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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/new-research-identifies-multiple-personal-social-and-biological-risk-factors-for-ptsd/" 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;">New research identifies multiple personal, social, and biological risk factors for PTSD</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 25th 2025, 10:00</div>
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<p><p>A study published in <a href="https://doi.org/10.1037/hum0000355"><em>The Humanistic Psychologist</em></a> shows that posttraumatic stress disorder (PTSD) is shaped not just by the trauma itself but also by personal history, biology, and the support systems people have around them.</p>
<p>The psychological toll of traumatic experiences—from wars and terrorism to natural disasters and severe illnesses—can be life changing, with PTSD standing out as one of the most common consequences. Despite decades of research, there is no single agreed-upon cause. Each year, approximately 13 million people worldwide develop the disorder, making PTSD not only a personal struggle but also a global public health issue.</p>
<p>Liana Spytska recognized that much of the research on PTSD risk factors has been conducted in Western, military-focused contexts, leaving important gaps in understanding civilian populations across diverse settings. By combining a thorough review of past research with new survey data, Spytska’s goal was to build a clearer picture of the numerous forces that shape who develops PTSD and why.</p>
<p>For the review, the researcher conducted a wide-ranging search in PubMed, Scopus, and UpToDate, focusing on peer-reviewed articles published since 2010. Keywords such as “posttraumatic stress disorder,” “childhood trauma,” “domestic violence,” and “risk factors” guided the search. This step provided a foundation for identifying which psychological, social, and biological factors had been most strongly linked to PTSD across prior research.</p>
<p>Alongside this review, the researcher carried out a survey among 250 adults aged 21-55, recruited from medical settings. The sample included 110 women and 140 men. To ensure the study focused on new cases, people with pre-existing psychiatric conditions, prior PTSD diagnoses, or acute medical conditions were excluded. Each participant’s health history was confirmed through medical records.</p>
<p>Participants completed the PTSD Checklist for DSM-5 (PCL-5), a well-established 20-item questionnaire that asks about symptoms of re-experiencing, avoidance, negative mood, and heightened arousal. The diagnostic thresholds followed DSM-5-TR criteria, meaning a participant had to report significant symptoms across multiple domains, or score above 33 points overall, for a PTSD diagnosis.</p>
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<p>The literature review highlighted that PTSD rarely occurs in isolation—it often coexists with depression, substance use, or physical illnesses. Severity of trauma exposure stood out as one of the most powerful predictors of PTSD, with prior traumatic experiences, lack of social support, and existing mental health conditions further elevating risk.</p>
<p>Biological vulnerabilities such as alterations in stress hormone regulation and structural differences in brain regions like the hippocampus and amygdala were also linked, while genetic and epigenetic findings suggested that vulnerability to PTSD may in part be inherited and shaped by early life adversity.</p>
<p>The survey results revealed surprisingly high rates of PTSD among participants: 190 of the 250 adults, or 76%, met diagnostic criteria. Most reported significant intrusion and avoidance symptoms, such as flashbacks and efforts to steer clear of trauma reminders, along with high levels of hyperarousal and negative thoughts. Age and injury severity strongly influenced outcomes; participants over 40 and those who had endured more serious injuries reported the most intense symptoms, while those with milder injuries displayed fewer symptoms of PTSD.</p>
<p>Social support emerged as a protective factor; individuals with stable employment and family backing had noticeably fewer symptoms.</p>
<p>Interestingly, no broad gender differences were found in the overall rate of PTSD diagnoses, though the patterns echoed prior findings that women are more vulnerable following sexual trauma, while men and older adults are more affected by serious medical conditions like heart attacks or strokes. Among the participants, nearly half lacked stable work, which was associated with more severe PTSD symptoms, underscoring the role of economic and social security in mental health resilience.</p>
<p>Taken together, the results point to PTSD as a condition that is deeply shaped not just by the traumatic event itself, but by the individual’s personal history, social environment, and biological susceptibility.</p>
<p>The reliance on a cross-sectional design captured PTSD symptoms only at a single time point, specifically within one to six months after the traumatic events, which may have inflated the prevalence (76%) by emphasizing more acute cases.</p>
<p>The research, “<a href="https://doi.org/10.1037/hum0000355">Study of Possible Risk Factors for Posttraumatic Stress Disorder</a>”, was authored by Liana Spytska.</p></p>
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<td><a href="https://www.psypost.org/psilocybin-and-mdma-may-reset-fear-related-brain-immune-signaling-scientists-find/" 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;">Psilocybin and MDMA may reset fear-related brain-immune signaling, scientists find</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 25th 2025, 08:00</div>
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<p><p>A new study published in Nature suggests that the immune system may play a more direct role in shaping fear and stress responses than previously thought — and that psychedelic compounds like psilocybin and MDMA may offer a way to therapeutically modify this neuroimmune pathway. Researchers found that a specific set of brain-immune interactions involving astrocytes, neurons, and inflammatory monocytes contributes to fear-related behavior in mice under chronic stress. The study also provides initial evidence that psychedelic treatments can disrupt this signaling cascade, reducing fear and inflammation, with parallel patterns found in human tissue.</p>
<p>Scientists have long known that the immune system communicates with the brain, especially during psychological stress. Immune cells can release molecules that cross into the brain and alter its activity, sometimes worsening symptoms of mental health conditions such as depression and anxiety. But many of the specific pathways and mechanisms by which these signals affect behavior have remained unclear.</p>
