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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-shed-new-light-on-the-mysterious-memory-altering-power-of-sleep/" 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 shed new light on the mysterious memory-altering power of sleep</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 7th 2025, 10:00</div>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41562-025-02117-5" target="_blank" rel="noopener">Nature Human Behaviour</a></em> suggests that sleep doesn’t just protect memories from fading—it transforms them. Researchers found that sleep selectively strengthens memory for the sequence of real-world events while allowing many of the perceptual details to fade. This transformation wasn’t short-lived: even 15 months after a one-time event, people better remembered the order in which things occurred—if they had slept soon after the experience.</p>
<p>The study addresses a long-standing question in memory research: does sleep simply preserve memories by protecting them from interference, or does it actively enhance and reshape them? Previous studies have shown that sleeping after learning improves memory, but many of those studies used artificial tasks like memorizing word lists or images on a screen. Researchers working in <a href="http://www.levinelab.ca/" target="_blank" rel="noopener">Brian Levine’s research lab</a> at Baycrest’s Rotman Research Institute took a different approach by examining memory for a real-world experience and tracking how it changed over time—days, weeks, and even more than a year later.</p>
<p>“For me, I’ve had a long-standing interest in how we remember complex personal past events (episodic memory),” said co-first author <a href="https://bsky.app/profile/stefsimpson.bsky.social" target="_blank" rel="noopener">Stephanie Simpson</a>, who is now a postdoctoral fellow at the Centre for Addiction and Mental Health. “When I joined the lab as a master’s student, I started reading about how factors like sleep can shape the way humans retrieve information, but to my knowledge most of these studies tested how people remembered words or simple images on a computer screen. Furthermore, most of these studies didn’t explore whether the effects of sleep on memory were long-lasting.”</p>
<p>“I was motivated to understand how the existing research I read about that was conducted in conventional, highly controlled experimental designs would extend to the ‘noisier’ real world. I was drawn to questions like: How can we bridge the study of fundamental research concepts into more naturalistic settings?”</p>
<p>“Like Steph, I’d always been fascinated by episodic memory – our ability to mentally time travel from the present to specific experiences from our past, reliving some amount of the perceptual, emotional, or contextual elements of that past event. Anything from the experience of eating a mediocre sandwich yesterday to my 10th birthday party,” added co-first author <a href="https://bsky.app/profile/diamondn.bsky.social" target="_blank" rel="noopener">Nicholas Diamond</a>, who currently works for the Government of Canada.</p>
<p>“One reason I’m interested is that this ability is disproportionately affected by some neuropathological diseases like Alzheimer’s. But episodic memory is also just cool and magical on its face, and in my opinion still pretty poorly understood at psychological and neurophysiological levels, even after 150 years or so of empirical research.”</p>
<p>“Some big, basic questions remain: how do single experiences – even non-exceptional ones – stick in our brains for delays beyond a few minutes? When we remember such experiences after a day or a month or a year, are we just making an inference about what happened based on our general knowledge, or can we really re-experience some amount of that original event? And lastly – we know that sleep helps memories stick in our brains, but how exactly does it transform our memories?”</p>
<p>“Saying a memory is ‘better’ or ‘worse’ isn’t really satisfying – I wanted to know how sleep makes a given memory different, and why does this difference lead to that memory being stickier over the long run?” Diamond continued. “I think our answers to these types of questions have been limited by the customs and conveniences of laboratory memory studies – artificial stimuli, delays on the order of seconds or minutes, and tests that assume something is simply remembered or not. We wanted to know how memory for rich real-life experiences – and different aspects of these experiences – changes on the order of weeks, months, and years.”</p>
<p>The researchers created a 20-minute audio-guided art tour through a Toronto healthcare center, where participants listened to descriptions of 33 artworks in a fixed sequence while walking through the space. The tour was designed to mimic how people naturally encounter and encode events in everyday life. After completing the tour, participants were tested on two aspects of memory: the details of each artwork (its color or shape, for example), and the sequence in which they encountered them. The same participants were tested again after sleeping, after a week, after a month, and in some cases, after 15 months.</p>
<p>While overall memory accuracy declined over time, people consistently remembered the order of events better than the specific details if they had gotten a full night’s sleep. In contrast, those who stayed awake during the same post-learning period showed no such advantage. In fact, only the sleep group demonstrated an actual improvement in sequence memory from before to after sleep, a rare finding that runs counter to the typical trend of gradual memory decay.</p>
<p>“Sleep can transform the way we remember complex, personal past experience,” Simpson told PsyPost. “Compared to a period of wakefulness, sleep enhances memory for the order of events from an art tour, but not the details of the event itself.”</p>
<p>To explore how sleep might be doing this, the researchers measured brain activity during sleep in a subgroup of participants using polysomnography, a technique that records electrical activity in the brain. They found that people who experienced more slow-wave sleep—the deep sleep stage associated with memory consolidation—showed stronger memory enhancement.</p>
<p>Even more telling, the degree of improvement in sequence memory was linked to a specific sleep phenomenon known as spindle–slow wave coupling. This occurs when two brain rhythms—sleep spindles and slow oscillations—sync up during deep sleep, creating conditions that support the reactivation and reorganization of memories.</p>
<p>“To help understand why and how sleep transforms memory, after completing our experimental art tour, we recorded people’s brains while they were sleeping using scalp electroencephalography (EEG),” Diamond explained. “Our results showed that one particular part of the sleep cycle – slow-wave sleep – was linked to sleep-related memory improvement. And more specifically, it was the synchronized occurrences of two particular brain rhythms occurring during slow-wave sleep – sleep spindles and slow waves – that was significantly related to overnight memory improvement.”</p>
<p>Interestingly, the sleep-related memory benefit was specific to sequential information. Participants’ memory for featural details—such as what material an artwork was made of—tended to fade over time, regardless of whether they had slept. This selective retention supports the idea that sleep may prioritize certain aspects of memory over others, perhaps because remembering the order of events is more useful for planning and understanding how experiences unfold over time.</p>
<p>“This is some of the first evidence that sleep can actually improve episodic memory – not just reduce forgetting,” Diamond told PsyPost. “In other words: people actually remember a given experience more accurately after a 12 or 24 hour delay (but only if they slept) than they did immediately after the experience. You can think of this as ‘anti-forgetting’ – memory getting better with time. The catch is that it’s one specific element of episodic memory that improves – sequence memory, or memory for the order in which experiences unfold.”</p>
<p>The long-term nature of the findings is especially compelling. Memory for sequences remained significantly better than for details even after 15 months, as long as participants had slept shortly after the event. This suggests that a single night of sleep can have enduring effects on how a memory is stored and retrieved.</p>
<p>“The sleep-related advantage for sequences is durable – it endured over 1 year later,” Simpson said.</p>
