities, the sympathetic nervous system can stay activated for too long, due to the cumulative effects of repeated exposure to different stressors. This is sometimes referred to as “<a href="https://www.sciencedirect.com/science/article/pii/S0306453019301581?casa_token=cLGoT4PMZPMAAAAA:Va1VdPprmyCgct-HxhagzAExcJqVicGoO0fGzcyTLuxp9OwHurXUDqHg0WlM8hgAiSVdA8mrNv3-">allostatic overload</a>”. It is when our nervous system becomes overwhelmed, keeping us in a heightened state of arousal, which can <a href="https://www.sciencedirect.com/science/article/pii/S0006322324014288#">increase our risk of anxiety</a>.</p>
<p>Eliminating the state of boredom deprives us of a simple and natural way to reset our sympathetic nervous system.</p>
<h2>Could boredom be good for us?</h2>
<p>In small doses, boredom is the necessary counterbalance to the overstimulated world in which we live. It can offer <a href="https://www.mayoclinichealthsystem.org/hometown-health/speaking-of-health/boost-your-brain-with-boredom#:~:text=Yet%20rest%20time%20is%20important,t%20include%20an%20electronic%20device.">unique benefits</a> for our nervous system and our mental health. This is opposed to long periods of boredom where increased default mode network activity <a href="https://www.researchgate.net/profile/James-Danckert-2/publication/269599951_Boredom_An_Emotional_Experience_Distinct_from_Apathy_Anhedonia_or_Depression/links/551d426a0cf2000f8f93898a/Boredom-An-Emotional-Experience-Distinct-from-Apathy-Anhedonia-or-Depression.pdf">may be associated with depression</a>.</p>
<p>There are several benefits of giving ourselves permission to be occasionally bored:</p>
<ul>
<li>improvements in <a href="https://hbr.org/2014/09/the-creative-benefits-of-boredom">creativity</a>, allowing us to build “flow” in our thoughts</li>
<li>develops <a href="https://childmind.org/article/the-benefits-of-boredom/">independence in thinking</a> and encourages finding other interests rather than relying on constant external input</li>
<li><a href="https://childmind.org/article/the-benefits-of-boredom/">supports self-esteem</a> and emotional regulation, because unstructured times can help us sit with our feelings which are important for managing anxiety</li>
<li>encourages periods without device use and breaks the loop of instant gratification that contributes to compulsive device use</li>
<li><a href="https://www.health.harvard.edu/staying-healthy/understanding-the-stress-response">rebalances the nervous system</a> and reduces sensory input to help calm anxiety.</li>
</ul>
<h2>Embrace the pause</h2>
<p>Anxiety levels are on the rise worldwide, especially among our youth. Many factors contribute to this trend. We are constantly “on”, striving to ensure we are scheduling for every moment. But in doing so, we are potentially depriving our brains and bodies of the downtime they need to reset and recharge.</p>
<p>We need to embrace the pause. It is a space where creativity can prosper, emotions can be regulated, and the nervous system can reset.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/255767/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/boredom-gets-a-bad-rap-but-science-says-it-can-actually-be-good-for-us-255767">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/choline-imbalance-in-the-brain-linked-to-with-cognitive-symptoms-in-young-depression-patients/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Choline imbalance in the brain linked to with cognitive symptoms in young depression patients</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 8th 2025, 14:00</div>
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<p><p>Young adults with major depressive disorder show distinct metabolic signals in two brain regions, and the pattern differs between those who struggle on thinking tasks and those who do not. In a new study published in the <em><a href="https://doi.org/10.1016/j.jad.2025.03.161" target="_blank">Journal of Affective Disorders</a></em>, researchers found that patients whose test scores indicated cognitive impairment had more choline relative to creatine in a part of the frontal midline called the anterior cingulate cortex, while all patients—impaired or not—had an elevated choline‑to‑creatine ratio in the putamen, a deep structure involved in motivation and learning. The ratio in the putamen also rose in step with the number of past depressive episodes among the impaired patients.</p>
<p>While many studies have examined mood-related symptoms of depression, less is known about the biological basis of cognitive changes in this condition, especially in younger adults. Prior research suggested that metabolic changes in the brain might be linked to these symptoms, but the specific patterns and brain regions involved remained unclear.</p>
<p>To investigate this, the researchers recruited 105 right-handed young adults between the ages of 18 and 35 who had recently been diagnosed with major depressive disorder but had not yet received treatment. They also included a control group of 68 healthy young adults matched for age and demographic factors. All participants completed a widely used cognitive test battery, known as the MATRICS Consensus Cognitive Battery, which measures skills like memory, attention, and processing speed.</p>