<p>The new study was designed to explore how chronic stress might disrupt communication between the brain and immune system — particularly in the amygdala, a region known to be involved in emotional processing and fear. The team of researchers from Brigham and Women’s Hospital, Massachusetts General Hospital, and Harvard Medical School focused on astrocytes, a type of glial cell that supports and regulates neurons. Prior work has suggested that astrocytes may help dampen inflammatory signals in the brain, and the researchers suspected they might be key players in mediating the behavioral effects of chronic stress.</p>
<p>In addition, the team was interested in whether psychedelic compounds, known to influence mood and perception, might interact with this brain-immune circuit. Psychedelics have recently attracted attention for their potential to treat depression and posttraumatic stress disorder, but the biological mechanisms behind these effects are not fully understood. (← missing period added)</p>
<p>“We are interested in trying to understand how interactions between the brain and body might contribute to psychiatric disorders. Importantly, these interactions have not been studied in deep mechanistic detail before. Hence, we hope that if we uncover new mechanisms that control this communication network, we can develop novel therapies for diseases like depression,” explained <a href="https://www.thewheelerlab.org/" target="_blank">Michael Wheeler</a>, an assistant professor of neurology at Harvard Medical School based out of Brigham and Women’s Hospital.</p>
<p>To examine the effects of stress on fear behavior, the researchers subjected mice to 18 days of restraint stress and assessed their responses using behavioral tests such as contextual fear conditioning and the elevated plus maze. Mice exposed to chronic stress displayed significantly more fear-related behaviors, including freezing, compared to unstressed controls. Blood samples revealed increased levels of corticosterone and several inflammatory cytokines, including interleukin-1 beta, suggesting an activated stress and immune response.</p>
<p>The researchers then analyzed astrocytes in the amygdala using single-cell RNA sequencing. They discovered a distinct population of astrocytes that expanded in response to chronic stress. These stress-sensitive astrocytes had lower expression of a receptor known as EGFR, or epidermal growth factor receptor. EGFR has been previously linked to anti-inflammatory functions, and its downregulation suggested that these astrocytes might be less able to buffer against inflammation under stress.</p>
<p>To test the causal role of EGFR in these cells, the researchers used a gene-editing approach to reduce EGFR expression specifically in amygdala astrocytes. Mice with this targeted knockdown showed exaggerated fear responses even after just seven days of stress — a time point that normally does not produce significant behavioral changes. Additional molecular analyses revealed increased inflammation and signs of heightened neuronal activity, suggesting that loss of EGFR made astrocytes less effective at regulating stress-induced brain signaling.</p>
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<p>The research team also found that astrocyte-neuron communication was altered in stressed animals. Loss of EGFR in astrocytes led to changes in neurons expressing a transcription factor called NR2F2, which was linked to increased excitatory signaling and fear behavior. Suppressing NR2F2 in neurons reduced fear responses, providing further evidence that this pathway plays a functional role.</p>
<p>Beyond changes within the brain itself, the researchers found that stress affected the immune system in peripheral tissues. Mice subjected to chronic stress had increased numbers of inflammatory monocytes in the meninges — the protective membranes surrounding the brain. These monocytes, known for their pro-inflammatory properties, were not seen in elevated numbers in the spleen or lymph nodes, suggesting a specific recruitment to the brain’s outer layers.</p>
<p>To probe the importance of these cells, the team conducted several experiments. Transferring monocytes into the meninges of stressed mice amplified fear behavior and reduced EGFR-related gene activity in the amygdala. Conversely, depleting these monocytes reduced fear responses and boosted protective signaling in astrocytes. The researchers also showed that monocytes could release inflammatory molecules like interleukin-1 beta that may reach the brain through leaky barriers during chronic stress.</p>
<p>Together, these results suggest a signaling loop in which chronic stress draws inflammatory immune cells to the meninges, where they influence brain astrocytes and neurons, ultimately shaping behavior.</p>
<p>“Our study shows that dialogue between the brain and body is a crucial driver of behavior, meaning that environmental changes that impact cells in our body can start to modify brain circuits implicated in mood disorders,” Wheeler told PsyPost.</p>
<p>With this brain-immune-fear circuit in place, the researchers turned to psilocybin and MDMA. These compounds were administered to mice following chronic stress exposure. Both psychedelics reduced fear-related behaviors and decreased the number of inflammatory monocytes in the meninges. At the molecular level, psychedelics restored EGFR signaling in astrocytes and dampened the inflammatory transcriptional programs seen in monocytes.</p>
<p>In cell culture experiments, psilocybin and MDMA also reduced the expression of pro-inflammatory genes in mouse and human immune cells treated with stress-related hormones. These effects were blocked by antagonists of serotonin receptors, indicating that serotonin signaling — a known target of psychedelics — may help mediate these immune changes.</p>
<p>“We were surprised to find that psychedelic compounds also impacted cell types that don’t directly contribute to hallucinations — in this particular case, immune cells that typically fight off infections,” Wheeler said. “Those findings told us that perhaps psychedelic therapy may have broader therapeutic applicability beyond mental health diseases.”</p>
<p>The team explored whether these results might apply to people by analyzing human amygdala tissue from individuals with major depressive disorder. They found that a subset of astrocytes in patients with depression had lower EGFR expression and that a group of excitatory neurons expressed elevated levels of NR2F2 and other genes linked to fear-related circuitry. These patterns mirrored what was observed in the stressed mice, providing a tentative bridge from animal models to human disease.</p>