<p>The idea that the brain reshapes memories during sleep is not new. In animal studies, researchers have observed that the hippocampus—a brain region critical for memory—replays patterns of activity related to recent experiences, sometimes at a faster pace, during sleep. These replays are thought to strengthen connections between neurons and transfer memories to more permanent storage areas in the cortex. The current study provides evidence that a similar process occurs in humans, and that it may specifically benefit our ability to remember the order in which things happen.</p>
<p>“Why does sleep specifically benefit memory for the sequence of our experiences? We think that this might have something to do with a brain phenomenon called ‘neural replay’, which has been heavily studied in rodents, and only more recently in humans,” Diamond said. “The idea is that, while we’re sleeping, patterns of neural firing that occurred during our waking life repeatedly ‘replay’ in a super time-compressed way, like a movie on fast forward.”</p>
<p>“This may strengthen neural connections between memories for sequences of events, bridging temporal gaps. We didn’t actually measure neural replay – you need to stick wires in people’s brains to do that with high fidelity – but we do know that replay occurs during slow-wave sleep and especially during spindle-slow wave coupling, which is why we expected that to be the key neural marker of memory transformation, which we indeed found to be the case.”</p>
<p>To ensure the findings weren’t just a fluke or the result of test design, the researchers replicated their results across multiple groups. One group slept after the tour, another stayed awake for 12 hours before their second test, and a third had their brain activity monitored during sleep. Across all groups, the same pattern emerged: sleep helped participants retain the sequence of events better than those who stayed awake, and this effect was strongest among those who spent more time in deep sleep and showed more spindle–slow wave coupling.</p>
<p>The study’s design also controlled for several possible confounds. For example, memory tests were matched in difficulty, and test items were randomly assigned and counterbalanced to avoid learning effects. Participants were excluded if they had sleep disorders, neurological conditions, or prior exposure to the tour site. These precautions strengthened the validity of the results.</p>
<p>Still, the study has limitations. While the authors found clear associations between sleep physiology and memory performance, the study cannot definitively establish causality. It’s also possible that individual differences in learning ability or motivation influenced how much benefit people got from sleep.</p>
<p>“A general issue that can not only apply to this study, but the whole field, is relying on a convenience sample of primarily young undergraduate students,” Simpson noted. “These samples tend to overrepresent people who are White, westernized, and well-educated. It would be great to test this in a sample of more diverse adults from a variety of ethnic and socioeconomic backgrounds.”</p>
<p>“In this study we tested how one night of sleep (within the confines of a sleep lab) influenced subsequent memory performance. In an ideal world without financial restrictions, we would investigate how participants slept over multiple nights to get an even more reliable measure of their sleeping brain activity. Alternatively, researchers could opt to use more portable devices (e.g. actigraphy watches) that can be worn at home over multiple nights. However, this comes at the cost of your signal to noise ratio.”</p>
<p>Future studies could explore how these sleep-related memory effects change across the lifespan, especially given that both memory and sleep patterns shift with age. Older adults often experience less slow-wave sleep and more fragmented sleep overall, which may contribute to difficulties with memory for the order of events.</p>
<p>“With age, both episodic memory and sleep habits change considerably,” Simpson explained. “We know that there is a strong connection between sleep and cognitive aging. For example, people with chronic sleep problems are at greater risk of developing Alzheimer’s disease. I think an interesting area of future research would be to explore sleep mechanisms as a biomarker for neurodegenerative diseases marked by significant memory impairment and determine if using sleep alongside memory measures may aid in the earlier diagnosis of individuals at risk for Alzheimer’s disease.”</p>
<p>“Memory for the sequence, or temporal order, of our experiences seems to be a key organizing principle of our real-life memories, sticking around in our brains even for years after a single experience,” Diamond concluded. “And sleep – especially slow-wave sleep – is the key ingredient for boosting sequence memory. So, make sure you get your sleep!”</p>
<p>The study, “<a href="https://doi.org/10.1038/s41562-025-02117-5" target="_blank" rel="noopener">Sleep selectively and durably enhances memory for the sequence of real-world experiences</a>,” was authored by N. B. Diamond, S. Simpson, D. Baena, B. Murray, S. Fogel, and B. Levine.</p></p>
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<td><a href="https://www.psypost.org/genetic-risk-for-alcoholism-alters-brain-immune-cell-response-to-alcohol-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Genetic risk for alcoholism alters brain immune cell response to alcohol, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 7th 2025, 08:00</div>
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<p><p>People who carry a high genetic risk for alcohol use disorder may have brain immune cells that respond differently to alcohol exposure, according to new research published in <em><a href="https://www.science.org/doi/10.1126/sciadv.ado5820" target="_blank" rel="noopener">Science Advances</a></em>. Using human-derived cell models, researchers found that microglia—immune cells in the brain—exhibited exaggerated responses to alcohol in individuals with elevated genetic susceptibility, potentially shedding light on the biological roots of alcohol dependence.</p>
<p>Alcohol use disorder is influenced by both genetic and environmental factors, with genetic components accounting for roughly half of the variation in who develops problematic drinking behaviors. Scientists have long suspected that immune and inflammatory processes in the brain contribute to this risk, but the exact cellular mechanisms have remained unclear. One challenge has been the lack of human-specific models that can accurately reflect how genetic risk plays out in brain cells.</p>
<p>“Alcohol use disorder has a strong genetic component, but we know little about how genetic risk actually translates to cellular and molecular changes in the brain,” said study author <a href="https://pang-lab.org/" target="_blank" rel="noopener">Zhiping Pang</a>, the Henry Rutgers Professor of NeuroMetabolism and director of the <a href="https://neurometabolism.org/" target="_blank" rel="noopener">Center for NeuroMetabolism</a> at Rutgers University. “Microglia, as the brain’s immune cells, are increasingly recognized as central players in how the brain responds to alcohol and other insults. We were interested in whether polygenic risk for alcohol use disorder might shape microglial responses to alcohol exposure and influence neuroimmune function in a human cellular context.”</p>
<p>Pang and his colleagues used induced pluripotent stem cells (cells reprogrammed from adult blood samples) to generate microglia from people with high or low genetic risk for alcohol use disorder. These cells were then exposed to ethanol in a controlled lab environment, allowing the team to examine how genetic predispositions shape microglial responses to alcohol. The participants were drawn from the Collaborative Study on the Genetics of Alcoholism, a long-running project that links genetic data with clinical diagnoses of alcohol use disorder.</p>
<p>The study focused on 18 participants: eight with alcohol use disorder and polygenic risk scores in the top 75th percentile, and ten controls with low risk scores and no history of the disorder. From each participant, the researchers created stem cell lines that were then developed into microglial cells. These cells were confirmed to be functionally similar to adult human microglia, based on both their appearance and gene expression patterns.</p>
<p>Once developed, the microglia were exposed to ethanol for seven days at concentrations mimicking heavy drinking. The team monitored how the cells changed at both a molecular and functional level, comparing those derived from high-risk versus low-risk individuals.</p>
<p>The first major difference emerged in the baseline state of the microglia: even before alcohol exposure, high-risk cells showed elevated expression of genes involved in cell division and reduced expression of genes related to immune signaling and antigen presentation. This suggests that the genetic risk for alcohol use disorder may influence microglial development and function from the outset.</p>
