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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/scientists-identify-key-brain-mechanism-behind-ayahuascas-ability-to-reduce-ptsd-symptoms/" 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 identify key brain mechanism behind ayahuasca’s ability to reduce PTSD symptoms</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 9th 2026, 06:00</div>
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<p><p>New research published in <em><a href="https://doi.org/10.1016/j.euroneuro.2025.11.009" target="_blank" rel="noopener">European Neuropsychopharmacology</a></em> provides evidence that the psychedelic brew ayahuasca can facilitate the extinction of severe, trauma-like fear memories in rats. The findings suggest that this effect depends on specific neuroplasticity mechanisms within the prefrontal cortex involving a protein known as brain-derived neurotrophic factor. By targeting these pathways, the treatment also appears to reduce the tendency to perceive safe environments as threatening.</p>
<p>Post-traumatic stress disorder is characterized by fear memories that are overgeneralized and resistant to standard extinction procedures. Standard laboratory models often use mild aversive conditioning that does not fully capture the persistence or intensity of traumatic memories found in humans.</p>
<p>The authors of the new study sought to address this gap by utilizing protocols that induce stronger, more resilient fear memories. They aimed to determine if ayahuasca could help attenuate these maladaptive memories and to identify the specific brain mechanisms responsible for such effects.</p>
<p>Previous studies have indicated that the infralimbic region of the medial prefrontal cortex is essential for fear extinction. This brain area exerts inhibitory control over fear circuits in the amygdala. It is also rich in serotonin receptors, which are the primary targets of the psychoactive compounds found in ayahuasca. The researchers hypothesized that the brew might enhance extinction learning by modulating plasticity in this region through brain-derived neurotrophic factor signaling.</p>
<p>“Rodent studies showing that psychedelic compounds enhance memory extinction have used standard fear conditioning procedures, producing moderate and specific aversive memories that do not capture key features of the memories underlying post-traumatic stress disorder (PTSD), including a relative resistance to extinction and fear overgeneralization,” explained study author <a href="https://orcid.org/0000-0003-2876-1146" target="_blank" rel="noopener">Leandro J. Bertoglio</a>, a professor of pharmacology at the Federal University of Santa Catarina.</p>
<p>“We aimed to test whether ayahuasca, a brew containing the serotonergic psychedelic N,N-dimethyltryptamine (DMT), could facilitate fear extinction and reduce generalization under more trauma-like conditions, and to examine the brain mechanisms involved. We focused on brain-derived neurotrophic factor (BDNF)-tyrosine kinase B (TrkB) receptor signaling in the infralimbic cortex because fear extinction depends on this neuroplastic pathway.”</p>
<p>The researchers employed a total of 303 adult Wistar rats, split almost evenly between males and females. The study utilized a batch of ayahuasca donated by a branch of the Santo Daime church in Brazil. The brew was analyzed to ensure specific concentrations of its active alkaloids, including DMT and harmine. The animals received an oral dose containing 0.3 mg/kg of DMT. This dose was selected because prior research indicated it enhances fear extinction without causing significant changes in locomotor activity.</p>
<p>The researchers conducted four distinct experiments to isolate variables and mechanisms. In the first experiment, they investigated the effect of prior stress on fear extinction. Half of the rats were subjected to restraint stress, where they were confined in a perforated plastic tube for 30 minutes. This procedure is known to impair the ability to extinguish fear later. On the following day, all animals underwent fear conditioning, where they were placed in a specific chamber (Context A) and received mild electric foot shocks.</p>
<p>After conditioning, the rats underwent two extinction sessions on consecutive days. During these sessions, they were placed back in the dangerous context without receiving any shocks. The researchers administered either ayahuasca or a water vehicle orally one hour before each of these sessions. The primary measure of fear was “freezing behavior,” defined as the complete absence of movement except for breathing.</p>
<p>The results showed that the rats exposed to restraint stress exhibited deficits in extinguishing their fear compared to non-stressed controls. They continued to freeze at high rates even after repeated exposure to the safe context. However, the stressed rats treated with ayahuasca showed a marked improvement. They learned that the context was safe much faster than the vehicle-treated stressed rats.</p>
<p>In addition to extinction, the researchers measured fear generalization. This occurs when an animal shows fear in a neutral, novel environment (Context B) that was never associated with pain. Stressed animals typically show high fear generalization. The study found that ayahuasca treatment reduced freezing in the neutral context, effectively restoring the ability of the rats to discriminate between dangerous and safe environments.</p>
<p>The second experiment tested whether ayahuasca could mitigate the effects of high-intensity trauma. Instead of restraint stress, the researchers varied the intensity of the electric shock during the initial conditioning phase. One group received standard shocks (1.0 mA), while another received high-intensity shocks (1.3 mA). The high-intensity group displayed persistent fear that was difficult to extinguish and showed high levels of generalization.</p>
<p>Consistent with the first experiment, ayahuasca treatment facilitated extinction in the high-intensity shock group. These rats reduced their freezing levels more than the control group receiving the same high-intensity shocks. The treatment also successfully reduced fear generalization in both male and female rats, preventing them from freezing in the neutral environment.</p>
<p>“Ayahuasca with low DMT content helped both female and male rats learn and later remember that an environment previously associated with danger (footshocks) was now safe,” Bertoglio told PsyPost. “This treatment also decreased the tendency to misinterpret a neutral environment as threatening (and thus express fear responses).”</p>
<p>The third and fourth experiments were designed to pinpoint the biological mechanism behind these behavioral changes. The researchers focused on the infralimbic cortex. They performed stereotaxic surgery to implant guide cannulas directly into this brain region. This allowed them to infuse drugs locally to block specific molecular pathways.</p>
<p>In the third experiment, the researchers infused an antibody that neutralizes brain-derived neurotrophic factor (BDNF) directly into the infralimbic cortex. This was done ten minutes before the extinction sessions, following the oral administration of ayahuasca. The goal was to see if removing available BDNF would prevent ayahuasca from working.</p>
<p>The data revealed that blocking BDNF in the infralimbic cortex completely abolished the beneficial effects of ayahuasca on fear extinction. Rats treated with ayahuasca and the anti-BDNF antibody froze just as much as the vehicle-treated controls. This suggests that the presence of BDNF in this brain region is required for ayahuasca to enhance the relearning of safety.</p>
<p>The researchers also observed a sex difference regarding fear generalization in this experiment. Blocking BDNF in the infralimbic cortex prevented the reduction of generalized fear in female rats. However, in male rats, the antibody did not stop ayahuasca from reducing fear in the neutral context.</p>
<p>The fourth experiment targeted the TrkB receptor, which is the primary receptor that BDNF activates. The researchers infused a selective antagonist called ANA-12 into the infralimbic cortex. This drug prevents BDNF from binding to its receptor and initiating intracellular signaling.</p>
<p>The results mirrored those of the antibody experiment. Blocking the TrkB receptor prevented ayahuasca from facilitating fear extinction in both male and female rats. This confirms that the entire BDNF-TrkB signaling pathway in the infralimbic cortex is necessary for the therapeutic-like effects of the drug on traumatic memories. Similar to the previous experiment, blocking this receptor prevented the reduction of fear generalization in females but not in males.</p>