<p>Based on test results, the depressed participants were divided into two groups: those with cognitive impairment and those without. A person was considered to have cognitive impairment if they scored at least 1.5 standard deviations below the average in two or more areas of the test. Using this standard, 39 of the 105 depressed participants were classified as having cognitive impairment, while the remaining 66 did not meet this threshold.</p>
<p>In addition to the cognitive testing, participants underwent a brain scan known as proton magnetic resonance spectroscopy. This imaging technique measures the concentration of certain chemicals in specific brain regions. The researchers focused on two areas: the anterior cingulate gyrus and the putamen. These regions are involved in emotional regulation, attention, memory, and motivation—all of which are often affected in depression.</p>
<p>The scans looked at the levels of choline-containing compounds (a marker related to cell membrane turnover and inflammation), creatine (a marker of energy metabolism), and N-acetylaspartate (a marker of neuronal health). The researchers then calculated the ratio of choline to creatine (Cho/Cr) and N-acetylaspartate to creatine (NAA/Cr) in both brain regions.</p>
<p>The results revealed several key differences. Participants with both depression and cognitive impairment had significantly higher Cho/Cr ratios in the right anterior cingulate gyrus compared to both healthy controls and depressed individuals without cognitive impairment. This suggests a possible link between changes in this region’s chemistry and the presence of cognitive difficulties.</p>
<p>Additionally, both depressed groups—those with and without cognitive impairment—showed elevated Cho/Cr ratios in the left putamen when compared to the control group. This finding implies that metabolic changes in the putamen may be common among people with depression, even if cognitive performance is relatively preserved.</p>
<p>The study also found a correlation between the number of depressive episodes and higher Cho/Cr levels in the left putamen among those with cognitive impairment. In other words, people with more frequent depressive episodes tended to show greater chemical changes in this brain region, which might suggest that these alterations accumulate over time.</p>
<p>Interestingly, the researchers did not find any significant differences between the groups in terms of NAA/Cr ratios, which are thought to reflect overall neuronal integrity. This might mean that the observed differences in choline levels are more reflective of inflammation, cell membrane activity, or changes in glial cells rather than outright neuron loss.</p>
<p>The anterior cingulate gyrus has long been thought to play a key role in balancing emotional and cognitive processes. It helps regulate attention, monitors performance, and contributes to learning and adapting to new rules. Previous studies have shown that people with depression often have disrupted connectivity in this area, especially in parts that coordinate with other brain regions involved in mood and cognition. The higher choline levels seen in the right anterior cingulate among cognitively impaired patients could reflect inflammation or other stress-related cellular changes that interfere with its normal functioning.</p>
<p>The putamen, on the other hand, is part of the striatum and is typically associated with motivation, reward processing, and motor control. In depression, this area has been linked to symptoms such as low motivation and reduced pleasure. Changes in the putamen’s chemistry, as seen in this study, could be part of the broader brain dysfunction that contributes to these symptoms.</p>
<p>Importantly, the study emphasizes that not all individuals with depression show cognitive impairment, and the biological changes associated with these impairments may be distinct from those linked to mood symptoms. While both depressed groups had some abnormalities in the putamen, only those with cognitive impairment showed the additional changes in the anterior cingulate.</p>
<p>This distinction could help explain why some patients respond well to antidepressants while others continue to struggle with concentration, memory, or other cognitive functions. Understanding these differences may help guide more personalized treatment approaches in the future, such as combining standard antidepressants with cognitive interventions or anti-inflammatory treatments for those with cognitive symptoms.</p>
<p>Despite its strengths, the study has some limitations. The sample size, while relatively large for a brain imaging study, was still limited to young adults from a single hospital. The findings may not generalize to older adults, who may have different patterns of brain aging or inflammation. The researchers also focused only on two brain regions, so it’s possible that other areas involved in cognition may show relevant changes as well. Additionally, the study only measured metabolites at one point in time, so it cannot determine whether the observed changes preceded or followed the onset of cognitive problems.</p>
<p>The authors suggest that future research should explore a broader range of brain regions, examine how these changes evolve over time, and include inflammatory markers like C-reactive protein to further investigate the potential role of immune system activity. They also highlight the need to investigate sex differences and the effects of treatments on brain chemistry and cognitive function.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.jad.2025.03.161" target="_blank">The abnormal choline to creatine ratio of the right anterior cingulate gyrus is linked to cognitive impairment in youth with major depressive disorder</a>,” was authored by Shijie Luo, Shunkai Lai, Linna Chu, Ying Wang, Pan Chen, Xiaojie Ye, Jinping Zhuo, Munila Abula, Yikun Liang, Dongxue Wei, Meiqi Zhang, Jie Yin, Xiaodan Lu, Jianzhao Zhang, Yiliang Zhang, Shuming Zhong, and Yanbin Jia.</p></p>