<p>After alcohol exposure, microglia from high-risk individuals exhibited more pronounced changes. Both high- and low-risk cells showed activation, but high-risk cells shifted more dramatically from a branched, resting state to a rounded, activated shape—indicative of heightened immune reactivity. These cells also displayed stronger gene expression changes, particularly in pathways related to immune responses and phagocytosis—the process by which microglia engulf and break down cellular debris, pathogens, or even synapses.</p>
<p>One gene, CLEC7A, stood out. It was significantly upregulated in high-risk microglia following ethanol exposure. This gene encodes a receptor involved in recognizing foreign particles and initiating phagocytosis. Follow-up experiments confirmed that CLEC7A protein levels also rose, and phagocytic activity increased substantially in high-risk cells—both when using artificial particles and synaptic material from neurons.</p>
<p>“What stood out was the distinct difference in microglial behavior between individuals with high and low genetic risk for alcohol use disorder,” Pang told PsyPost. “The enhanced phagocytic activity and elevated CLEC7A expression in high-PRS microglia after ethanol exposure suggest that these cells are biologically primed to respond differently to alcohol, which we did not fully anticipate.”</p>
<p>This finding led researchers to test how microglia might influence neurons in the context of alcohol exposure. They created co-cultures combining neurons and microglia and observed the effects of alcohol. In the absence of microglia, neurons exposed to alcohol showed increased synaptic activity. This effect persisted when low-risk microglia were added. But when neurons were co-cultured with high-risk microglia, alcohol no longer enhanced synaptic connections—suggesting that these immune cells were pruning or removing synapses in response to ethanol.</p>
<p>These results highlight a potential mechanism through which genetic predisposition could heighten vulnerability to alcohol use disorder. If microglia in genetically susceptible individuals are more prone to immune activation and synapse pruning, alcohol might accelerate the loss of healthy brain connectivity, potentially reinforcing problematic behaviors and impairing cognitive function.</p>
<p>“Genetic risk for alcohol use disorder doesn’t just influence behavior—it may also alter how the brain’s immune cells respond to alcohol,” Pang explained. “People with a higher genetic risk for alcohol use disorder may have brain immune cells (called microglia) that react more strongly to alcohol. This heightened response could lead to unnecessary trimming of brain connections over time, which may change how the brain functions and, ultimately, how a person behaves, such as increasing their risk of heavy drinking.”</p>
<p>As with all research, the study has limitations. The microglia were studied in a two-dimensional culture system, which does not fully replicate the complexity of the human brain. Although the cells were derived from real people, they were reprogrammed and studied in an artificial environment that may not perfectly capture long-term effects of alcohol use.</p>
<p>Additionally, the researchers focused on a short window of alcohol exposure—just seven days—rather than chronic exposure over months or years. It’s also unclear how past drinking behavior might have influenced the stem cells used, given that some were taken from individuals already diagnosed with alcohol use disorder.</p>
<p>Despite the limitations, the study provides a valuable model for understanding how genetic risk translates into functional changes in the brain’s immune system. By using human-derived microglia and polygenic risk scores, the researchers were able to link inherited risk directly to cellular behavior. Their findings suggest that treatments for alcohol use disorder might one day be tailored to an individual’s genetic profile—especially if interventions can target overactive microglial responses.</p>
<p>“Our next steps include integrating human neurons and microglia in more advanced 3D culture systems, i.e. brain organoids, to better understand how these immune changes affect synaptic connectivity,” Pang said. “We also aim to explore therapeutic interventions that could mitigate the harmful effects of alcohol in genetically vulnerable individuals.”</p>
<p>“This work highlights the importance of studying human-specific biology in psychiatric disorders. By combining genetic risk scores with human cellular models, we can start to unravel how inherited risk influences brain cell function—and ultimately behavior—in a way that animal models may not fully capture.”</p>
<p>The study, “<a href="https://doi.org/10.1126/sciadv.ado5820" target="_blank" rel="noopener">Polygenic risk for alcohol use disorder affects cellular responses to ethanol exposure in a human microglial cell model</a>,” was authored by Xindi Li, Jiayi Liu, Andrew J. Boreland, Sneha Kapadia, Siwei Zhang, Alessandro C. Stillitano, Yara Abbo, Lorraine Clark, Dongbing Lai, Yunlong Liu, Peter B. Barr, Jacquelyn L. Meyers, Chella Kamarajan, Weipeng Kuang, Arpana Agrawal, Paul A. Slesinger, Danielle Dick, Jessica Salvatore, Jay Tischfield, Jubao Duan, Howard J. Edenberg, Anat Kreimer, Ronald P. Hart, and Zhiping P. Pang.</p></p>
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<td><a href="https://www.psypost.org/neuroscientists-uncover-a-fascinating-fact-about-social-thinking-in-the-brain/" 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 uncover a fascinating fact about social thinking in the brain</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 7th 2025, 06:00</div>
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<p><p>When we think about people in our social circle, our brains appear to keep track of two different kinds of comparisons: how others relate to each other, and how others relate to ourselves. A new study published in <em><a href="https://doi.org/10.1177/09567976251328430" target="_blank" rel="noopener">Psychological Science</a></em> shows that these two types of social knowledge—called allocentric and egocentric similarity—are represented by entirely different brain systems. Using functional brain imaging and a unique design involving real-world social groups, the research reveals that the brain independently processes these reference frames when we consider the traits of people we know.</p>
<p>Prior research has shown that people are quick to form impressions of others and often rely on perceived similarities—either between others or between others and themselves—when navigating social relationships. But it was not clear whether these two types of comparisons are computed by the same brain mechanisms or whether they rely on separate systems. Drawing inspiration from spatial cognition, where scientists distinguish between allocentric (object-to-object) and egocentric (self-to-object) frames of reference, the researchers aimed to test whether similar distinctions exist in how we mentally represent people.</p>
<p>“When we are driving a car down the road, we need to how both far we are from an upcoming car but also how close that car is from other cars next to it,” explained study author Robert S. Chavez, an associate professor in psychology and the <a href="https://csnl.uoregon.edu/" target="_blank" rel="noopener">Center for Translational Neuroscience</a> at University of Oregon. “In other words, it needs to know the self-to-other distance (egocentric distance) and the other-to-other distance (allocentric distance) to drive safely. There had been previous work on how the brain processes these reference frames in spatial cognition, but we were inspired to see if the brain processes social information using similar processes.”</p>
<p>To explore this, the researchers recruited 108 participants from 20 real-world social groups, such as student clubs, coworker teams, and friend groups. Each group consisted of six people who were familiar with one another. The study used a round-robin design in which every participant rated themselves and each other member of their group on traits related to warmth (e.g., friendliness) and competence (e.g., effectiveness). These ratings were used to construct models of allocentric similarity (how similar group members were to each other) and egocentric similarity (how similar each person was to themselves compared to others).</p>
<p>In a separate session, the same participants underwent functional magnetic resonance imaging (fMRI) while completing a trait-judgment task. During the task, they were shown names of themselves or their peers along with descriptive words (like “happy” or “clumsy”) and asked to decide whether the trait applied to the person. This task was designed to elicit neural patterns reflecting mental representations of each individual. The researchers then used statistical modeling to compare how similar the brain’s responses were when participants thought about each peer and how that matched up with the behavioral similarity ratings.</p>
