<table style="border:1px solid #adadad; background-color: #F3F1EC; color: #666666; padding:8px; -webkit-border-radius:4px; border-radius:4px; -moz-border-radius:4px; line-height:16px; margin-bottom:6px;" width="100%">
<tbody>
<tr>
<td><span style="font-family:Helvetica, sans-serif; font-size:20px;font-weight:bold;">PsyPost – Psychology News</span></td>
</tr>
<tr>
<td> </td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/highly-irritable-teens-are-more-likely-to-bully-others-but-anxiety-mitigates-this-tendency/" 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;">Highly irritable teens are more likely to bully others, but anxiety mitigates this tendency</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 12th 2025, 10:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A study of adolescents found that social anxiety weakens the association between irritability and bullying perpetration. In other words, highly irritable adolescents were more likely to bully others—but this link was weaker among those who also had symptoms of social anxiety. The paper was published in <a href="https://doi.org/10.1017/S0954579424000439"><em>Development and Psychopathology</em></a>.</p>
<p>Bullying among adolescents is a deliberate and repeated form of aggressive behavior intended to harm, intimidate, or control another person perceived as vulnerable. It can be physical, verbal, relational (e.g., social exclusion), or digital (cyberbullying). Bullying is most often discussed in the context of school environments but can also occur online or in other social settings. It typically involves a power imbalance between the perpetrator and the victim.</p>
<p>Several factors contribute to bullying perpetration. Exposure to violence or aggression at home can normalize aggressive behavior. Peer dynamics also play a significant role, as adolescents may bully to gain approval or status within a group. Psychological factors such as poor emotion regulation and low empathy are linked to a higher risk of bullying. School climate and weak adult supervision may also increase the likelihood of bullying. In some countries, exposure to bullying is among the top factors influencing academic performance.</p>
<p>Study author Michael T. Perino and his colleagues sought to replicate findings from previous research showing that anxiety can moderate the relationship between irritability and bullying perpetration. Earlier studies suggested that while irritability is linked to a higher likelihood of bullying others, the strength of this association may depend on anxiety. The authors of the current study hypothesized that this moderating effect would be specific to social anxiety, rather than anxiety more broadly.</p>
<p>Participants were adolescents enrolled in the Preschool Depression Study, a long-term research project conducted at Washington University School of Medicine. These participants were originally recruited as preschoolers but were assessed again in early adolescence. The current study used data from 169 adolescents, with an average age of about 12 to 13 years.</p>
<p>Researchers assessed participants’ anxiety symptoms using the Kiddie-Schedule for Affective Disorders and Schizophrenia – Present and Lifetime Version (K-SADS-PL). Irritability was measured using the Preschool Age Psychiatric Assessment, and bullying behavior was reported by parents using the Health and Behavior Questionnaire. All measures were based on either clinician interviews or parent reports.</p>
<p>The results showed that adolescents who engaged in more bullying behavior tended to be more irritable and less socially anxious. As expected, bullying perpetration was not significantly associated with generalized anxiety. Irritable adolescents were also more likely to show generalized aggression (such as fighting), which was associated with higher generalized anxiety but not with social anxiety.</p>
<p>The researchers then tested a statistical model to examine whether social anxiety moderated the relationship between irritability and bullying. The analysis supported this hypothesis: as social anxiety increased, the link between irritability and bullying became weaker. At low levels of social anxiety, irritability was strongly linked to bullying. But at higher levels of social anxiety, that link diminished or even reversed.</p>
<p>“This study demonstrates that social anxiety significantly impacts the relationship between irritability and bully perpetration. Bully perpetration is a persistent and damaging problem, and current interventions have positive, albeit small, effects,” the study authors concluded.</p>
<p>The study sheds light on the role of social anxiety in bullying behaviors. However, it should be noted that the design of this study does not allow any causal inferences to be derived from the results. While it is possible that irritability makes one more likely to bully others, it might also be the case that successfully bullying others can make an adolescent more irritable. Other explanations of the nature of these relationships also remain open.</p>