<p>“If we suspect that psychedelics are candidate molecules to control not just inflammatory signals in the brain, but tissue plasticity more broadly through their control of neural-immune interactions, we might be able to find use for them in completely new diseases where neural-immune communication is disturbed — for example, inflammatory diseases,” Wheeler explained.</p>
<p>Still, the researchers caution that these results are early and based largely on animal studies. Further work is needed to determine how these mechanisms operate in humans and whether they can be effectively targeted in clinical settings.</p>
<p>“We aren’t suggesting that psychedelics are a panacea for every disease,” Wheeler said. “But rather, we think that they may have applicability in unanticipated diseases marked by similar inflammatory mechanisms as mental health disorders. In other words, diseases that are not brain diseases — something akin to chronic inflammation. There is still a substantial amount of mechanistic work needed to determine their utility in these and other disorders, but we are excited at this possibility.”</p>
<p>“We want to understand the extent to which our findings apply to humans, so we are collaborating with colleagues at Massachusetts General Hospital on a clinical trial to understand how psilocybin therapy impacts the immune system. Likewise, we want to test our ideas that psychedelics may modify tissue plasticity in inflammatory diseases, to see what use cases they may have outside of the brain.”</p>
<p>“We think that harnessing the therapeutic power of the immune system in psychiatry could potentially usher in revolutionary therapies,” Wheeler added. “We hope that the mechanisms we defined in this study are early steps in this process.”</p></p>
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<td><a href="https://www.psypost.org/acetaminophen-use-during-pregnancy-linked-to-higher-risk-of-autism-adhd-in-children/" 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;">Acetaminophen use during pregnancy linked to higher risk of autism, ADHD in children</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 25th 2025, 06:00</div>
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<p><p>A new comprehensive analysis published in <em><a href="https://ehjournal.biomedcentral.com/articles/10.1186/s12940-025-01208-0" target="_blank">Environmental Health</a></em> suggests that children exposed to acetaminophen in the womb may face a heightened risk of developing neurodevelopmental disorders, including autism spectrum disorder and attention-deficit/hyperactivity disorder (ADHD). The study systematically reviewed 46 existing studies and found that most of the higher-quality research reported a statistically significant association between prenatal acetaminophen use and increased rates of these conditions in offspring.</p>
<p>Acetaminophen, also known as paracetamol, is widely considered a go-to option for pain and fever relief during pregnancy. Over half of pregnant women around the world use the drug, often due to its perceived safety compared to alternatives like non-steroidal anti-inflammatory drugs, which are known to carry teratogenic risks. However, over the past decade, several studies have raised questions about whether frequent or prolonged exposure to acetaminophen during pregnancy could disrupt the developing brain.</p>
<p>The brain undergoes rapid and sensitive developmental processes during gestation, and this makes it particularly susceptible to environmental influences—including medications. Given acetaminophen’s known ability to cross the placental barrier and interact with systems involved in hormone regulation, immune signaling, and oxidative stress, researchers aimed to determine whether consistent patterns exist between its prenatal use and later diagnosis of neurodevelopmental disorders.</p>
<p>“We decided to look into this because acetaminophen, like Tylenol, is something over half of pregnant women use worldwide for pain or fever, and it’s often seen as the safest option,” said study author <a href="https://www.linkedin.com/in/diddier-prada-89051435/" target="_blank">Diddier Prada</a>, an assistant professor at <a href="https://scholars.mssm.edu/en/persons/diddier-prada" target="_blank">the Icahn School of Medicine at Mount Sinai</a>. </p>
<p>“But we started noticing that some studies were hinting that it might be linked to kids developing issues like autism or ADHD later on. This got our attention because pregnancy is such a critical time for a baby’s brain to grow, and we wanted to figure out if this common medicine could be playing a role. With so many families relying on it, we felt it was important to dig deeper and get a clearer picture using a careful, step-by-step methodological approach.”</p>
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<p>The researchers employed the Navigation Guide, a systematic methodology developed to assess environmental health risks through observational data. They searched PubMed, ISI Web of Science, and Google Scholar through February 2025 for studies examining links between prenatal acetaminophen exposure and neurodevelopmental outcomes. The focus was on children diagnosed with ADHD, autism, or related developmental challenges, and the review included both prospective and retrospective studies, some of which used biological markers such as acetaminophen levels in cord blood or meconium.</p>
<p>A total of 46 human studies met the inclusion criteria. These included large-scale cohort studies, sibling-controlled studies, and case-control designs. The researchers excluded animal studies and duplicated datasets. Each study was evaluated for its methodological quality, potential sources of bias, and strength of evidence. The team applied structured rating systems to judge how well each study accounted for key confounding variables, such as maternal age, chronic illness, substance use, and reasons for taking acetaminophen in the first place.</p>
<p>Due to significant variation in study designs, exposure measurements, and outcome definitions, the researchers opted not to conduct a meta-analysis. Instead, they synthesized the findings qualitatively, placing special emphasis on studies with stronger methodological rigor and prospective designs.</p>
<p>Of the 46 studies included, 27 reported positive associations between prenatal acetaminophen use and neurodevelopmental problems in children. Nine studies found no significant relationship, while four reported possible protective effects, and the remainder produced mixed findings. Importantly, the strongest associations were observed in studies with more rigorous designs—those that used biomarkers to assess exposure, adjusted for a wide range of confounding variables, and tracked participants over time.</p>