<p>The key finding was that both allocentric and egocentric similarities were reflected in brain activity patterns—but in completely different sets of brain regions. Allocentric similarity was associated with increased neural similarity in areas such as the ventromedial prefrontal cortex, posterior cingulate cortex, and lateral orbitofrontal cortex.</p>
<p>These regions have previously been linked to social cognition and are part of the brain’s default mode network, which is active when we think about other people or ourselves. Notably, these regions also overlap with those involved in spatial navigation using allocentric reference frames, supporting the idea that the brain may repurpose spatial mapping systems for social mapping.</p>
<p>In contrast, egocentric similarity was associated with neural activity in the dorsal medial prefrontal cortex and anterior cingulate cortex—areas involved in social comparison, self-other distinctions, and mentalizing.</p>
<p>“When we think of other people, our brain spontaneously represents information about both the similarities among others in our social world as well as our position in that similarity space,” Chavez told PsyPost. “Our results show that how these similarities are computed is carried out in independent brain systems at the same time. Just like the example of a car driving down the road, we need both of these calculations to make sense of complex social information.”</p>
<p>Interestingly, the relationship between perceived similarity and brain response went in the opposite direction: the more similar participants thought someone was to themselves, the more dissimilar their brain patterns were when thinking about that person. This suggests that the brain may actively maintain a distinction between the self and others, even when those others are perceived as similar. This kind of neural separation could help prevent confusion between our own thoughts and those of others, especially in socially close relationships.</p>
<p>“One finding that might surprise some folks was the finding that greater the closer people were in egocentric similarity, the more dissimilar their brain responses were in the dorsal medial prefrontal cortex which is often implicated in mentalizing and processes related to empathy,” Chavez explained. “We think this is interesting because it dovetails with theories on the need for cognitive separation between self and others that may help facilitate.”</p>
<p>Another important aspect of the study was the comparison between individual ratings and group consensus ratings. The researchers tested whether the average ratings of each person by the group better predicted brain responses than the individual’s own ratings. Across the board, they found that within-perceiver ratings were more closely aligned with neural patterns than group-averaged ones. This suggests that how a person personally evaluates others—even if biased—is more consistent with their brain’s internal representation than how others see those same people.</p>
<p>The study’s results provide strong evidence that the brain uses distinct systems to encode different kinds of social similarity. Allocentric and egocentric reference frames were associated with nonoverlapping brain regions, supporting the idea that they are processed separately rather than as part of a single, unified social-evaluation system. This finding helps clarify long-standing debates in the field about whether different types of social information are handled by shared or separate neural mechanisms.</p>
<p>Although the study sheds new light on how the brain encodes different types of social similarity, it also has limitations. The sample consisted mostly of young adults from a university setting, many of whom were White and middle-class. As such, the findings may not generalize to people from other backgrounds or to different types of social relationships, such as family members or long-term romantic partners. The task also involved relatively passive trait judgments, which might engage different processes than more interactive or emotionally charged social experiences.</p>
<p>“It is important to remind ourselves that these subjects are lying on their back in a noisy tube (the MRI machine), which is about the most non-social place in the world,” Chavez noted. “Although we think these results speak to the way the brain processes social information, it clearly cannot capture the richness of these processes in the real world.”</p>
<p>Future research could explore how these brain systems function in more diverse groups and during more natural social interactions. The researchers also plan to investigate how these patterns longitudinally, particularly as relationships change and evolve. Another promising direction is to examine how social reference frames are affected in conditions where social processing is impaired, such as in autism or certain personality disorders.</p>
<p>“We are hoping to continue to use real-world groups of people in combination with more naturalistic stimuli and methods to address some of the limitations of this study and provide even more detailed understanding about how the brain represents dynamic information about the relationship between self and others and how this unfolds over time,” Chavez said.</p>
<p>The study, “<a href="https://doi.org/10.1177/09567976251328430" target="_blank" rel="noopener">Person Knowledge Is Independently Encoded by Allocentric and Egocentric Reference Frames Within Separate Brain Systems</a>,” was authored by Robert S. Chavez, Taylor D. Guthrie, and Jack M. Kapustka.</p></p>
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<td><a href="https://www.psypost.org/a-neuroscientist-explains-how-cancer-hijacks-the-brains-motivation-circuit/" 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 neuroscientist explains how cancer hijacks the brain’s motivation circuit</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 6th 2025, 20:00</div>
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<p><p>A cruel consequence of advanced cancer is the profound apathy many patients experience as they lose interest in once-cherished activities. This symptom is part of a syndrome called cachexia, which affects about <a href="https://www.cancer.gov/about-cancer/treatment/research/cachexia">80% of late-stage cancer patients</a>, leading to severe muscle wasting and weight loss that leave patients bone thin despite adequate nutrition.</p>
<p>This loss of motivation doesn’t just deepen patients’ suffering, it isolates them from family and friends. Because patients <a href="https://doi.org/10.1002/pon.5476">struggle to engage with demanding therapies</a> that require effort and persistence, it also strains families and complicates treatment.</p>
<p>Doctors typically assume that when late-stage cancer patients withdraw from life, it is an inevitable <a href="https://doi.org/10.1111/j.1365-2354.2002.00283.x">psychological response to physical deterioration</a>. But what if apathy isn’t just a byproduct of physical decline but an integral part of the disease itself?</p>
<p>In our newly published research, my colleagues <a href="https://kepecslab.org/">and I</a> have discovered something remarkable: Cancer doesn’t simply waste the body – it <a href="https://science.org/doi/10.1126/science.adm8857">hijacks a specific brain circuit that controls motivation</a>. Our findings, published in the journal Science, challenge decades of assumptions and suggest it might be possible to restore what many cancer patients describe as <a href="https://doi.org/10.1097/ppo.0b013e3181f45b90">most devastating to lose</a> – their will to engage with life.</p>
<h2>Untangling fatigue from physical decline</h2>
<p>To unravel the puzzle of apathy in cancer cachexia, we needed to trace the exact path inflammation takes in the body and peer inside a living brain while the disease is progressing – something impossible in people. However, neuroscientists have advanced technologies that make this possible in mice.</p>
<p>Modern neuroscience equips us with a powerful <a href="https://theconversation.com/illuminating-the-brain-one-neuron-and-synapse-at-a-time-5-essential-reads-about-how-researchers-are-using-new-tools-to-map-its-structure-and-function-187607">arsenal of tools</a> to probe how disease changes brain activity in mice. Scientists can <a href="https://theconversation.com/mapping-how-the-100-billion-cells-in-the-brain-all-fit-together-is-the-brave-new-world-of-neuroscience-170182">map entire brains</a> at the cellular level, <a href="https://theconversation.com/illuminating-the-brain-one-neuron-and-synapse-at-a-time-5-essential-reads-about-how-researchers-are-using-new-tools-to-map-its-structure-and-function-187607">track neural activity</a> during behavior, and precisely <a href="https://theconversation.com/brain-stimulation-can-rewire-and-heal-damaged-neural-connections-but-it-isnt-clear-how-research-suggests-personalization-may-be-key-to-more-effective-therapies-182491">switch neurons on or off</a>. We used these neuroscience tools in a mouse model of cancer cachexia to study the effects of the disease on the brain and motivation.</p>