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<td><a href="https://www.psypost.org/scientists-who-relocate-more-often-start-nobel-research-up-to-two-years-earlier/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists who relocate more often start Nobel research up to two years earlier</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 8th 2025, 12:00</div>
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<p><p>Top scientists may improve their chances of producing breakthrough discoveries by changing where they work—or by dividing their time between multiple locations—according to a new study published in the <em><a href="https://onlinelibrary.wiley.com/doi/10.1111/iere.12768" target="_blank">International Economic Review</a></em>. The research found that Nobel Prize winners who moved to new locations more frequently began their prize-winning work nearly two years earlier than those who stayed put, while those who held multiple affiliations at the same time started their influential research even earlier.</p>
<p>While past research has shown that working alongside high-quality colleagues can improve productivity, the new study focuses on a different kind of interaction: the creative spark that comes from encountering unfamiliar ideas. The authors propose that being exposed to a wider variety of viewpoints, theories, and methods helps researchers generate novel combinations of knowledge—a process they describe as “recombinant innovation.”</p>
<p>“There is considerable interest in where vital, new ideas originate. Most of it focuses on being at the same institution as other innovators. We thought it would be interesting to look not just at being around other important innovators, but also at the changes and unique mixes of colleagues,” explained study authors Bruce A. Weinberg, the Eric Byron Fix-Monda Professor of Economics and Public Affairs at The Ohio State University, and <a href="https://sites.google.com/site/johnhamecon/home" target="_blank">John C. Ham</a>, a professor of economics at NYU Abu Dhabi and Global Network Professor of Economics at the NYU Wagner School of Public Service.</p>
<p>To explore this idea, the researchers examined the detailed career histories of 488 recipients of the Nobel Prize in chemistry, medicine, and physics, spanning from 1901 to 2003. The study focused on the time interval between when these scientists began their careers and when they started the line of research that ultimately led to their Nobel Prize. Importantly, the authors used biographical information, committee statements, and autobiographies to identify when each scientist began their prize-winning research—not when they won the prize, which often happens many years later.</p>
<p>The researchers looked closely at two patterns: whether the laureates moved to a new location during their careers, and whether they held appointments in more than one place at the same time. A “new location” was defined as a place the scientist hadn’t worked in for at least five years, while “multiple locations” referred to any year in which the scientist spent significant time in more than one place. These movements were tracked year by year across the scientists’ careers and combined with other data such as the quality of colleagues and the scientist’s field of research.</p>
<p>To make their estimates, the authors built a statistical model that calculated the likelihood of starting prize-winning work at any given point in a scientist’s career, while accounting for other influences like field, time period, and the presence of other highly accomplished scientists in the same city. This approach allowed them to compare the average time it took to begin Nobel work under different scenarios—such as moving frequently versus staying in one location, or working across multiple institutions versus staying at just one.</p>
<p>Weinberg and Ham found that scientists who moved to a new location every two years began their Nobel-worthy research an average of 2.6 years earlier than those who never moved. Those who moved every three years started 1.9 years earlier, while those who moved every five years started nearly one year earlier. Working across multiple locations had an even stronger relationship: scientists who were always in multiple locations began their breakthrough research about 2.6 years earlier, on average, than those who consistently worked in a single location.</p>
<p>To put these numbers in perspective, the average Nobel laureate in the sample took about 10.5 years from the start of their career to the beginning of their prize-winning work. Shaving two or more years off that timeline represents a meaningful shift, especially considering that the laureates already belong to the most elite group of scientists.</p>
<p>The study also provided a broader picture of how scientific careers have evolved over the past century. The average time to begin Nobel-worthy research varied somewhat across disciplines and time periods.</p>