<p>“We found that blocking BDNF-TrkB receptor signaling in the infralimbic cortex prevented the beneficial effects of ayahuasca on fear extinction, providing evidence of a causal mechanism,” Bertoglio explained. “Interestingly, we observed sex-dependent effects on fear generalization. The tested experimental interventions prevented ayahuasca-induced reductions in fear generalization in females but not in males.”</p>
<p>“These findings indicate biological differences that warrant further study. Brain circuits responsible for fear overgeneralization differ between sexes, which could lead to personalized therapeutic strategies based on sex/gender differences.”</p>
<p>These findings suggest that the infralimbic cortex is a critical site of action for ayahuasca. The drug appears to stimulate plasticity in this region, likely by increasing the excitability of neurons and promoting the release of neurotrophic factors. This plasticity allows the brain to overwrite the traumatic memory with a new safety memory.</p>
<p>“The effects were replicated in two protocols that induce aversive memories with PTSD-like features, including prior stress exposure and stronger, trauma-like conditioning,” Bertoglio said. “The measured effect size was large, with a decrease in the fear response of more than 70% relative to the control groups. These data indicate that the effects are substantial and not limited to normative laboratory conditions, suggesting potential translational relevance.”</p>
<p>But the study still has some limitations. The experiments were conducted on rodents, and translational research in humans is necessary to confirm if similar mechanisms apply. The researchers utilized a specific low dose of DMT within the brew, and it is unknown if higher, hallucinogenic doses would recruit different mechanisms or brain regions.</p>
<p>“These results come from controlled animal experiments and do not indicate that ayahuasca is ready for clinical use in treating trauma,” Bertoglio noted. “Instead, the study identifies mechanisms and conditions that may guide future research and clinical translation.”</p>
<p>The sex differences observed in the mechanism of fear generalization also warrant further investigation. While the infralimbic cortex was essential for females, males appeared to rely on other neural circuits for this specific aspect of fear processing. Other regions such as the hippocampus or the amygdala might play a more prominent role in males for distinguishing between contexts under the influence of ayahuasca.</p>
<p>The research highlights the potential of psychedelic compounds to treat conditions involving rigid, maladaptive memories. By combining behavioral protocols that mimic the severity of trauma with precise molecular manipulations, the study provides a detailed map of how ayahuasca may help the brain recover from intense stress.</p>
<p>“The following steps include testing boundary conditions and potential moderating factors in rodents and translating these mechanistic findings and insights into clinical research through our human studies arm,” Bertoglio said. “We are particularly interested in how psychedelics can safely enhance extinction-based treatments.”</p>
<p>“A noteworthy aspect of the work is that the oral ayahuasca treatment was repeated twice but did not alter locomotion or anxiety, suggesting that neuroplastic mechanisms may be sufficient to enhance extinction. This supports the idea that therapeutic effects may not require strong acute behavioral effects. For context, the DMT content in our rodent study is approximately one-third of that typically used in human studies.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.euroneuro.2025.11.009" target="_blank" rel="noopener">Ayahuasca modulation of traumatic-like fear memories requires infralimbic cortex BDNF-dependent mechanisms in rats</a>,” was authored by Isabel Werle, Francisco S. Guimarães, Rafael G. dos Santos, Jaime E.C. Hallak, and Leandro J. Bertoglio.</p></p>
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<td><a href="https://www.psypost.org/personality-traits-shape-how-pilots-react-to-simulated-in-flight-crises/" 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;">Personality traits shape how pilots react to simulated in-flight crises</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 20:00</div>
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<p><p>A recent psychological analysis suggests that a pilot’s inherent personality traits may predict their stress levels during in-flight emergencies more accurately than their professional experience does. The findings indicate that pilots with a natural disposition toward anxiety experience heightened stress during simulated hazards, regardless of how many hours they have flown. This research was published in the journal <em><a href="https://doi.org/10.1027/2192-0923/a000283" target="_blank">Aviation Psychology and Applied Human Factors</a></em>.</p>
<p>Commercial aviation maintains an exceptional safety record, yet accidents involving a loss of control in-flight remain a primary concern for the industry. These catastrophic events often begin with an unexpected disruption, such as a sudden system failure or a severe weather event. When a pilot encounters such a threat, the immediate human reaction is often a physiological startle response.</p>
<p>This reflex can be followed by a cognitive state known as surprise. Surprise occurs when there is a mismatch between what a pilot expects the aircraft to do and what is actually happening. This mental disconnect can impair a pilot’s ability to process information and execute the correct procedures.</p>
<p>Airlines typically select pilots based on their emotional stability and ability to handle pressure. Researchers aimed to determine if subtle individual differences within this highly selected group still influence performance during critical moments. Jiayu Chen, a researcher at the Delft University of Technology in the Netherlands, led the investigation.</p>
<p>Chen worked alongside colleagues to better understand how specific personality profiles interact with sudden cockpit crises. The team sought to identify whether a pilot’s baseline anxiety or their ability to regulate emotions could predict their reaction to a startle. They also investigated whether the accumulation of flight hours provided a buffer against the psychological shock of an emergency.</p>
<p>To answer these questions, the researchers compiled and analyzed data from four separate experiments. These studies were conducted in high-fidelity, motion-based flight simulators. The combined dataset included eighty-nine licensed commercial airline pilots.</p>
<p>Before entering the simulator, each pilot completed a series of standardized psychological questionnaires. The researchers used these surveys to assess “trait anxiety.” This psychological concept describes a stable behavioral disposition to perceive a wide range of situations as threatening.</p>
<p>The team also measured a trait known as “action orientation.” This metric assesses a person’s capacity to stay focused on a goal and regulate their emotions under pressure. It distinguishes between individuals who can detach from irrelevant concerns and those who tend to dwell on a problem.</p>
<p>Pilots also provided their total flight hours to allow the researchers to gauge their experience levels. Once the preliminary data was collected, the pilots entered the simulator to perform routine flight tasks. During these flights, the researchers introduced a variety of startling and surprising scenarios.</p>
<p>The simulated hazards included engine failures, malfunctions with the rudder, or erroneous readings on the airspeed indicators. These events were designed to be unpredictable and jarring. After handling each emergency, the pilots rated their subjective experiences on several scales.</p>
<p>Participants scored how startled and surprised they felt during the specific event. They also rated their acute stress levels and the amount of mental workload required to manage the situation. The researchers then used statistical methods to look for correlations between the pilots’ personality traits and their reported reactions.</p>
<p>The analysis revealed a specific link between a pilot’s inherent anxiety levels and their physiological reaction to the hazards. Pilots with higher scores in trait anxiety reported feeling higher levels of stress during the simulated emergencies. This suggests that a baseline disposition toward anxiety makes an individual more sensitive to the pressure of an unexpected crisis.</p>