<p>For ADHD specifically, 14 out of 20 studies found a significant link between acetaminophen exposure in the womb and increased diagnosis rates. In some cases, a dose-response pattern emerged, suggesting that longer or more frequent use of the medication may elevate risk. For autism, five out of eight studies reported a positive association. Studies that examined other forms of neurodevelopmental disruption, such as language delays or behavioral dysregulation, also tended to find increased risk linked to prenatal acetaminophen use.</p>
<p>“We were a bit surprised by how many of the 46 studies we looked at—over half—showed a connection between acetaminophen use and these brain development issues, especially when the studies were well done,” Prada told PsyPost. “We also didn’t expect that a few studies suggested it might even help a little, though that was rare. The fact that the best studies kept pointing to a link was eye-opening and made us realize this is something we can’t ignore, even though it’s a medicine so many trust.”</p>
<p>The researchers also looked at evidence from sibling-controlled studies, which aim to account for shared genetic and environmental factors within families. These studies produced mixed results, with some showing null associations. However, the authors caution that sibling designs may suffer from reduced statistical power and higher susceptibility to certain types of measurement error, especially when exposure is based on self-reported data.</p>
<p>The consistency of findings across multiple cohorts, countries, and methods—combined with emerging evidence from biological studies—led the authors to conclude that the observed associations are unlikely to be explained solely by confounding factors. Laboratory studies and animal models have shown that acetaminophen can influence hormone signaling, immune function, and oxidative stress in ways that could plausibly interfere with brain development.</p>
<p>“The main thing people should know is that our research suggests using acetaminophen during pregnancy might affect a child’s brain development, possibly increasing the chance of conditions like autism or ADHD,” Prada explained. “It’s not a definite cause, but it’s a signal to be careful. If you’re pregnant or planning to be, it’s smart to use it only when you really need to, in small amounts and for a short time, and chat with your doctor about it. Untreated pain or fever can also harm the baby, so it’s about finding the right balance, and doctors are the best guides for that.”</p>
<p>While the review provides a strong argument for caution, it does not claim that acetaminophen <em>causes</em> neurodevelopmental disorders. The authors note that observational studies, no matter how well-designed, cannot definitively establish causality. Unmeasured confounding factors, such as maternal stress or infection, might still play a role in the observed associations.</p>
<p>Another limitation is that the studies included in the review varied widely in how they measured acetaminophen exposure—some relied on maternal recall, while others used biomarkers or medical records. Timing of exposure also varied, and some studies lacked detailed data on dosage or frequency. This heterogeneity makes it difficult to identify specific windows of heightened vulnerability or safe thresholds of use.</p>
<p>“Since all the studies we reviewed were observational—meaning they watched people rather than testing something directly—we can’t say for sure that acetaminophen causes these issues; it might be something else, like the reason for taking it, like a fever, playing a part,” Prada noted. “Also, some studies relied on moms remembering what they took, which isn’t always accurate, and the studies varied a lot in how they were done. So, while the evidence is strong enough to raise concern, it’s not the final word, and more research is needed to be certain.”</p>
<p>“Looking ahead, we want to do more detailed studies that follow bigger, more varied groups of people over time, checking things like traces of acetaminophen in babies’ bodies to see the impact on neurodevelopment in the children. Our goal is to figure out if this link is real and why it might occur, so we can protect kids’ brain development. We also hope to find safer ways to help pregnant women with pain or fever, like new medicines or other non-pharmacological approaches, like cool cloths, and work with doctors and health groups to update advice based on what we learn.”</p>
<p>“We’re really proud that this is the first time we’ve used such a careful method to pull together all this information, giving a clearer view than ever before,” Prada added. “It’s a team effort with experts from places like Mount Sinai, Harvard, UCLA, and UMass Lowell. We’re excited to see it spark conversations about how to keep moms and babies healthy. We also want to make sure everyone, especially those who might not have easy access to good healthcare, gets the message and support they need, because this is about fairness in health for all families.”</p>
<p>The study, “<a href="https://doi.org/10.1186/s12940-025-01208-0" target="_blank">Evaluation of the evidence on acetaminophen use and neurodevelopmental disorders using the Navigation Guide methodology</a>,” was authored by Diddier Prada, Beate Ritz, Ann Z. Bauer, and Andrea A. Baccarelli.</p></p>
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<td><a href="https://www.psypost.org/neuroscientists-find-evidence-of-an-internal-brain-rhythm-that-orchestrates-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 find evidence of an internal brain rhythm that orchestrates memory</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 24th 2025, 16:00</div>
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<p><p>A new study sheds light on how our brains rhythmically organize memories at the level of individual nerve cells. Researchers in Germany have found that single neurons in the human medial temporal lobe tend to synchronize their activity with slow brain waves, particularly during memory formation and retrieval. These patterns, known as theta-phase locking, appear to reflect an internal rhythm that helps structure cognitive processes. The findings were published in <em><a href="https://doi.org/10.1038/s41467-025-62553-9" target="_blank">Nature Communications</a>.</em></p>