<p>We identified a small brain region called the <a href="http://dx.doi.org/10.1177/1073858407311100">area postrema</a> that acts as the brain’s inflammation detector. As a tumor grows, it releases cytokines − molecules that trigger inflammation − into the bloodstream. The area postrema lacks the typical blood-brain barrier that keeps out toxins, pathogens and other molecules from the body, allowing it to directly sample circulating inflammatory signals.</p>
<p>When the area postrema detects a rise in inflammatory molecules, it triggers a neural cascade across multiple brain regions, ultimately suppressing dopamine release in the brain’s motivation center − the <a href="https://doi.org/10.1016/j.neuron.2019.03.003">nucleus accumbens</a>. While commonly misconstrued as a “pleasure chemical,” dopamine is actually associated with drive, or the <a href="https://doi.org/10.1038/422573a">willingness to put in effort to gain rewards</a>: It tips the internal cost-benefit scale toward action.</p>
<p>We <a href="https://science.org/doi/10.1126/science.adm8857">directly observed this shift</a> using two quantitative tests designed with behavioral economics principles to measure effort. In the first, mice repeatedly poked their noses into a food port, with progressively more pokes required to earn each food pellet. In the second task, mice repeatedly crossed a bridge between two water ports, each gradually depleting with use and forcing the mice to switch sides to replenish the supply, similar to picking berries until a bush is empty.</p>
<p>As cancer progressed, mice still pursued easy rewards but quickly abandoned tasks requiring greater effort. Meanwhile, we watched dopamine levels fall in real time, precisely mirroring the mice’s decreasing willingness to work for rewards.</p>
<p>Our findings suggest that cancer isn’t just generally “wearing out” the brain − it sends targeted inflammatory signals that the brain detects. The brain then responds by rapidly reducing dopamine levels to <a href="https://science.org/doi/10.1126/science.adm8857">dial down motivation</a>. This matches what patients describe: “Everything feels too hard.”</p>
<h2>Restoring motivation in late-stage disease</h2>
<p>Perhaps most exciting, we found <a href="https://science.org/doi/10.1126/science.adm8857">several ways to restore motivation</a> in mice suffering from cancer cachexia − even when the cancer itself continued progressing.</p>
<p>First, by genetically switching off the inflammation-sensing neurons in the area postrema, or by directly stimulating neurons to release dopamine, we were able to restore normal motivation in mice.</p>
<p>Second, we found that giving mice a drug that blocks a particular cytokine − working similarly to existing FDA-approved arthritis treatments − also proved effective. While the drug did not reverse physical wasting, it restored the mice’s willingness to work for rewards.</p>
<p>While these results are based on mouse models, they suggest a treatment possibility for people: Targeting this specific inflammation-dopamine circuit could improve quality of life for cancer patients, even when the disease remains incurable.</p>
<p>The boundary between physical and psychological symptoms is an <a href="https://plato.stanford.edu/entries/dualism/">artificially drawn line</a>. Cancer ignores this division, using inflammation to commandeer the very circuits that drive a patient’s will to act. But our findings suggest these messages can be intercepted and the circuits restored.</p>
<h2>Rethinking apathy in disease</h2>
<p>Our discovery has implications far beyond cancer. The inflammatory molecule driving loss of motivation in cancer is also <a href="https://onlinelibrary.wiley.com/doi/full/10.1155/2011/765624">involved in numerous other conditions</a> − from autoimmune disorders such as rheumatoid arthritis to chronic infections and depression. This same brain circuit might explain the <a href="https://doi.org/10.3390/jcm13072058">debilitating apathy</a> that millions of people suffering from various chronic diseases experience.</p>
<p>Apathy triggered by inflammation may have originally <a href="https://doi.org/10.1038/nri.2015.5">evolved as a protective mechanism</a>. When early humans faced acute infections, dialing down motivation made sense − it conserved energy and directed resources toward recovery. But what once helped people survive short-term illnesses turns harmful when inflammation persists chronically, as it does in cancer and other diseases. Rather than <a href="https://theconversation.com/feeling-sick-is-an-emotion-meant-to-help-you-get-better-faster-126915">aiding survival</a>, prolonged apathy deepens suffering, worsening health outcomes and quality of life.</p>
<p>While translating these findings into therapies for people requires more research, our discovery reveals a promising target for treatment. By intercepting inflammatory signals or modulating brain circuits, researchers may be able to restore a patient’s drive. For patients and families watching motivation slip away, that possibility offers something powerful: hope that even as disease progresses, the essence of who we are might be reclaimed.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/254043/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/cancer-hijacks-your-brain-and-steals-your-motivation-new-research-in-mice-reveals-how-offering-potential-avenues-for-treatment-254043">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/womens-attitudes-toward-masturbation-predict-key-outcomes/" 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;">Women’s attitudes toward masturbation predict key outcomes</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 6th 2025, 18:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1093/jsxmed/qdad173" target="_blank" rel="noopener">The Journal of Sexual Medicine</a></em> suggests that young women who feel empowered and satisfied during masturbation tend to report better sexual function and more positive perceptions of their own genitals. In contrast, those who experience shame or guilt during masturbation show lower levels of sexual desire, satisfaction, and genital self-image.</p>
<p>The authors of the new study sought to better understand the emotional and psychological factors linked to female masturbation and how these factors might relate to broader aspects of sexual well-being. Cultural shifts have encouraged women to explore their own bodies, yet masturbation remains a sensitive topic.</p>
<p>Past research has pointed to potential benefits of masturbation, such as increased self-esteem, better sexual responsiveness, and improved body image. However, few studies have focused specifically on how emotional reactions to masturbation relate to sexual function and genital self-image, particularly among young women.</p>
<p>To address this gap, the researchers surveyed female undergraduate students in Brazil. Participants were recruited through social media platforms including Instagram and WhatsApp and were eligible if they were over 18 and currently enrolled in university. A total of 113 women completed the online survey, although three were excluded because they did not meet the inclusion criteria.</p>
<p>The survey took about 15 minutes to complete and consisted of several parts. It included questions about demographic information, relationship status, and medication use. It also included a detailed section on masturbation habits, such as how often participants masturbated, what techniques they used, and how they felt during the activity. Feelings like empowerment, satisfaction, guilt, and shame were rated on a 5-point scale. The researchers used two standardized tools to assess sexual health and genital self-image: the Female Sexual Function Index, which measures aspects like desire, arousal, and satisfaction, and the Female Genital Self-Image Scale, which evaluates how positively a woman views her genitals.</p>
<p>About three-quarters of participants reported masturbating at least once a month, and around 10% said they did so nearly every day. The majority reported initiating masturbation between the ages of 10 and 16. Clitoral stimulation was the most common technique, and most women (over 80%) reported that they frequently or always achieved orgasm through masturbation.</p>
<p>One of the most consistent patterns in the results was that positive feelings during masturbation—particularly empowerment and satisfaction—were associated with better scores on both the sexual function and genital self-image scales. Women who felt powerful when masturbating tended to score higher in the domains of desire, orgasm, and satisfaction. In contrast, those who reported feeling ashamed or guilty during masturbation scored lower in these areas, suggesting that emotional experiences during self-pleasure may play a more meaningful role in sexual well-being than how often someone masturbates.</p>