<p>This correlation held true even though the participants were professional pilots who had passed rigorous industry selection processes. The study supports the idea that personality traits interact with the environment to amplify acute stress. A pilot prone to anxiety appears to experience the “fight-or-flight” response more intensely when things go wrong.</p>
<p>The study produced results regarding flight experience that contradict common assumptions. The data showed that the number of hours a pilot had flown did not possess a statistically significant correlation with their reported levels of startle, surprise, or stress. A veteran captain was just as likely to feel overwhelmed by a sudden malfunction as a pilot with much less time in the cockpit.</p>
<p>This finding implies that familiarity with routine flying does not necessarily blunt the physiological shock of a startling event. The novelty of the hazard affects experienced and novice pilots in a similar fashion. This challenges the notion that experience alone is a sufficient shield against the cognitive effects of surprise.</p>
<p>The researchers also looked for effects related to action orientation. They hypothesized that pilots who are naturally better at regulating their emotions would report lower stress or startle. The data did not provide evidence to support this prediction.</p>
<p>There were no statistically significant effects of action orientation on how the pilots perceived the startle or workload. This lack of correlation might be due to the nature of the pilot population. The participants generally possessed high levels of action orientation, making it difficult to distinguish effects based on this trait.</p>
<p>The study did find strong internal connections between the different sensations the pilots reported. If a pilot felt a high level of mental workload, they were very likely to also report high levels of stress and surprise. This suggests these cognitive and emotional responses feed into one another.</p>
<p>When a pilot struggles to understand a confusing situation, the mental effort required rises. This increased demand appears to drive up their acute stress levels. The findings highlight the complex mental environment a pilot must navigate when a routine flight turns dangerous.</p>
<p>There are several limitations to this analysis that provide context for the results. The pilots involved in the study were a relatively uniform group who volunteered for the research. They generally possessed lower anxiety and better emotional regulation than the general population.</p>
<p>This lack of diversity in the sample might have masked the influence of certain personality traits. Additionally, the study relied on the pilots to rate their own feelings after the fact. Self-reported data can sometimes be less accurate than physiological measurements taken in real-time.</p>
<p>The simulated scenarios were also flown manually in a specific aircraft model. This setup might not perfectly replicate the highly automated environment of a modern airliner cruising at high altitude. The workload in the study was generated by manual flying rather than complex system management.</p>
<p>Chen and the team suggest that future research should incorporate physiological sensors to track stress markers like heart rate. They also recommend testing these dynamics in scenarios that require crew collaboration. Understanding these individual differences is necessary for designing better training programs.</p>
<p>The study, “<a href="https://doi.org/10.1027/2192-0923/a000283" target="_blank">The Effect of Personality Traits and Flight Experience on Pilots’ Cognitive and Affective Responses to Simulated In-Flight Hazards</a>,” was authored by Jiayu Chen, Annemarie Landman, Olaf Stroosma, M. M. van Paassen, and Max Mulder.</p></p>
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<td><a href="https://www.psypost.org/sex-differences-in-brain-volume-emerge-before-birth-groundbreaking-research-suggests/" 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;">Sex differences in brain volume emerge before birth, groundbreaking research suggests</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 18:00</div>
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<p><p>A new study published in <em><a href="http://dx.doi.org/10.1038/s41598-025-33981-w" target="_blank">Scientific Reports</a></em> provides a detailed model of how the human brain develops during the transition from the womb to early infancy. The findings indicate that distinct growth patterns for different brain tissues and sex-based differences in brain volume are established between mid-pregnancy and the first weeks of life. This research offers a continuous view of how the brain expands during a foundational period that was previously difficult to map.</p>
<p>The perinatal period involves rapid biological changes that establish the core architecture of the human brain. This phase includes the processes where cells proliferate, migrate to their correct locations, and begin forming complex connections. Scientists have often studied prenatal development and postnatal development separately because of the technical challenges involved in imaging fetuses compared to newborns. This separation has historically made it difficult to understand exactly how growth trajectories evolve as a fetus becomes an infant.</p>
<p>To bridge this gap, a research team led by the University of Cambridge aimed to create a unified model of early brain growth. Yumnah T. Khan, a PhD student at the Autism Research Centre at the University of Cambridge, led the investigation. The team sought to determine when specific tissues dominate growth and when sex differences in brain size first appear. By combining data from before and after birth, they hoped to capture the dynamic nature of brain structural changes.</p>
<p>The researchers utilized data from the Developing Human Connectome Project, which is a large-scale initiative designed to map brain connectivity. The final dataset included 798 magnetic resonance imaging scans collected from 699 unique individuals. These participants included 263 fetuses scanned while in the womb and 535 newborns.</p>
<p>The sample consisted of 380 males and 319 females. The scans covered a developmental window ranging from just over 21 weeks to nearly 45 weeks after conception. This allowed the team to track changes across the second and third trimesters of pregnancy and into the first month after birth.</p>
<p>The team used advanced statistical modeling to chart the volume of different brain tissues against the age of the individuals. They applied corrections to account for the natural variance that increases as infants grow older. The analysis focused on total brain volume as well as specific compartments like gray matter, white matter, and cerebrospinal fluid.</p>
<p>The analysis revealed that the total volume of the brain grows at an increasing rate leading up to birth. When the researchers accounted for the exact age at the time of the scan, they observed a slight slowing of this growth rate in the weeks immediately following birth. This suggests the most rapid expansion occurs just before and shortly after delivery.</p>
<p>Different types of brain tissue followed their own unique timelines. White matter, which forms the connections between brain cells, was the primary driver of growth during mid-pregnancy. However, its proportional contribution to the total brain size decreased over time. This suggests the brain prioritizes establishing core connectivity pathways early in gestation.</p>
<p>In contrast, gray matter, which contains the cell bodies of neurons and is involved in processing information, became the dominant driver of growth during late pregnancy and the postnatal period. This shift indicates a transition from laying down connections to the proliferation and maturation of processing centers. The rapid growth of gray matter likely supports the development of sensory and motor abilities needed for survival after birth.</p>
<p>The study also looked at deep brain structures known as subcortical regions. These areas, such as the amygdala and thalamus, showed an earlier peak in their growth rates compared to the outer layer of the brain, the cortex. The cortex is typically associated with higher-level cognitive functions.</p>
<p>The finding that subcortical structures mature faster aligns with the understanding that regions responsible for basic physiological and sensory functions develop before those involved in complex thought. The researchers observed that the cerebellum, a region critical for motor control, showed exponential growth throughout the studied period. This rapid expansion likely facilitates the early coordination required for an infant’s movements.</p>