<p>For example, physicists who graduated before 1918 took around 11.3 years to begin their prize-winning work, while those who graduated after 1945 took closer to 9.4 years. In medicine, the average time to begin dropped from about 9.9 years in earlier cohorts to 7.6 years in more recent ones. The data also reflected larger historical shifts, such as the growing dominance of the United States as a home for top scientists, especially after the Second World War.</p>
<p>Most Nobel laureates spent the majority of their careers in a single location. But the periods leading up to their most important work were more likely to involve change. In the years just before starting their Nobel work, about 10% of laureates were in a new location, and 13% were in both a new and multiple locations. That share rose to 21% in the year they began their breakthrough research, before dropping sharply afterward. These patterns suggest that new environments may be especially helpful at the outset of an innovative project.</p>
<p>The study builds on a broader body of research about knowledge spillovers and how ideas travel. Traditional models have emphasized clustering—bringing top researchers together in physical spaces such as academic departments or research institutes. But this new research suggests that movement between different environments, and exposure to a wider mix of perspectives, may be just as important for sparking breakthroughs.</p>
<p>“If our results also apply to high-quality scientists, as opposed to laureates, from a policy perspective, we believe it suggests that cross-pollination has significant value, exposing people to ideas they might not otherwise encounter,” Weinberg and Ham told PsyPost.</p>
<p>“From a personal-interest angle, readers may want to try to expose themselves to ideas or people they don’t usually encounter. Individual scholars should aim to visit other campuses via sabbaticals, for example. To their universities, having faculty on leave is likely a mixed blessing, as these faculty members will increase their visibility, making them more attractive to other schools, while also raising their productivity.”</p>
<p>“We also believe that our study demonstrates the value of sophisticated statistical work, as we were dealing with a highly non-random sample of exceptionally talented scientists,” the researchers said.</p>
<p>Although the researchers accounted for several potential confounding factors—such as the quality of colleagues or early career advantages—they acknowledge that the study is not designed to prove that moving causes earlier innovation. It is possible, for instance, that more ambitious or productive scientists are more likely to seek out multiple appointments or relocate frequently.</p>
<p>However, the authors argue that their focus on Nobel laureates helps reduce this concern, since all individuals in the sample were already exceptionally successful. Moreover, they note that while the effects may not generalize to all scientists, they appear meaningful among those working at the very highest levels.</p>
<p>“We think that the impact of moving to new places or working across multiple locations is impressive even after accounting for the number of other innovators that people are around—it really suggests that exposure to new ideas and novel combinations of ideas has a huge benefit,” Weinberg and Ham said.</p>
<p>The authors highlight that their approach differs from earlier studies that looked at the influence of colleagues on publication counts or immediate research output. Instead, they focus on the timing of major discoveries, using the Nobel Prize as a retrospective indicator of scientific significance. Their method captures how combining different ideas—often from different fields or institutions—can lead to unusually creative or high-impact outcomes.</p>
<p>There are limitations to the study. The data set is restricted to Nobel Prize winners, which may not reflect patterns among the broader scientific community. The definitions of “new” and “multiple” locations, while carefully selected, are still approximations. The measure of colleague quality is also somewhat indirect, relying on the number of future laureates in a given city. And while the researchers attempted to control for differences in ability and background, unmeasured factors could still play a role.</p>
<p>“This is a single study,” Weinberg and Ham noted. “We are using historical data, which could be a strength—because it isn’t about one episode—but things may have changed with the internet, for instance. We also want to be circumspect in extrapolating to different groups. That is, the study may well be valid for the group that it studies—Nobel laureates—but people may want to be cautious applying it more generally. We would like to apply our model to a group of scientists who are not as elite as laureates. The problem here is a lack of data for doing this.”</p>
<p>“Bruce is currently using natural language processing to identify important new ideas and see how they move around in networks of innovators,” the researchers added. “It seems valuable to trace the actual flows of ideas. John is continuing to work on statistical models that will let us analyze data sets with less standard sampling schemes.”</p>
<p>The study, “<a href="https://doi.org/10.1111/iere.12768" target="_blank">Recombinant Innovation, Novel Ideas, and the Start of Nobel Prize–Winning Work</a>,” was authored by John C. Ham, Brian Quistorff, and Bruce A. Weinberg.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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