<p>Interestingly, the frequency of masturbation was only weakly related to most aspects of sexual function. The only clear link was found in the domain of sexual desire, where women who masturbated daily or more reported higher levels of desire. Other domains such as arousal and satisfaction did not show strong associations with how frequently women masturbated. This finding supports the idea that frequency alone may not determine sexual health; rather, the context and emotional meaning of the activity may be more important.</p>
<p>The study also looked at other factors that might be related to sexual well-being. Being in a stable relationship was associated with higher scores on the sexual function index, compared to being single or in a casual relationship. This supports previous research suggesting that stable partnerships may offer emotional security and sexual fulfillment, which in turn contribute to better sexual functioning.</p>
<p>One notable finding was the link between the use of psychiatric medications and lower sexual function. About 20% of the participants reported using medications for mental health, and these women tended to score lower on the sexual function index. This is consistent with prior research indicating that many psychiatric drugs, especially antidepressants, can have side effects that interfere with sexual desire and responsiveness.</p>
<p>The study also explored the use of sex toys, particularly vibrators. While vibrators were commonly used among women who masturbated daily, their use was associated with lower reported sexual satisfaction. The authors suggest this may not reflect the effects of vibrators themselves, but rather that women who use them more frequently may be doing so to compensate for dissatisfaction in other areas of their sexual lives.</p>
<p>Negative feelings during masturbation were not common, but when present, they appeared to be meaningful. Around 17% of participants reported feeling shame, and 10% reported guilt. Those who felt shame had notably lower scores in desire, arousal, orgasm, satisfaction, and genital self-image. These findings echo other studies showing that shame and guilt related to sexual activity can diminish overall sexual health and satisfaction.</p>
<p>Motivations for masturbation varied among participants. The most frequently reported reason was to achieve sexual satisfaction when a partner was not available. Other common motivations included stress relief, pleasure, and increased sexual awareness.</p>
<p>A significant relationship was also found between positive genital self-image and sexual function. Women who reported more positive feelings toward their genitals tended to have higher levels of satisfaction, arousal, and orgasm. This connection between body image and sexual responsiveness highlights the psychological dimensions of sexual health.</p>
<p>The study has several limitations. Because it was conducted online and relied on voluntary participation, there may be a bias toward women who feel more comfortable discussing masturbation. The use of self-report measures can also lead to inaccuracies due to memory errors or social desirability. In addition, the Female Sexual Function Index is not well-suited for women who have not been sexually active in the past four weeks, which may limit its accuracy in some cases. The cross-sectional nature of the study also means it cannot determine cause-and-effect relationships. Finally, although the sample included women of different ages, most were university students, which may not reflect the broader population.</p>
<p>Despite these limitations, the study offers new insights into how emotional responses to masturbation relate to sexual function and genital self-image among young women. The findings suggest that how a woman feels about masturbation may matter more than how often she does it. Promoting positive attitudes and reducing stigma surrounding female masturbation could play a role in enhancing sexual well-being.</p>
<p>The study, “<a href="https://doi.org/10.1093/jsxmed/qdad173" target="_blank" rel="noopener">Masturbation, sexual function, and genital self-image of undergraduate women: a cross-sectional study</a>,” was authored by Renata Fernandes Soares, Gabriela Tomedi Leites, Tatiane Gomes de Araujo, Gabriela Paludo Pedreti, Taís Marques Cerentini, and Patricia Viana da Rosa.</p></p>
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<td><a href="https://www.psypost.org/daily-use-of-cannabis-is-strongly-associated-with-chronic-inflammation-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Daily use of cannabis is strongly associated with chronic inflammation, study finds</a>
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<p><p>Recent research has found that individuals who use cannabis daily or nearly daily tend to have elevated levels of soluble urokinase plasminogen activator receptor (suPAR), a marker of chronic inflammation. In contrast, less frequent cannabis use was not associated with increased levels of this inflammation indicator. The research was published in <a href="https://doi.org/10.1017/S0033291724002848"><em>Psychological Medicine</em></a>.</p>
<p>Cannabis is a plant genus that includes species such as Cannabis sativa, Cannabis indica, and Cannabis ruderalis. It is widely known for its psychoactive properties, primarily due to compounds called cannabinoids—especially tetrahydrocannabinol (THC). Another major cannabinoid, cannabidiol (CBD), is non-psychoactive and is often used for therapeutic purposes.</p>
<p>Cannabis can be consumed in a variety of forms, including smoking, vaporizing, edibles, and oils. It has a long history of both recreational and medicinal use, with applications in pain relief, anxiety, nausea, and epilepsy. Legal status varies around the world, with some countries fully legalizing it, others permitting only medical use, and many maintaining strict prohibitions.</p>
<p>Long-term or heavy cannabis use has been linked to cognitive impairment, dependence, and mental health issues. More recently, researchers have proposed that frequent cannabis use may contribute to chronic inflammation in the body. This inflammation could in turn play a role in the development of psychosis and other serious mental illnesses associated with cannabis use.</p>
<p>Study author Emmet Power and his colleagues sought to investigate whether cannabis use—particularly daily or near-daily use—is associated with immune system activity and inflammation.</p>
<p>To do this, the researchers examined levels of four biomarkers: interleukin-6 (IL-6), tumor necrosis factor-alpha (TNFα), C-reactive protein (CRP), and soluble urokinase plasminogen activator receptor (suPAR). These markers are involved in immune and inflammatory responses, and elevated levels can indicate infection, chronic inflammation, or increased risk for conditions such as cardiovascular disease, cancer, or sepsis.</p>
<p>The researchers used data from the Avon Longitudinal Study of Parents and Children (ALSPAC), a long-term cohort study that enrolled 14,541 pregnant women living in a specific region of southwest England with expected delivery dates between April 1, 1991, and December 31, 1992. The study initially gathered health-related data from the parents and later continued collecting data from the children themselves.</p>
<p>When the children reached age 24, 3,257 of them were still participating. For the current analysis, the researchers used data from 914 participants in this group. Among them, 22% met criteria for major depressive disorder, 29% for anxiety, and 10% had experienced psychotic symptoms in the previous six months.</p>
<p>Participants provided blood samples, allowing researchers to assess biomarker levels. They also answered a single question about how often they used cannabis and provided additional health and demographic information.</p>
<p>The results showed that just under 5% of participants used cannabis daily, 7% used it weekly or monthly, and 21% reported using it less than once a month. Cannabis use was not associated with IL-6, CRP, or TNFα levels.</p>
<p>However, daily or near-daily cannabis use was strongly associated with elevated suPAR levels. In other words, people who used cannabis frequently tended to have higher levels of this particular marker of inflammation. Less frequent cannabis use did not show this association.</p>
<p>“In summary, our study found that daily/near daily cannabis use is strongly associated with elevated levels of suPAR, a marker of chronic inflammation, at age 24. The relationship between cannabis use and elevated suPAR in particular raise intriguing questions about mechanisms that may underpin the relationship between cannabis exposure; psychotic disorder; and potential roles of frequent cannabis use in oxidative stress, and potential role in chronic diseases in multiple systems,” the study authors concluded.</p>