<p>A major component of the analysis involved comparing brain development between males and females. The data showed that, on average, males experienced greater increases in brain volume as they aged compared to females. This difference was observable across the entire brain and within specific regions.</p>
<p>The researchers found that these sex differences were generally linear, meaning males consistently showed faster growth. This provides evidence that sex differences in brain structure are not solely a result of social or environmental influences after birth. Instead, biological factors present during pregnancy appear to initiate these divergence patterns.</p>
<p>While males exhibited faster overall growth, the shape of the growth trajectories was largely similar between the sexes. Both males and females followed the same general patterns of tissue expansion. However, there were specific exceptions in regional development.</p>
<p>For example, parts of the temporal lobe showed more pronounced gray matter increases in males. Additionally, the team identified a distinct growth pattern in the left anterior cingulate gyrus. In this region, males showed an S-shaped growth curve, whereas females showed a linear trajectory.</p>
<p>The study faces certain limitations regarding the available data. The scans for fetuses did not begin until after 21 weeks of gestation, leaving the first half of pregnancy unmapped in this analysis. Additionally, the number of scans available for younger fetuses was smaller than for older infants, which could impact the precision of the early growth models.</p>
<p>The researchers also noted technical differences between how fetal and neonatal scans were acquired. Although the same scanner was used, the settings had to be adjusted for the different environments of the womb and the nursery. This could potentially introduce variations in the measurements, though the team observed strong continuity in the data.</p>
<p>While the study documents when sex differences emerge, it does not confirm the biological mechanisms causing them. The authors suggest that prenatal hormones like testosterone likely play a role. Male fetuses are exposed to a surge of testosterone between 14 and 18 weeks of gestation.</p>
<p>The timing of the observed structural differences, appearing after 18 weeks, corresponds with the aftermath of this hormonal surge. Future research will need to directly investigate the link between hormone levels and these structural changes to confirm causality. The researchers emphasize that understanding these typical growth trajectories provides a baseline for identifying atypical development.</p>
<p>This baseline could eventually help explain why certain neurodevelopmental conditions are more common in one sex than the other. For instance, autism is diagnosed more frequently in males. Understanding if and how early brain overgrowth relates to these conditions remains a priority for the field.</p>
<p>The team calls for further longitudinal studies to validate these findings over longer periods. Following the same individuals from pregnancy through childhood would provide even stronger evidence for these developmental patterns. The current study represents a significant step toward a complete map of early human brain development.</p>
<p>The study, “<a href="http://dx.doi.org/10.1038/s41598-025-33981-w" target="_blank">Mapping brain growth and sex differences across prenatal to postnatal development</a>,” was authored by Yumnah T. Khan, Alex Tsompanidis, Marcin A. Radecki, Carrie Allison, Meng-Chuan Lai, Richard A. I. Bethlehem and Simon Baron-Cohen.</p></p>
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<td><a href="https://www.psypost.org/changes-in-breathing-patterns-may-predict-moments-of-joy-before-they-happen/" 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;">Changes in breathing patterns may predict moments of joy before they happen</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 16:00</div>
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<p><p>Recent research suggests that the way a person breathes does more than simply sustain life. Respiratory patterns may actually predict moments of joy and excitement before they occur. A study published in the <em><a href="https://doi.org/10.1016/j.jad.2025.120686" target="_blank">Journal of Affective Disorders</a></em> found that specific changes in breathing dynamics are linked to surges in high-energy positive emotions. This connection appears to be particularly strong for individuals with a history of depression.</p>
<p>The findings offer a fresh perspective on the relationship between physiological processes and mental health. While traditional advice often focuses on slow breathing to calm the nerves, this new data indicates that more active breathing patterns may precede positive states of high arousal. The study was conducted by a team of researchers led by Sean A. Minns and Jonathan P. Stange from the University of Southern California.</p>
<p>Mental health professionals have long recognized a connection between the lungs and the mind. The field of psychology itself derives its name from the Greek word psyche, which shares a root with the word for breath. This relationship is often studied in the context of Major Depressive Disorder. This condition is characterized by persistent sadness and a broad impairment in daily functioning.</p>
<p>One of the most debilitating aspects of depression is anhedonia. This symptom refers to a reduced ability to experience pleasure or interest in life. Even after a person has recovered from a depressive episode, they may still struggle to experience positive emotions. This lingering deficit can increase the risk of the depression returning.</p>
<p>Most previous research has focused on how negative emotions alter breathing. For example, stress might cause a person to sigh more often or breathe erratically. There has been less investigation into how breathing relates to positive moods. This represents a gap in scientific understanding. Positive affect is a strong predictor of long-term recovery.</p>
<p>Psychologists often categorize emotions using a model that includes two dimensions. The first dimension is valence, which ranges from pleasant to unpleasant. The second dimension is arousal, which ranges from low energy to high energy. Joy and excitement are examples of high-arousal positive affect. Calmness and contentment are examples of low-arousal positive affect.</p>
<p>Individuals with depression often show a specific reduction in high-arousal positive emotions. They may feel calm, but they rarely feel enthusiastic. The researchers wanted to see if breathing patterns in daily life could predict these elusive states of high energy. They also wanted to know if this relationship worked differently for people who had previously suffered from depression compared to those who had not.</p>
<p>To investigate these questions, the team recruited seventy-three adults. The participants were divided into two groups. One group consisted of thirty-six individuals with a history of Major Depressive Disorder who were currently in remission. The second group consisted of thirty-seven healthy volunteers with no history of psychiatric issues.</p>
<p>The study employed a method known as Ecological Momentary Assessment. This approach allows scientists to collect data in the real world rather than in an artificial laboratory setting. For seven days, participants went about their normal lives while wearing a specialized piece of technology. This device was a “smart shirt” called the Hexoskin.</p>
<p>The Hexoskin is a garment worn under regular clothes. It contains sensors woven into the fabric that measure the expansion and contraction of the chest and abdomen. This allowed the researchers to continuously monitor respiratory metrics. The device measured breathing rate and the volume of air moved with each breath.</p>
<p>While wearing the shirts, participants received surveys on their smartphones at random times throughout the day. These surveys asked them to rate their current mood. The participants rated the intensity of various emotions, such as feeling cheerful, happy, or confident. They also reported on the strategies they were using to manage their emotions.</p>
<p>The researchers focused their analysis on the thirty-minute window immediately preceding each survey. By looking at the physiological data leading up to the mood report, they hoped to see if breathing changes happened before the emotional shift. This time-lagged design helps clarify the direction of the relationship.</p>