<p>The study, led by neuroscientists at the University Hospital Bonn, the University of Bonn, and the University of Freiburg, examined how single-neuron activity in the human brain aligns with local electrical rhythms during memory tasks. The team focused on theta waves—slow oscillations typically occurring between 1 and 10 Hz—which have long been associated with memory processes in animal research. While studies in rodents have shown that hippocampal neurons often fire at specific phases of the theta rhythm, it has remained unclear whether similar dynamics hold in the human brain during real-time memory use.</p>
<p>“In <a href="https://spatialmemorylab.com/" target="_blank" rel="noopener">the Bonn Spatial Memory Lab</a>, we study how the brain forms memories about places and locations. Previous research showed that single brain cells can synchronize with rhythmic brain activity. We wanted to understand this synchronization more deeply and explored its role during both learning and remembering of spatial memories,” explained Tim Guth of the University of Bonn. “Our goal is to understand the memory system of the brain at the level of individual cells and populations of cells. Ultimately, we hope to help improve the treatment of memory disorders.”</p>
<p>The research took advantage of a unique clinical context. Patients with treatment-resistant epilepsy often undergo surgery to implant electrodes in the brain, helping doctors locate the source of seizures. With informed consent, these electrodes can also record brain activity at an extremely fine resolution—down to individual neurons. This setup allowed the researchers to directly observe how nerve cells behave as people form and recall memories.</p>
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<p>Eighteen patients took part in a virtual navigation task called “Treasure Hunt,” which asked them to explore a computer-generated beach and memorize the locations of hidden objects. During each trial, participants navigated to chests containing objects, learned their locations, and later recalled either the object associated with a specific location or the location linked to a particular object. Each session provided dozens of such encoding and retrieval episodes. The researchers recorded both behavioral accuracy and neural activity throughout.</p>
<p>Using advanced computational techniques, the research team analyzed how well individual neurons fired in sync with theta waves. To do this, they estimated the phase of the local field potential—a measure of the average electrical activity near each electrode—across a broad 1–10 Hz frequency range. This approach allowed them to track the timing of each spike relative to ongoing slow-wave activity.</p>
<p>The results provide evidence that neurons in the human medial temporal lobe—including the hippocampus, entorhinal cortex, and amygdala—frequently exhibit theta-phase locking. That is, neurons tended to fire at the same point in the theta cycle across time. About 86% of neurons showed significant phase locking across the full task, and many of them were aligned near the trough of the theta wave.</p>
<p>“Much like musicians in an orchestra follow a shared rhythm, many brain cells in the human memory system time their activity to the brain’s electrical oscillations,” Guth told PsyPost.</p>
<p>Importantly, the strength of this phase locking varied depending on the characteristics of the brain’s electrical background. Neurons were more tightly synchronized with theta waves during periods of high theta power and when the field potentials displayed steep aperiodic slopes—conditions thought to reflect greater neural inhibition. This suggests that theta-phase locking is not a fixed feature but is modulated by moment-to-moment changes in the local neural environment.</p>
<p>The presence of clear theta oscillations, identified using a cycle-by-cycle algorithm, also predicted stronger phase locking. Yet, even outside of these clearly rhythmic periods, neurons continued to show non-random firing relative to theta phase, suggesting that some degree of synchronization persists even when oscillations are less apparent.</p>
<p>“While most brain cells fired at the same point in the rhythm during both learning and recall, a small group shifted their timing,” Guth said. “This shift may help the brain separate the processes of storing new memories from retrieving old ones.”</p>
<p>The researchers also examined whether this rhythmic coordination related to successful memory performance. Surprisingly, they found no strong evidence that theta-phase locking was more pronounced during correctly remembered trials compared to forgotten ones. This held true during both the encoding and retrieval phases of the task. While previous studies using static images or verbal tasks have reported such effects, the dynamic and continuous nature of the spatial navigation task used here may have played a role in blunting phase-reset phenomena that typically enhance phase locking at stimulus onset.</p>
<p>Even though the overall strength of phase locking didn’t predict memory success, the study did find that a subset of neurons shifted their preferred firing phase between encoding and retrieval. About 9% of neurons exhibited such phase shifts, and these shifts tended to be slightly more common during successful memory trials. This observation lends partial support to theoretical models like the SPEAR (Separate Phases of Encoding And Retrieval) model, which proposes that encoding and retrieval occur at different points in the theta cycle to avoid interference.</p>
<p>The degree of phase shift between encoding and retrieval was relatively modest—typically around 40 to 90 degrees—falling short of the full 180-degree separation proposed in some models. Yet even smaller shifts may help segregate memory-related processes and reduce crosstalk between new learning and recall.</p>
<p>Theta-phase locking also varied by brain region. The parahippocampal cortex showed the highest percentage of neurons exhibiting phase locking, while the hippocampus had the lowest. This was not explained by differences in spike count or theta power across regions, indicating possible functional specialization in how different medial temporal areas contribute to rhythmic coordination.</p>
<p>In their analysis, the researchers also explored how both oscillatory (periodic) and non-oscillatory (aperiodic) components of the local field potential shaped phase locking. Steeper aperiodic slopes—reflecting greater inhibition—were associated with stronger phase locking, while flatter slopes corresponded with reduced synchronization. The study used a method called SPRiNT to estimate these aperiodic features over time, offering a more granular view of how internal dynamics fluctuate during memory tasks.</p>