<p>The study sheds light on the links between cannabis use and immune system activity. However, it should be noted that the design of this study does not allow any causal inferences to be derived from the results.</p>
<p>The paper, “<a href="https://doi.org/10.1017/S0033291724002848">Cannabis use in youth is associated with chronic inflammation,</a>” was authored by Emmet Power, David Mongan, Colm Healy, Subash Raj Susai, Melanie Föcking, Stanley Zammit, Mary Cannon, and David Cotter.</p></p>
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<td><a href="https://www.psypost.org/experimental-vaccine-targeting-tau-protein-shows-promise-for-alzheimers-disease/" 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;">Experimental vaccine targeting tau protein shows promise for Alzheimer’s disease</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 6th 2025, 14:00</div>
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<p><p>A new study published in the journal <em><a href="https://doi.org/10.1002/alz.70101" target="_blank" rel="noopener">Alzheimer’s & Dementia</a></em> reports that a novel vaccine targeting a toxic form of the tau protein generated a strong and long-lasting immune response in mice and monkeys. The vaccine, which uses a virus-like particle to display a key phosphorylated tau fragment, reduced the buildup of pathological tau in the brain, prevented brain shrinkage, and improved memory performance in mice prone to tau-related neurodegeneration. These results offer a potential path forward for treating Alzheimer’s disease and other tauopathies with an approach that could be longer-lasting and more cost-effective than current antibody-based therapies.</p>
<p>The research was motivated by ongoing failures in developing effective treatments for Alzheimer’s disease, especially therapies targeting tau protein. Tau forms tangles in the brains of patients with Alzheimer’s and related disorders, and one specific version of tau—phosphorylated at threonine 181 (pT181)—is known to appear early in disease progression.</p>
<p>While monoclonal antibody therapies have recently gained approval for targeting amyloid beta, efforts to develop antibodies against tau have often failed in human trials. In addition to limited efficacy, antibody treatments are expensive and require repeated intravenous infusions. The researchers behind this new study aimed to overcome those barriers by designing a vaccine that could train the immune system to produce its own antibodies against pT181.</p>
<p>“I am interested in developing a vaccine for Alzheimer’s disease because, when I was young, my grandfather had late-stage confusion and dementia,” said study author <a href="https://hsc.unm.edu/directory/bhaskar-kiran.html" target="_blank" rel="noopener">Kiran Bhaskar</a>, a professor at the University of New Mexico School of Medicine, director of the Brain and Behavioral Health Institute, and co-director of the New Mexico Alzheimer’s Disease Research Center. “At that time, we didn’t even know that his state of confusion was due to Alzheimer’s disease or another type of dementia. Since I got my PhD in neuropathology in 2002, I’ve been working on this topic, and ever since, my team has been trying to understand the disease mechanisms and find a cure.”</p>
<p>To create the vaccine, the team attached a synthetic version of the pT181 tau fragment to the surface of a virus-like particle (VLP) derived from the Qß bacteriophage. These VLPs mimic the structure of real viruses without carrying infectious material, making them a powerful tool for presenting antigens to the immune system. The resulting vaccine, called pT181-Qß, was tested in several animal models of tauopathy, including two different strains of genetically modified mice and a small group of rhesus macaques.</p>
<p>In one set of experiments, mice engineered to develop severe tau pathology (PS19 model) received two intramuscular doses of either the pT181-Qß vaccine or a control treatment. The researchers measured antibody levels, brain pathology, and behavior over several months. Mice that received the pT181-Qß vaccine produced high levels of antibodies targeting pT181, and these levels remained elevated months after the final injection. These mice showed less tau buildup in the hippocampus and cortex, areas of the brain important for memory and learning. They also had fewer tau tangles, reduced brain inflammation, and less brain atrophy, as measured by MRI scans.</p>
<p>“We all age and continue to live longer than our parents and grandparents,” Bhaskar told PsyPost. “Age is the main risk factor for dementia. Without a cure, many of us will end up having either Alzheimer’s disease or another type of dementia. In fact, 1 in 2 people over the age of 80 is diagnosed with Alzheimer’s disease or another type of cognitive disability.”</p>
<p>“Lately, there are reliable blood markers that can detect the disease 10–20 years before the onset of clinical symptoms. When we have this window of opportunity to treat and prevent the disease—or delay its onset—with a vaccine approach, we may have a better quality of life later on as we age.”</p>
<p>Bhaskar and his colleagues observed similar benefits in another mouse model (hTau mice), which expresses non-mutated human tau and mimics features of late-onset Alzheimer’s disease. In these animals, the vaccine again led to strong anti-pT181 antibody responses and reduced tau pathology, including a decline in a key inflammation-related protein (ASC). Mice that received the vaccine also performed better in a Y-maze memory test, suggesting that targeting pT181 helped preserve cognitive function.</p>
<p>To assess the safety and effectiveness of the vaccine in a species more closely related to humans, the scientists also vaccinated six adult rhesus macaques. Three received the experimental vaccine and three received a control. The vaccinated monkeys developed high levels of antibodies against pT181, which were also detected in their cerebrospinal fluid—suggesting the antibodies crossed into the brain. No adverse effects were reported, and extensive blood tests and tissue analysis after death showed no signs of toxicity or immune-related damage.</p>
<p>“Because our approach is built on a dummy virus as a means to attach tau protein—which forms tangles in the brains of people with Alzheimer’s—and then inject it as a vaccine to trick the immune system into thinking that there is a viral attack, which then leads to the production of antibodies against tau, we thought it might cause some unwanted side effects,” Bhaskar explained. “Surprisingly, in three mouse models of Alzheimer’s disease we tested, and also in the rhesus macaques, we did not see any major changes in blood biochemistry or blood cell counts. But the vaccine did the job it was supposed to do—reducing tangles in the brain and improving memory.”</p>
<p>Importantly, the researchers also showed that the antibodies generated by the vaccine were able to bind to tau found in the brains of human Alzheimer’s patients. Using tissue samples from deceased donors and blood from patients with mild cognitive impairment, they found that the vaccine-induced antibodies could detect pT181 and immunoprecipitate tau from human brain lysates. This suggests that the vaccine’s antibodies could recognize the same pathological targets in humans as they did in the animal models.</p>
<p>Although the results in animal models are promising, mouse and monkey brains differ from those of humans, especially in the context of age-related neurodegeneration.</p>
<p>“Humans are not mice,” Bhaskar said. “Although the vaccine worked great even in monkeys in terms of safety and making the antibodies against ‘bad’ tau, until we test it in humans, we always face uncertainties about whether it will work because of the high degree of variability due to various factors.”</p>
<p>One of the main challenges is funding the production of clinical-grade vaccine batches, which can cost millions of dollars. The researchers hope to pursue a combination vaccine strategy similar to existing multivalent vaccines, like Gardasil-9 for human papillomavirus (HPV). Their vision includes targeting multiple forms of tau, amyloid beta, and neuroinflammatory molecules in a single shot to better address the complex biology of Alzheimer’s disease.</p>
<p>“We have an array of ‘bad’ tau-targeting vaccines that we’d like to test as a combination vaccine,” Bhaskar explained. “For example, the FDA-approved vaccine Gardasil-9, which is typically given to teenagers, is also built on this ‘dummy’ virus-like particle platform. It has a cocktail of nine different vaccines targeting different strains of HPV. We want to develop a similar cocktail vaccine approach for Alzheimer’s disease by combining vaccines that target different types of ‘bad’ tau, amyloid beta, and brain inflammation—all of which we are also developing in my lab. That way, the major drivers of dementia—at least in Alzheimer’s disease, which is likely caused by amyloid beta, tau, and inflammation—can be removed from the brain.”</p>