<p>The paper “<a href="https://doi.org/10.1017/S0954579424000439">Social anxiety moderates the association between adolescent irritability and bully perpetration</a>” was authored by Michael T. Perino, Jennifer C. Harper-Lednicky, Alecia C. Vogel, Chad M. Sylvester, Deanna M. Barch, and Joan L. Luby.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/neuroscientists-identify-brain-pathway-that-prioritizes-safety-over-other-needs/" 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 identify brain pathway that prioritizes safety over other needs</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 12th 2025, 08:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41593-025-01975-6" target="_blank">Nature Neuroscience</a></em> has identified a brain circuit in mice that overrides basic needs like hunger or social contact in favor of seeking safety. Researchers found that a connection between the lateral hypothalamus and the brainstem initiates movement toward shelter in threatening contexts, even when mice are motivated by food or social interaction.</p>
<p>Animals, including humans, are constantly balancing competing needs—such as hunger, social connection, and safety. While the brain must continually assess environmental cues to prioritize which need to address, little was known about the specific deep brain circuits that govern this prioritization. This study set out to uncover whether certain neural pathways could drive safety-seeking behavior even when other needs are pressing.</p>
<p>“We are interested in how the brain controls behaviors through movement and wanted to explore how lateral hypothalamic circuits communicate with brainstem circuits that initiate locomotion,” said study author Ole Kiehn, a professor of neuroscience at the University of Copenhagen and Karolinska Institutet.</p>
<p>The research team focused on the lateral hypothalamus, a region long associated with drives like feeding, and the pedunculopontine nucleus in the brainstem, which plays a key role in initiating movement. Prior studies suggested that electrical or chemical stimulation of the lateral hypothalamus could induce movement in animals, but the precise neurons involved and their role in context-specific behaviors remained unclear.</p>
<p>To explore this, the researchers conducted a series of experiments using genetically modified mice that allowed them to precisely identify and manipulate specific populations of neurons. They focused on excitatory neurons in the lateral hypothalamus that send projections to the pedunculopontine nucleus. Using optogenetics—a method that uses light to control neuron activity—they stimulated these neurons and observed the behavioral outcomes.</p>
<p>When these lateral hypothalamic neurons were activated, the mice rapidly initiated movement. The direction of this movement depended on the context. In situations where the animals faced a potential threat, such as an aversive sound or air puff, they moved toward shelter—even if they were hungry or engaged in social exploration. This behavior was specific to stimulation of this circuit; control stimulations using different wavelengths of light or non-targeted viral injections did not produce the same response.</p>
<p>In behavioral tests, the team showed that activation of this circuit reliably caused mice to abandon food or social interactions and seek shelter. For example, in a test where food and shelter were placed in opposite corners of an arena, hungry mice that had been fasting for over 16 hours chose to retreat to the shelter when the circuit was activated. The same was true when the competing option was the opportunity to investigate another mouse of the opposite sex.</p>
<p>Additional experiments confirmed that this safety-seeking behavior was not a byproduct of general discomfort or motor activation. When the researchers broadly stimulated movement-related neurons elsewhere in the brainstem, the mice became active but did not consistently head for shelter. This suggested that the observed behavior was not just general locomotion but a directed, purposeful action prioritizing safety.</p>
<p>“We initially we thought that lateral hypothalamic to pedunculopontine nucleus circuits would be involved in food seeking, which involves approach to food rather than running to safety away from food,” Kiehn told PsyPost. “It was a surprise to discover the innate and generalized nature of the safety circuits.”</p>
<p>To further test the circuit’s role, the researchers used chemogenetics to artificially increase or decrease the activity of these neurons over longer periods. When they increased activity, mice spontaneously returned to the shelter more often, even in the absence of explicit threats. When they suppressed activity, the animals were slower to respond to threats and less likely to seek shelter. These changes occurred without affecting overall movement levels, indicating that the circuit plays a specific role in driving safety-related behavior.</p>
<p>Neural recordings supported these findings. Using fiber photometry, the researchers tracked real-time activity in the circuit as mice encountered cues linked to potential threats. Activity in the lateral hypothalamus–pedunculopontine circuit rose just before the animals initiated movement toward safety. The increase in neural activity preceded the actual motion, indicating that this pathway likely initiates the decision to retreat.</p>