<p>The results revealed a clear pattern. When participants exhibited increases in minute ventilation and breathing rate, they were more likely to report high-arousal positive emotions thirty minutes later. Minute ventilation refers to the total amount of air a person breathes in one minute. Essentially, breathing faster and moving more air was a precursor to feeling joy and excitement.</p>
<p>The researchers then compared the two groups of participants. They found that this physiological link was present in both groups. However, the strength of the connection varied based on the participant’s medical history. The relationship between breathing and positive mood was notably stronger in the group with a history of depression.</p>
<p>For healthy controls, an increase in ventilation predicted a subtle increase in positive mood. For those with remitted depression, the same increase in ventilation predicted a much larger boost in positive mood. This suggests that for these individuals, physiological activation may be a requisite for experiencing joy.</p>
<p>The study also examined the role of emotion regulation strategies. The researchers looked specifically at a strategy called acceptance. Acceptance involves experiencing thoughts and feelings without judging them or trying to change them. It emphasizes openness to the present moment.</p>
<p>Participants who reported using acceptance more frequently showed a stronger link between their breathing and their mood. For those who rarely used acceptance, the connection between minute ventilation and positive emotion was statistically insignificant. This suggests that being open to one’s internal experience may allow physiological changes to more effectively influence emotional states.</p>
<p>The team also found a connection between breathing variability and regulation style. At the level of individual differences, people who had more variable depth of breath tended to use acceptance more often. This variability might reflect a flexible physiological system that adapts readily to different situations.</p>
<p>These findings challenge the common assumption that slower breathing is always better for mental health. While slow breathing can help reduce anxiety, it may not be the best tool for generating excitement or enthusiasm. High-energy positive states appear to be supported by a more active respiratory pattern.</p>
<p>The authors propose that individuals with a history of depression may rely more heavily on this physiological “ramp-up” to feel good. In healthy individuals, positive emotions might arise more easily without requiring such a strong physiological push. For those in remission, the body may need to work harder to generate the same level of joy.</p>
<p>There are several caveats to consider regarding this research. The study relied on wearable sensors that come in standard sizes. This led to issues with sensor fit for some participants with atypical body proportions. As a result, a portion of the respiratory data had to be excluded to ensure accuracy.</p>
<p>Additionally, the study was observational. It showed that breathing changes predict mood changes, but it cannot definitively prove that breathing causes the mood to change. It is possible that an unmeasured third variable influences both factors. The sample size was also relatively small, which limits how broadly the results can be generalized.</p>
<p>Despite these limitations, the implications for treatment are promising. The study suggests that respiratory patterns could serve as a target for new interventions. Therapies could potentially harness breathing techniques to help individuals with depression access high-energy positive states.</p>
<p>The researchers envision the possibility of “just-in-time” interventions. Wearable devices could monitor a person’s breathing in real time. If the device detects a pattern associated with low mood or disengagement, it could prompt the user to engage in specific breathing exercises. These exercises would be designed to increase ventilation and potentially spark a positive emotional shift.</p>
<p>This approach could be particularly useful for preventing relapse. Since the loss of joy is a major risk factor for the return of depression, finding ways to boost positive affect is a treatment priority. By understanding the physiological precursors of joy, clinicians may be able to offer more precise tools to their patients.</p>
<p>Future research will need to confirm these findings in larger groups. Scientists also need to determine if these patterns hold true for people currently experiencing a major depressive episode. The current study focused only on those in remission. It remains to be seen if the same dynamics apply during the acute phase of the illness.</p>
<p>The study provides a first step toward understanding the dynamic interplay between breath and joy in everyday life. It highlights the importance of looking beyond the laboratory to see how physiology functions in the real world. As technology improves, the ability to monitor and influence these processes will likely expand.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.jad.2025.120686" target="_blank">When breath lifts your mood: Dynamic everyday links between breathing, affect, and emotion regulation in remitted depression</a>,” was authored by Sean A. Minns, Bruna Martins-Klein, Sarah L. Zapetis, Ellie P. Xu, Jiani Li, Gabriel A. León, Margarid R. Turnamian, Desiree Webb, Archita Tharanipathy, Emily Givens, and Jonathan P. Stange.</p></p>
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<td><a href="https://www.psypost.org/attachment-anxiety-shapes-how-emotions-interfere-with-self-control/" 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;">Attachment anxiety shapes how emotions interfere with self-control</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 14:00</div>
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<p><p>Attachment anxiety shapes how people handle emotional conflict, and brief reminders of security or threat can shift that balance, according to research published in <a href="https://doi.org/10.1080/02699931.2025.2476679"><em>Cognition & Emotion</em></a>.</p>
<p>Everyday life requires us to focus on what matters while ignoring emotionally distracting information; this is known as emotional conflict control. Previous research shows that people differ in how well they manage this kind of emotional interference, and attachment theory suggests that these differences may stem from how secure or insecure people feel in close relationships. Individuals with anxious attachment, for example, tend to be highly sensitive to emotional cues, whereas avoidantly attached individuals often suppress emotional information in favor of control.</p>
<p>Drawing on the functional neuro-anatomical model of attachment, Mengke Zhang and colleagues conducted two experiments to examine how attachment styles and short-term attachment “priming” experiences relate to emotional conflict control.</p>
<p>In Experiment 1, 225 Chinese undergraduate students completed the Experiences in Close Relationships questionnaire, which assesses two core dimensions of adult attachment, including attachment anxiety and attachment avoidance. Participants then completed an emotional face-word Stroop task that required them to identify whether a face displayed a happy or fearful expression while ignoring a word superimposed on the face.</p>
<p>These words varied in emotional valence and in whether they were related to close relationships, allowing the task to generate emotional conflict when facial expressions and words conveyed mismatched emotional information.</p>
<p>Performance on the Stroop task was used to index emotional interference, with slower or less accurate responses on emotionally incongruent trials indicating greater difficulty resolving conflict between emotional and task-relevant information.</p>
<p>The second experiment extended this approach by examining situational influences on emotional conflict control. A separate sample of 185 undergraduates first completed the same attachment questionnaire and baseline mood ratings, then completed a brief writing-based priming task. Participants were randomly assigned to recall either a supportive attachment-related experience (attachment security priming), a distressing attachment-related experience (attachment threat priming), or a neutral interpersonal memory.</p>