<p>Despite the robust evidence for theta-phase locking, the study has some limitations. The number of encoding and retrieval events may have been too small to detect subtle performance-related effects, and the lack of a sharply defined stimulus onset may have reduced the likelihood of observing phase resets. The wide frequency range used to define theta (1–10 Hz) may also differ from narrower bands used in other studies, potentially complicating comparisons. Additionally, while the presence of phase locking suggests temporal organization, the functional consequences for memory processing remain a topic for further research.</p>
<p>“Although this synchronization was active during memory processes, we still don’t know exactly why it happens or how essential it is for memory,” Guth said. “More research is needed to see how it changes across different memory tasks.”</p>
<p>The study, “<a href="https://doi.org/10.1038/s41467-025-62553-9" target="_blank">Theta-phase locking of single neurons during human spatial memory</a>,” was authored by Tim A. Guth, Armin Brandt, Peter C. Reinacher, Andreas Schulze-Bonhage, Joshua Jacobs, and Lukas Kunz.</p></p>
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<td><a href="https://www.psypost.org/high-fat-fructose-diet-linked-to-anxiety-like-behavior-via-disrupted-liver-brain-communication/" 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;">High-fat fructose diet linked to anxiety-like behavior via disrupted liver-brain communication</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 24th 2025, 14:00</div>
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<p><p>A study on mice fed a high-fat fructose diet to induce a condition resembling non-alcoholic fatty liver disease in humans suggests that liver damage from this diet triggers neuroinflammation and anxiety-like behaviors by disrupting communication between the liver and the brain. The research was published in <a href="https://doi.org/10.1007/s00213-025-06820-z"><em>Psychopharmacology</em></a>.</p>
<p>Non-alcoholic fatty liver disease (NAFLD) is a condition in which excess fat builds up in the liver of individuals who consume little or no alcohol. It has become one of the most common liver disorders worldwide and is associated with obesity, type 2 diabetes, and metabolic syndrome. NAFLD can range from simple steatosis (fat accumulation without inflammation) to non-alcoholic steatohepatitis, which involves liver inflammation and can progress to fibrosis or cirrhosis—the most severe stages of liver damage.</p>
<p>Many people with NAFLD have no symptoms, although some may experience fatigue, discomfort in the upper right abdomen, or mild liver enlargement. The exact cause of NAFLD remains unclear, but insulin resistance, poor diet, and physical inactivity are considered major risk factors.</p>
<p>Currently, lifestyle changes such as weight loss, healthy eating, and regular exercise are the primary treatments, as no specific medications for NAFLD have been approved. Without intervention, the disease can increase the risk of liver failure, cardiovascular disease, and liver cancer. Prevention strategies focus on maintaining a healthy weight, managing blood sugar, and limiting processed foods and added sugars.</p>
<p>Study author Hongmei Du and colleagues aimed to explore the relationship and underlying mechanism between liver injury caused by a high-fat fructose diet and the emergence of anxiety-like behaviors in mice. They also sought to determine whether corilagin—a natural compound with hepatoprotective properties—could mitigate the behavioral and physiological effects of liver injury.</p>
<p>Corilagin is an ellagitannin (a type of hydrolysable tannin) found in various medicinal plants. It is one of the main phenolic compounds in longan fruit (Dimocarpus longan), especially concentrated in the seed and pericarp. Prior research has shown that corilagin can reverse fatty liver changes in mice by reducing blood lipid levels, hepatic lipid accumulation, and abnormal lipid metabolism.</p>
<p>In this study, 26 male mice were randomly assigned to three groups. The first group received a standard diet. The second group was fed a high-fat diet and given 12.5% fructose syrup as drinking water to induce NAFLD. The third group received the same high-fat fructose diet along with intraperitoneal injections of corilagin every other day (2.5 mg/kg).</p>
<p>To test whether corilagin had direct effects on anxiety independent of liver damage, the researchers also established four additional groups with another 27 mice. One group was fed a normal diet, the second received corilagin while on a normal diet, the third was exposed to chronic social defeat stress (CSDS) to induce anxiety-like behavior, and the fourth received corilagin during CSDS exposure. Importantly, the CSDS model induces anxiety symptoms through social stress rather than metabolic damage, allowing the researchers to isolate liver-dependent effects.</p>
<p>After these treatments, all mice underwent a battery of behavioral tests to assess anxiety-like behavior. Researchers then conducted biochemical analyses on blood and brain tissue to assess inflammation and glutamate levels.</p>
<p>The results showed that mice fed the high-fat fructose diet developed anxiety-like behaviors, along with elevated levels of fat and glutamate in the blood. They also developed liver damage, with fat accumulation in hepatic tissue and elevated levels of liver injury markers (ALT and AST). In addition, inflammation markers—including IL-6, IL-1β, and TNF-α—were elevated not only in the liver but also in the hippocampus and cortex, suggesting that liver damage triggered neuroinflammation.</p>
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<p>Treatment with corilagin alleviated these physiological and behavioral changes. It reduced hepatic fat accumulation, normalized glutamate levels in the blood and brain, lowered inflammatory markers, and reduced anxiety-like behaviors in the mice fed the high-fat fructose diet.</p>
<p>However, when anxiety-like behavior was induced through chronic social defeat stress in mice without liver damage, corilagin did not improve symptoms. This suggests that its behavioral benefits are tied to its ability to protect liver function and prevent downstream effects on the brain, rather than a direct anxiolytic effect.</p>
<p>“Our results indicated that the HFFD-induced NAFLD [high-fat fructose diet-induced non-alcoholic fatty liver disease] and mild hepatic fibrosis led to elevated levels of glutamate and aminotransferases, which infiltrated the brain, causing inflammation, and subsequently induced anxiety-like behaviors in mice. These pathological and behavioral manifestations were ameliorated through corilagin intervention. This study provides a possible underlying mechanism between HFFD and neurological disorders,” the study authors concluded.</p>