<p>“It costs about $4–5 million just to make a small amount of clinical-grade vaccine for clinical trials. We are trying to find funding to get this off the ground. Until we do human testing, no big pharmaceutical company is likely to risk joining our team. We are now in a ‘gap’ period and really bootstrapping in terms of funding.”</p>
<p>The study, “<a href="https://doi.org/10.1002/alz.70101" target="_blank" rel="noopener">Targeting of phosphorylated tau at threonine 181 by a Qβ virus-like particle vaccine is safe, highly immunogenic, and reduces disease severity in mice and rhesus macaques</a>,” was authored by Nicole M. Maphis, Jonathan Hulse, Julianne Peabody, Somayeh Dadras, Madelin J Whelpley, Manas Kandath, Colin Wilson, Sasha Hobson, Jeff Thompson, Suttinee Poolsup, Danielle Beckman, Sean P Ott, Jennifer W. Watanabe, Jodie L. Usachenko, Koen K Van Rompay, John Morrison, Reed Selwyn, Gary Rosenberg, Janice Knoefel, Bryce Chackerian, and Kiran Bhaskar.</p></p>
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<td><a href="https://www.psypost.org/classical-music-may-promote-calmer-more-stable-fetal-heart-rhythms-study-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;">Classical music may promote calmer, more stable fetal heart rhythms, study suggests</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 6th 2025, 12:00</div>
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<p><p>New research published in the journal <em><a href="https://doi.org/10.1063/5.0236416" target="_blank" rel="noopener">Chaos</a> </em>provides insight into how music affects the developing fetus. By examining changes in fetal heart rate variability in response to classical music, scientists found that exposure to music led to more regular and predictable patterns of fetal heartbeats—suggesting a soothing effect on the fetal autonomic nervous system.</p>
<p>Previous work has suggested that music can stimulate fetal movements or heart rate accelerations, and some studies have hinted at long-term cognitive benefits. However, most studies have relied on conventional ways of measuring fetal heart rate that may miss more subtle changes. This new study aimed to go further by using a mathematical approach known as recurrence quantification analysis to examine the more complex, nonlinear patterns in fetal heart rate fluctuations.</p>
<p>“Our interest arose from a broader effort to understand how early sensory experiences shape autonomic and neurodevelopmental trajectories,” explained Eric Alonso Abarca‑Castro of Universidad Autónoma Metropolitana–Lerma and his co‑authors. “We had seen evidence in newborns that auditory stimulation can modulate heart rate variability, so we wondered whether similar effects could already be detected in utero, using advanced tools like Recurrence Quantification Analysis (RQA). While we cannot yet claim any direct effects on long‑term neurodevelopment, these preliminary findings open the door to future research into how prenatal sensory environments might influence the developing nervous system.”</p>
<p>The research team, based in Mexico, recruited 100 pregnant women in their third trimester from a maternal hospital in Toluca. After screening out cases with signal loss or pregnancy complications, they analyzed high-quality fetal heart data from 37 participants. Each fetus was exposed to two five-minute segments of classical music played through headphones placed on the mother’s abdomen.</p>
<p>The music included “The Swan” by Camille Saint-Saëns and “Arpa de Oro” by Abundio Martínez. The session was divided into four stages: five minutes before music (PRE), five minutes for the first song (STIM1), five minutes for the second song (STIM2), and five minutes after the music ended (POST).</p>
<p>To assess how the music influenced fetal heart rhythms, the researchers used both traditional and advanced measures. Traditional metrics included average heart rate and standard deviation of heartbeat intervals. The more sophisticated recurrence quantification analysis looked at patterns in the timing between beats to assess regularity, complexity, and predictability. Specific measures included determinism, average and maximum line lengths, entropy, and trapping time—each capturing different aspects of the heart rhythm’s dynamics.</p>
<p>After the music ended, fetal heart rate patterns became more predictable and regular. There was a significant increase in determinism, line length, and trapping time from the PRE to POST stage, meaning that the heartbeats followed more stable patterns. Entropy, a measure of signal complexity, decreased after the music, suggesting that the heart rate dynamics became less chaotic. These changes suggest the music may have a calming effect on the fetal autonomic nervous system, which controls involuntary bodily functions such as heartbeat.</p>
<p>“Exposing a fetus to calm, classical music appears to make its heartbeat patterns more regular—and even slightly increases movement—during and immediately after the stimulus,” the researchers told PsyPost. “These changes suggest that simple, non‑invasive interventions like prenatal music might support healthy autonomic development, laying groundwork for better stress regulation after birth. Although we cannot assert that this will directly improve neurodevelopmental outcomes, our work invites further investigation into potential long‑term benefits.”</p>
<p>Interestingly, not all music appeared equally effective. The second piece, the traditional Mexican song “Arpa de Oro,” produced stronger changes in heart rate patterns than the first piece. During the STIM2 phase, the researchers saw increases in maximum line length and trapping time compared to the PRE phase, indicating a more stable and predictable response. The first song did not show statistically significant effects across these measures. This difference raises the possibility that musical characteristics—like melody, rhythm, or cultural familiarity—might influence how fetuses respond.</p>
<p>“Very few prior studies have applied detailed techniques such as RQA to fetal heart data, so it was striking to see clear, differential effects between two classical pieces—Saint‑Saëns’s ‘The Swan’ and Martínez’s ‘Arpa de Oro’—on the fetus’s heart‑rate dynamics,” the researchers said.</p>
<p>Despite the promising results, the study has some limitations. The final sample size was relatively small due to the strict requirements for signal quality. Additionally, the researchers did not assess the behavioral state of the fetus during the recordings, making it harder to link changes in heart rate variability to specific fetal actions like movement or sleep-wake cycles.</p>
<p>“Our sample was relatively small and limited to healthy, low‑risk pregnancies, and we only measured acute responses,” the researchers noted. “We cannot yet say whether these immediate changes translate into long‑term developmental improvements, nor how well they generalize across different populations or musical genres.”</p>
<p>Future studies are planned to explore whether different musical styles produce distinct responses and whether these early effects on heart rate are linked to later neurodevelopment. The team also hopes to follow infants over time to determine if prenatal exposure to music has lasting benefits for emotional or cognitive growth.</p>
<p>“We plan to conduct longitudinal follow‑ups comparing neurodevelopmental and autonomic outcomes in infants who received prenatal musical stimulation versus controls,” the researchers explained. “We also aim to explore a wider range of auditory environments—both soothing and potentially stressful—to map their developmental impacts more fully. Ultimately, we hope these studies will clarify whether and how prenatal music exposure can influence neurodevelopmental trajectories.”</p>
<p>“Beyond its applied implications, this research showcases how RQA can sensitively capture complex physiological responses in utero. We hope it encourages more interdisciplinary work combining psychophysiology, obstetrics, and musicology. While we make no claims about direct neurodevelopmental effects yet, our findings clearly open the door for future investigations into the role of prenatal sensory stimulation.”</p>
<p>The study, “<a href="https://doi.org/10.1063/5.0236416" target="_blank" rel="noopener">Response to music on the nonlinear dynamics of human fetal heart rate fluctuations: A recurrence plot analysis</a>,” was authored by José Javier Reyes-Lagos, Hugo Mendieta-Zerón, Migdania Martínez-Madrigal, Juan Carlos Santiago-Nuñez, Luis Emilio Reyes-Mendoza, Ximena Gonzalez-Reyes, Juan Carlos Echeverría, Eric Alonso Abarca-Castro, Ana Karen Talavera-Peña, Sara Avilés-Hernández, and Claudia Lerma.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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