<p>Following the priming manipulation, participants reported their momentary sense of attachment security or insecurity as well as changes in positive and negative emotions. They also completed a modified version of the emotional face-word Stroop task using attachment-related words only. This design allowed the researchers to test whether temporary shifts in attachment-related feelings altered emotional conflict control beyond individuals’ baseline attachment styles.</p>
<p>Across both experiments, attachment anxiety consistently emerged as the most important individual difference shaping emotional conflict control.</p>
<p>In the first experiment, individuals higher in attachment anxiety showed greater emotional interference on the Stroop task, particularly when distracting words were positive in emotional tone. This pattern suggests that anxiously attached individuals were more likely to have their attention drawn toward emotionally salient information, making it harder to suppress distractions and focus on the task at hand.</p>
<p>Attachment avoidance, in contrast, was not reliably associated with reduced emotional interference, indicating that the emotional demands of the face-word Stroop task may overwhelm avoidant individuals’ typical tendency to disengage from emotional material.</p>
<p>The second experiment showed that attachment security priming successfully increased participants’ immediate sense of attachment security, but it did not lead to uniform improvements in emotional control. Instead, among individuals high in attachment anxiety, greater feelings of security were associated with <em>increased</em> emotional interference, suggesting that security cues may heighten emotional engagement rather than dampen it for those who are chronically sensitive to relationship concerns. For individuals lower in attachment anxiety, security priming had little effect on emotional interference.</p>
<p>Attachment threat priming produced a different pattern. Compared to the neutral condition, threat priming reduced emotional interference overall, indicating improved emotional conflict control. This effect was especially pronounced among individuals low in attachment anxiety, who showed clear reductions in interference following threat cues.</p>
<p>Among individuals high in attachment anxiety, threat priming worked indirectly; increased feelings of attachment insecurity were associated with reduced emotional interference, suggesting that threat cues may shift attention away from emotional evaluation and toward cognitive control in this group.</p>
<p>Of note is that the study relied on undergraduate samples and laboratory-based tasks, which may limit how well the findings generalize to other populations or to real-world emotional challenges.</p>
<p>The research “<a href="https://doi.org/10.1080/02699931.2025.2476679">Attachment styles and attachment (in)security priming in relation to emotional conflict control</a>,” was authored by Mengke Zhang, Song Li, Xinyi Liu, Qingting Tang, Qing Li, and Xu Chen.</p></p>
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<td><a href="https://www.psypost.org/study-reports-associations-between-infants-head-growth-patterns-and-risk-of-autism/" 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 reports associations between infants’ head growth patterns and risk of autism</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 12:00</div>
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<p><p>A study of infants during their first year of life conducted in Israel found that children with consistently small or large head circumferences had around three times higher odds of being diagnosed with autism compared to infants whose head circumference was consistently medium. These odds were 6–10 times higher in the 5% of infants with the smallest head circumferences and the 5% of infants with the largest head circumferences. The research was published in <a href="https://doi.org/10.1002/aur.70172"><em>Autism Research</em></a>.</p>
<p>Autism, or autism spectrum disorder, is a neurodevelopmental condition characterized by differences in social communication, social interaction, and patterns of behavior, interests, or sensory processing. It is described as a spectrum because the type and intensity of characteristics vary widely between individuals.</p>
<p>Autism typically emerges in early childhood, although it may be formally diagnosed later in life. Researchers have investigated ways to detect autism in early childhood, and some studies suggested that abnormal head growth patterns in infancy may be associated with a subsequent diagnosis of autism.</p>
<p>Other studies have reported that children later diagnosed with autism spectrum disorder sometimes have very small heads at birth, followed by a period of accelerated growth of the head during infancy. There is some evidence that such an accelerated pace of head growth might begin before birth.</p>
<p>Study author Rewaa Balaum and her colleagues wanted to explore the relationship between head growth patterns during the first year of life and a later diagnosis of autism. They conducted a longitudinal study in which they looked into head circumference and height development trajectories.</p>
<p>Study participants included 262 children with autism and 560 non-autistic children born in the Negev, southern Israel, between 2014 and 2017. Their head circumference and height data during the first year of life were available in the databases of mother-child health clinics operated by the Israeli Ministry of Health.</p>
<p>Seventy-eight percent of participating children were boys, and 77% were Jewish. The ethnic groups living in the Negev are mainly Jews and Bedouin Arabs. Children with autism were less likely to come from families of high socioeconomic status compared to the control group. They also tended to have somewhat lower weight at birth (3.24 kg vs 3.32 kg) and somewhat lower head circumference (34.18 cm vs 34.88 cm).</p>
<p>Head circumference and height measurements of these infants were taken on multiple occasions during their first year of life. Using these data, study authors grouped participating infants into seven categories based on their head growth trajectories.</p>
<p>These trajectories were: infants with consistently small heads, infants with medium head circumference throughout infancy, infants with consistently large heads, infants whose head circumference increased from small to medium, those whose heads increased from medium to large, infants whose heads were large in the early days but decreased to medium by the end of the first year, and those whose heads were medium at birth but decreased to small near the end of the first year.</p>
<p>Results showed that infants with consistently large and consistently small heads were the most likely to be diagnosed with autism later. Their odds of being diagnosed with autism were around three times higher compared to infants with consistently medium-sized heads. These odds were 6–10 times higher in the 5% of infants with the smallest heads and the 5% of infants with the largest head circumferences.</p>
<p>Crucially, the researchers found that these head growth patterns were strongly linked to height. Children with atypical head sizes also tended to have atypical heights. The highest risk for autism was observed in children who had both atypical head size and atypical height, rather than those with isolated head growth issues.</p>
<p>“Our findings suggest that the reported associations between atypical head growth during infancy and ASD [autism spectrum disorder] may be attributed to broader physical growth anomalies. This conclusion highlights the importance of a multifaceted, longitudinal examination of such anthropometric measures in studies of child development,” the study authors concluded.</p>
<p>The study contributes to the scientific understanding of autism. However, it should be noted that the study only looked at children in the first year of life. It remains unknown whether these growth patterns continue beyond this period. It also remains unknown how much these findings can be generalized to human populations outside southern Israel.</p>
<p>The paper, “<a href="https://doi.org/10.1002/aur.70172">Head Growth Trajectories During the First Year of Life and Risk of Autism Spectrum Disorder,</a>” was authored by Rewaa Balaum, Leena Elbedour, Einav Alhozyel, Gal Meiri, Dikla Zigdon, Analya Michaelovski, Orly Kerub, and Idan Menashe.</p></p>
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<td><a href="https://www.psypost.org/blood-test-might-detect-parkinsons-disease-years-before-physical-symptoms-appear/" 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;">Blood test might detect Parkinson’s disease years before physical symptoms appear</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 10:00</div>