<p>The study sheds light on the effects of liver damage caused by the non-alcoholic fatty liver disease on brain and mental health. However, it should be noted that this was a study on mice, not on humans. While mice and humans share many physiological similarities, they are still very different species. Results on humans might not be identical.</p>
<p>The paper, “<a href="https://doi.org/10.1007/s00213-025-06820-z">High-fat Fructose diet induces neuroinflammation and anxiety-like behaviors by modulating liver-brain axis communication,</a>” was authored by Hongmei Du, Yuan Zhou, Jia Wang, Xianbing Bai, Borui Tao, and Ming Chen.</p></p>
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<td><a href="https://www.psypost.org/study-finds-trump-and-harris-used-distinct-rhetoric-in-2024-but-shared-more-similarities-than-expected/" 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;">Study finds Trump and Harris used distinct rhetoric in 2024—but shared more similarities than expected</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Aug 24th 2025, 12:00</div>
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<p><p>A new linguistic analysis published in <em><a href="https://doi.org/10.1371/journal.pone.0324715" target="_blank" rel="noopener">PLOS One</a></em> suggests that Donald Trump and Kamala Harris employed distinct rhetorical strategies during the U.S. presidential debate—but they also shared several unexpected linguistic similarities. The findings indicate that some stylistic differences commonly associated with Republican and Democratic rhetoric may have blurred during the high-stakes debate.</p>
<p>Political debates provide a unique opportunity to analyze how candidates craft their language in real time, under pressure, while addressing voters from across the political spectrum. The researchers behind the study aimed to determine whether Trump and Harris’ rhetorical styles aligned with broader patterns typically associated with their respective parties.</p>
<p>Previous work suggests that Democrats tend to emphasize inclusivity, empathy, and collective responsibility, while Republicans focus on individual authority, traditional values, and strength. The new study sought to examine whether such tendencies were reflected in the candidates’ language during the 2024 debate.</p>
<p>“My research group is funded by an EU grant for <a href="https://www.abstractionproject.eu/" target="_blank" rel="noopener">the ABSTRACTION Project</a>, where we investigate how language and word choice in particular shapes abstract thinking and social interaction,” explained corresponding author <a href="https://www.unibo.it/sitoweb/m.bolognesi/en">Marianna Bolognesi</a>, a professor of linguistics at the University of Bologna and principal investigator of the ABSTRACTION Project.</p>
<p>“The 2024 Trump–Harris debate offered a valuable case study to test whether the ‘red’ and ‘blue’ language styles identified in previous research would persist when both candidates were confronted with the same questions under identical constraints. We expected to find clear differences, but instead observed far fewer than anticipated, suggesting that both candidates adjusted their language to the context of the debate.”</p>
<p>For the study, Bolognesi and her co-author Philipp Wicke analyzed full transcripts of the September 2024 debate between Trump and Harris, broadcast on ABC News. The researchers used a mixed-methods approach combining large language models, lexical databases, and human annotation. They assessed over 100 individual responses from Trump and Harris, applying both manual and automated tools to identify linguistic patterns.</p>
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<p>Among the methods used were GPT-4o for figurative framing detection, SiEBERT for sentiment polarity analysis, and DeBERTa for political ideology classification. Word specificity was assessed using the WordNet hierarchy, while concreteness was evaluated using human-rated norms. The researchers also manually counted pronoun usage and tracked the number of direct references each candidate made to their opponent.</p>
<p>One of the most striking contrasts between the two candidates lay in their use of figurative frames. Trump frequently described the nation as being under siege, using metaphors of collapse and invasion. He portrayed immigration as a “flood” or “invasion,” the economy as being “sold down the tubes,” and societal decay as a “bloodbath” or “crime through the roof.” This framing leaned on hyperbole and catastrophe, aiming to evoke fear, urgency, and a need for drastic change.</p>
<p>Harris, on the other hand, used frames focused on resilience, rebuilding, and unity. She described economic recovery as “lifting up the middle class” and referred to American democracy as something to be “defended” and “restored.” Her use of metaphor tended to focus on collaboration and moving forward, such as “charting a new way forward” or “cleaning up Donald Trump’s mess.”</p>
<p>Harris used figurative framing more frequently than Trump. On average, she employed nearly three frames per response, while Trump used about one and a half. These frames were validated through a combination of large language model analysis and manual annotation, with high agreement between human raters.</p>
<p>Contrary to expectations, there were no meaningful differences in lexical specificity between the candidates. Both Trump and Harris used language with similar levels of detail, based on the depth of words within the WordNet semantic hierarchy. This finding challenges the assumption that Democrats tend to be more policy-dense and Republicans more slogan-driven in debates. It may reflect the fact that both candidates were responding to the same questions and attempting to appeal to a national audience.</p>
<p>“Most of the findings were surprising, but one unexpected result was that Trump and Harris did not differ significantly in the specificity of their answers, both blended general claims with specific examples,” Bolognesi told PsyPost.</p>
<p>Similarly, both candidates predominantly used abstract language. While Harris’ word choices were marginally more concrete, both fell near the abstract end of the concreteness scale. The authors suggest this may reflect a broader strategic aim: abstract language can invite broader interpretation and engagement, while more concrete language may narrow a candidate’s message.</p>