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<p><p>A new analysis of gene expression in blood samples suggests that specific biological signs of Parkinson’s disease are detectable years before physical symptoms appear. These molecular signatures, related to how cells repair DNA and handle stress, seem to fade once the disease is fully established. The findings were published in <em><a href="https://doi.org/10.1038/s41531-025-01194-7" target="_blank">npj Parkinson’s Disease</a></em>.</p>
<p>Parkinson’s disease is traditionally diagnosed only after significant brain damage has occurred, typically manifested by tremors, stiffness, and slowness of movement. Scientists have long sought ways to identify the condition during the “prodromal” phase. This phase represents a period when internal biological changes are happening, but the classic motor symptoms have not yet surfaced. Identifying the disease at this stage is a major goal for medical science because it offers a potential window for early intervention.</p>
<p>Danish Anwer, a doctoral student at the Department of Life Sciences at Chalmers University of Technology in Sweden, led a team to investigate whether these early internal changes could be tracked in the blood. The research team operated on the hypothesis that the body’s genetic instructions for repairing DNA might be overactive or dysregulated early in the disease process. </p>
<p>Dopamine-producing neurons in the brain are high-energy cells that naturally produce toxic byproducts during their activity. These byproducts can damage DNA, requiring a robust repair system to keep the cells healthy.</p>
<p>The researchers theorized that in the early stages of Parkinson’s, these repair systems might be working overtime to save the dying cells. If this activity could be detected in the blood, it would serve as an early warning system. To test this, they needed to look at how these biological processes change over time rather than just taking a single snapshot.</p>
<p>The research team utilized data from the Parkinson’s Progression Markers Initiative, a large-scale observational study that tracks the evolution of the disease. They analyzed blood samples collected over a period of up to three years. The study included 188 healthy individuals to serve as a control group.</p>
<p>In addition to the healthy controls, the study analyzed 393 patients who had already been diagnosed with established Parkinson’s disease. Crucially, the researchers also included 58 individuals in the prodromal phase. These are people who do not yet have the motor symptoms of Parkinson’s but exhibit early warning signs such as REM sleep behavior disorder or loss of smell.</p>
<p>The researchers used a technique called RNA sequencing to look at the activity levels of thousands of genes in these blood samples. While DNA is the instruction manual, RNA is the message that tells the cell what to do at any given moment. By sequencing the RNA, the team could see which genes were being turned on or off.</p>
<p>They specifically examined genes responsible for three key biological pathways. The first was mitochondrial DNA repair, which maintains the energy generators of the cell. The second was nuclear DNA repair, which protects the main genetic code. The third was the integrated stress response, a safety mechanism cells use to handle dangerous conditions.</p>
<p>To analyze this vast amount of data, the team employed machine learning algorithms known as logistic regression classifiers. These computer models were trained to distinguish between the different groups based on their gene expression profiles. The researchers assessed how accurately these models could identify a person as healthy, prodromal, or having established Parkinson’s based solely on their blood data.</p>
<p>The investigation revealed that gene activity related to DNA repair and stress responses could accurately distinguish prodromal individuals from healthy controls. The models achieved high accuracy in identifying those in the early, pre-symptomatic stages. The accuracy of these predictions tended to improve as the participants moved closer to the typical time of diagnosis.</p>
<p>In contrast, these same gene patterns could not effectively separate patients with established Parkinson’s disease from healthy people. This suggests that the molecular signals are strong and distinct during the early development of the disease but quiet down later. Once the disease is clinically apparent, the gene expression in the blood appears to return to a state similar to that of healthy individuals.</p>
<p>The researchers observed that gene expression in the prodromal group was highly variable at the beginning of the study. Over the course of two to three years, this variability decreased significantly. This pattern indicates that the body initially mounts a chaotic or intense effort to repair cellular damage. As the disease progresses, this protective response appears to burn out or fail.</p>
<p>This concept was further supported by the observation of non-linear patterns in gene activity. About half of the DNA repair genes did not simply increase or decrease in a straight line. Instead, they followed complex trajectories, rising and then falling, or vice versa. This suggests a dynamic and transient biological struggle occurring before the onset of motor symptoms.</p>
<p>The study highlighted specific genes that were particularly predictive of the prodromal state. These included ERCC6 and NEIL2, both of which are involved in fixing damage to DNA. ERCC6 is known to be important for repairing active genes and is linked to conditions involving premature aging. NEIL2 helps repair damage caused by oxidative stress, which is a known factor in the death of dopamine neurons.</p>
<p>Another notable gene identified was NTHL1. This gene showed high importance as a predictor early in the prodromal phase. However, its relevance declined sharply as time passed. This decline supports the theory that specific repair mechanisms are recruited early on but eventually become overwhelmed or inactivated as the neurodegeneration advances.</p>
<p>The team also compared these specific stress and repair genes against broader sets of genes usually associated with Parkinson’s disease. They found that the repair and stress response genes were superior at identifying the prodromal phase. This indicates that general Parkinson’s risk genes might be less useful for tracking the active disease process in its earliest stages compared to these specific repair pathways.</p>
<p>The inability of the models to distinguish established Parkinson’s from controls is a significant finding. It implies that by the time a patient sees a doctor for tremors, the systemic battle in the blood has largely subsided. This highlights a limited temporal window where blood tests based on these markers would be effective.</p>
<p>There are limitations to this research that should be considered when interpreting the results. Blood samples serve as a proxy and do not always perfectly reflect what is happening inside the brain. It is possible that the signals detected in the blood are distinct from the specific degeneration occurring in central nervous system cells. The changes in the blood might reflect a systemic response to the disease rather than the direct brain pathology.</p>
<p>Additionally, the sample size for the prodromal group was relatively small compared to the other groups. While the statistical methods used were robust, larger studies will be necessary to confirm these patterns. The researchers also noted that external factors like medication could influence gene expression in established patients, potentially masking some signals.</p>
<p>The researchers did not perform functional tests to see if the changes in RNA levels resulted in changes in actual protein levels or cellular function. Gene expression is only the first step in protein production. Future studies will need to bridge the gap between these genetic signals and the actual cellular machinery.</p>
<p>Despite these limitations, the study provides evidence that the prodromal phase of Parkinson’s is biologically distinct from the established phase. It suggests that the body fights the disease aggressively in the beginning. This insight could help in the design of clinical trials by allowing researchers to select patients who are in this active, early phase.</p>