<p>“The more interesting divergence emerged in word abstractness, that is, in their use of terms referring to intangible entities: Harris remained fairly consistent in relying on abstract terminology, while Trump shifted more sharply between concrete terms such as <i>jobs</i> and <i>borders</i> and sweeping abstractions like <i>American greatness</i>,” Bolognesi said. “This was unexpected, since prior research led us to anticipate Harris would rely more on abstract but specific terms, and Trump on concrete but generic language.”</p>
<p>While both candidates relied heavily on emotionally charged language, the study found no statistically significant difference in the overall emotional polarity of their responses. Both Trump and Harris tended toward negative sentiment, a pattern that aligns with prior research showing that modern political communication often uses fear and outrage to galvanize audiences.</p>
<p>However, Harris was found to use more subjective language than Trump. Her responses included more expressions of personal judgment and moral perspective, while Trump’s statements were more likely to be framed as statements of fact, even when they involved speculation or exaggeration. This subjectivity was measured using two independent models, both of which yielded consistent results.</p>
<p>“We also found no significant difference in the emotional valence of the words they used: both relied heavily on terms with slightly negative connotations, contrary to our expectation that Trump would be more negative and Harris more positive,” Bolognesi said. “Another striking finding was that Harris used more subjective language, framing issues in terms of empathy, moral judgment, and personal perspective, while Trump’s rhetoric appeared more objective, often presented as statements of fact.”</p>
<p>The researchers uncovered marked differences in how each candidate addressed their opponent and constructed social identity. Trump did not refer to Harris by name even once during the debate, while Harris mentioned Trump by name 70 times—more than half of her responses included direct references to him. This contrast likely reflects differing rhetorical strategies: Harris leaned into confrontation and accountability, while Trump avoided direct acknowledgment of his opponent, possibly to minimize her perceived legitimacy.</p>
<p>In terms of pronouns, Trump used first-person singular forms like “I” and “me” 245 times, while inclusive pronouns like “we” and “us” appeared only 133 times. Harris showed a more balanced ratio, using singular pronouns 144 times and inclusive ones 136 times. This supports the hypothesis that Republican rhetoric tends to emphasize individual leadership, while Democratic discourse emphasizes collective responsibility.</p>
<p>Using a political ideology classifier, the researchers assessed whether each candidate’s statements aligned more with Democratic or Republican ideals. As expected, the vast majority of Trump’s responses were labeled Republican, while Harris’ leaned Democratic.</p>
<p>“Word choice is never random: it shapes how issues are framed, and determines which audiences feel aligned and which feel alienated,” Bolognesi told PsyPost. “As expected, Harris tended to emphasize empowerment and recovery with positive figurative frames and metaphorical language (“we will move forward”), while Trump leaned on crisis narratives (‘our country is collapsing’), a pattern confirmed by our statistical analyses. We also found that Trump relied more on singular pronouns (‘I built’), whereas Harris balanced singular and plural forms (‘we will fight together’). Finally, Trump avoided mentioning Harris by name, while Harris frequently invoked Trump directly, another telling difference in rhetorical style.”</p>
<p>While the study provides a comprehensive look at how language shaped the 2024 debate, some limitations are worth noting. The use of automated tools, while powerful, may miss nuances in meaning or context. The sample also reflects just one debate, meaning the findings might not generalize to other events or forms of political speech.</p>
<p>“One key point we highlight in the interpretation of our findings is that this was a presidential debate addressed to the entire electorate, not a partisan rally,” Bolognesi noted. “Because the audience was broader and more heterogeneous, both candidates likely adjusted their linguistic strategies, which helps explain why some of the differences we expected based on previous research were less pronounced. This also shows that both candidates possess a flexible vocabulary, to adapt to different communicative contexts.”</p>
<p>Future research may investigate how these linguistic patterns shift across multiple debates or differ from spontaneous remarks made during town halls or campaign rallies. The researchers are also examining non-political contexts to determine whether similar rhetorical strategies appear outside the political arena.</p>
<p>“Political language is just one of the discourse genres we are examining,” Bolognesi explained. “Within the ERC ABSTRACTION project, we are also studying other domains—for example, everyday conversations, where we’ve found that abstract words tend to spark curiosity and keep dialogue going, while concrete words often close the exchange. We are also analyzing how the same scientific topic is explained differently depending on the audience’s expertise (children, adults, experts, non-experts), and how these choices shape understanding. Another strand of our work focuses on the development of language-mediated abstraction skills in children, exploring how word use influences their ability to think and reason abstractly.</p>
<p>“One of our key standpoints is that effective communication requires a repertoire of words across different levels of abstraction, allowing speakers to adapt to different audiences—whether experts, non-experts, children, or voters,” Bolognesi added. “In the debate, both Trump and Harris showed this skill, aligning more closely with each other than with the partisan styles typical of campaign rallies. To foster this ability in children and adults, in both English and Italian, we developed Word Ladders, a research-based linguistic game that trains users to move flexibly between concrete and abstract words. The app is free, ad-free, and available here: <a href="https://www.abstractionproject.eu/playthegame" target="_blank" rel="noopener">https://www.abstractionproject.eu/playthegame</a>.”</p>
<p>The study, “<a href="https://doi.org/10.1371/journal.pone.0324715" target="_blank" rel="noopener">Red and blue language: Word choices in the Trump and Harris 2024 presidential debate</a>,” was published June 3, 2025.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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