<p>The research team aims to understand exactly how these early repair mechanisms work and why they eventually fail. Developing these findings into a practical blood test for clinical use will require further testing and regulatory approval. The scientists estimate that such a test could potentially begin trials in healthcare settings within five years.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41531-025-01194-7" target="_blank">Longitudinal assessment of DNA repair signature trajectory in prodromal versus established Parkinson’s disease</a>,” was authored by Danish Anwer, Nicola Pietro Montaldo, Elva Maria Novoa-del-Toro, Diana Domanska, Hilde Loge Nilsen, and Annikka Polster.</p></p>
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<td><a href="https://www.psypost.org/a-common-enzyme-linked-to-diabetes-may-offer-a-new-path-for-treating-alzheimers/" 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;">A common enzyme linked to diabetes may offer a new path for treating Alzheimer’s</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 8th 2026, 08:00</div>
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<p><p>A protein long implicated in diabetes and obesity may hold the key to treating Alzheimer’s disease by reinvigorating the brain’s immune system. New research suggests that blocking this protein, known as PTP1B, allows immune cells to clear toxic waste more effectively and restores cognitive function in mice. The findings were published in the <em><a href="https://doi.org/10.1073/pnas.2521944123" target="_blank">Proceedings of the National Academy of Sciences</a></em>.</p>
<p>Alzheimer’s disease is characterized by the accumulation of sticky protein clumps called amyloid-beta. These plaques disrupt communication between brain cells and are widely believed to drive memory loss and neurodegeneration. The brain relies on specialized immune cells called microglia to maintain a healthy environment. In a healthy brain, microglia locate and engulf toxic clumps like amyloid-beta through a process called phagocytosis.</p>
<p>However, in patients with Alzheimer’s, these immune cells often become lethargic. They fail to keep up with the accumulating waste, allowing plaques to spread. Scientists have struggled to find ways to safely reactivate these cells without causing damaging inflammation.</p>
<p>There is a growing body of evidence linking Alzheimer’s to metabolic disorders. Conditions like type 2 diabetes are well-established risk factors for dementia. This connection led researchers to investigate a specific enzyme called protein tyrosine phosphatase 1B, or PTP1B. </p>
<p>This enzyme acts as a brake on signaling pathways that control how cells use energy and respond to insulin. Nicholas K. Tonks, a professor at Cold Spring Harbor Laboratory who discovered PTP1B in 1988, led the investigation along with graduate student Yuxin Cen. They hypothesized that PTP1B might be preventing microglia from doing their job.</p>
<p>To test this theory, the team used a mouse model genetically engineered to develop Alzheimer’s-like symptoms. These mice, known as APP/PS1 mice, typically develop amyloid plaques and memory deficits as they age. The researchers created a group of these mice that lacked the gene responsible for producing PTP1B. When these mice reached an age where memory loss typically begins, the researchers assessed their cognitive abilities.</p>
<p>The mice lacking the enzyme performed better on memory tests than the standard Alzheimer’s mice. One test involved a water maze where mice had to remember the location of a hidden platform. The mice without PTP1B found the escape route faster, indicating superior spatial learning. Another test measured how much time mice spent exploring a new object versus a familiar one. The genetically modified mice showed a clear preference for the new object, a sign of intact recognition memory.</p>
<p>The team also tested a drug designed to inhibit PTP1B to see if pharmacological intervention could mimic the genetic deletion. They administered a compound called DPM1003 to older mice that had already developed plaques. After five weeks of treatment, these mice showed similar improvements in memory and learning. This suggested that blocking the enzyme could reverse existing deficits and was not just a preventative measure.</p>
<p>Next, the investigators examined the brains of the animals to understand the biological changes behind these behavioral improvements. They used staining techniques to visualize amyloid plaques. Both the mice lacking the PTP1B gene and those treated with the inhibitor had considerably fewer plaques in the hippocampus. This region of the brain is essential for forming new memories.</p>
<p>To understand how the plaques were being cleared, the researchers analyzed the gene activity in individual brain cells. They performed single-cell RNA sequencing to look at the genetic profiles of thousands of cells. They found that PTP1B is highly expressed in microglia. When the enzyme was absent, the microglia shifted into a unique state.</p>
<p>These cells began expressing genes associated with the consumption of cellular debris. This state is often referred to as “disease-associated microglia,” or DAM. While the name sounds negative, this profile indicates cells that are primed to respond to injury. The lack of PTP1B appeared to push the microglia toward this beneficial, cleaning-focused phenotype.</p>
<p>The researchers then isolated microglia in a dish and exposed them to amyloid-beta to observe their behavior directly. Cells lacking PTP1B were much more efficient at swallowing the toxic proteins. “Over the course of the disease, these cells become exhausted and less effective,” says Cen. “Our results suggest that PTP1B inhibition can improve microglial function, clearing up Aβ plaques.”</p>
<p>The study revealed that this boost in activity was powered by a change in cellular metabolism. Phagocytosis is an energy-intensive process. The immune cells without PTP1B were able to ramp up their energy production to meet this demand. They increased both their glucose consumption and their oxygen use.</p>
<p>This metabolic surge was driven by the PI3K-AKT-mTOR signaling pathway. This is a well-known cellular circuit that regulates growth and energy survival. In the absence of PTP1B, this pathway remained active, providing the fuel necessary for the microglia to function.</p>
<p>Finally, the team identified the specific molecular switch that PTP1B controls to regulate this process. They found that the enzyme directly interacts with a protein called spleen tyrosine kinase, or SYK. SYK is a central regulator that tells microglia to activate and start eating. PTP1B normally removes phosphate groups from SYK, which keeps the kinase in an inactive state.</p>
<p>When PTP1B is removed or inhibited, SYK becomes overactive. This triggers a cascade of signals that instructs the cell to produce more energy and engulf amyloid. The researchers confirmed this by adding a drug that blocks SYK to the cells. When SYK was blocked, the benefits of removing PTP1B disappeared, and the microglia stopped clearing the plaque. This proved that PTP1B works by suppressing SYK.</p>
<p>The researchers utilized a “substrate-trapping” technique to confirm this direct interaction. They created a mutant version of PTP1B that can grab onto its target protein but cannot let go. This allowed them to isolate the PTP1B enzyme and see exactly what it was holding. They found it was bound tightly to SYK, confirming the direct relationship between the two proteins.</p>
<p>While these results are promising, the study was conducted in mice. Animal models mimic certain aspects of Alzheimer’s pathology but do not perfectly replicate the human disease. Future research will need to determine if similar metabolic and immune pathways are active in human patients. Additionally, PTP1B regulates many systems in the body, so widespread inhibition must be tested for safety.</p>
<p>The researchers are now interested in developing inhibitors that can specifically target the brain to minimize potential side effects. The Tonks lab is working to refine these compounds for potential clinical use. Tonks envisions a strategy where these inhibitors are used alongside existing treatments. “The goal is to slow Alzheimer’s progression and improve quality of life of the patients,” says Tonks. “Using PTP1B inhibitors that target multiple aspects of the pathology, including Aβ clearance, might provide an additional impact,” says Ribeiro Alves.</p>
<p>The study, “<a href="https://doi.org/10.1073/pnas.2521944123" target="_blank">PTP1B inhibition promotes microglial phagocytosis in Alzheimer’s disease models by enhancing SYK signaling</a>,” was authored by Yuxin Cen, Steven R. Alves, Dongyan Song, Jonathan Preall, Linda Van Aelst, and Nicholas K. Tonks.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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