<p>The researchers also examined whether this circuit had connections to other areas of the brain involved in emotion and motivation. They found that many of the same neurons projected to regions like the ventral tegmental area, the locus coeruleus, and the periaqueductal gray—areas linked to reward, arousal, and defensive behavior. However, only the projection to the pedunculopontine nucleus appeared to directly initiate shelter-seeking locomotion.</p>
<p>To rule out the influence of these other regions, the team selectively inhibited neurons in the ventral tegmental area during activation of the hypothalamus–brainstem pathway. The safety-seeking behavior remained unchanged. This suggests that while other regions may be coactivated, the primary driver of the shelter-seeking response was the connection between the lateral hypothalamus and the pedunculopontine nucleus.</p>
<p>Interestingly, the study also addressed the question of whether the response was related to traditional escape behaviors. Unlike rapid fleeing responses triggered by immediate threats such as predators, the behavior observed here resembled a slower, more deliberate retreat to shelter. This suggests that the circuit may help the animal weigh current needs against potential risks and choose a course of action that favors long-term survival.</p>
<p>The study also ruled out the involvement of a well-known group of hypothalamic neurons called orexin neurons, which are implicated in arousal and feeding. Although these neurons share some characteristics with the population studied here, they were found to be anatomically and functionally distinct.</p>
<p>One of the most intriguing aspects of the study is the possibility that this circuit can be shaped by experience. The researchers observed that external cues, such as sounds previously paired with air puffs, could activate the circuit even in the absence of a physical threat. This suggests that the pathway could play a role in learned avoidance or anxiety-related behaviors.</p>
<p>“Basically, what we have discovered is an evolutionary survival mechanism in the mouse’s brain,” Kiehn explained. “It connects part of the hypothalamus (the lateral hypothalamus) to and area of the brainstem – the pedunculopontine nucleus- that plays a key role in initiating movement. When active, the network sets aside other needs such as food seeking and social contact and makes the mouse run for cover.”</p>
<p>While the findings come from studies in mice, the researchers noted that both the lateral hypothalamus and the pedunculopontine nucleus are found in all vertebrates, including humans. This raises the possibility that similar mechanisms may underlie how other animals—and potentially people—prioritize safety in complex environments.</p>
<p>But the researchers also noted that mice are prey animals with highly developed threat avoidance behaviors, so it is unclear whether the same prioritization system exists in animals that face fewer natural predators. “Even though a lot of species, humans included, are not prey as such, it is possible that similar circuits are vital to the universal balancing of needs fulfilment and avoiding danger,” Kiehn said. “Because the circuit we have discovered can also be affected by external signals that may serve as learning cues, it is possible that the circuit is affected by stressful situations that may eventually lead to increased anxiety.”</p>
<p>Future research will need to determine how this circuit interacts with higher-level decision-making processes and how it may be modulated in different internal states, such as hunger, fatigue, or stress. It is also possible that dysfunction in this circuit could contribute to disorders where threat perception is altered, such as anxiety or post-traumatic stress.</p>
<p>The study, “<a href="https://www.nature.com/articles/s41593-025-01975-6" target="_blank">A hypothalamus–brainstem circuit governs the prioritization of safety over essential needs</a>,” was authored by Nathalie Krauth, Lara K. Sach, Giacomo Sitzia, Christoffer Clemmensen, and Ole Kiehn.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/liberals-and-conservatives-live-differently-but-people-think-the-divide-is-even-bigger-than-it-is/" 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;">Liberals and conservatives live differently — but people think the divide is even bigger than it is</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 12th 2025, 06:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A new study published in the <em><a href="https://doi.org/10.1037/pspp0000545" target="_blank">Journal of Personality and Social Psychology</a></em> has found that political identity is related to some of the most basic aspects of daily life, from how students move through their day to what they do for fun. Although the differences between liberal and conservative students were small, they were consistent and measurable. However, a follow-up study revealed a striking mismatch between reality and perception: students on campus believed the behavioral divide between liberals and conservatives was far larger than it actually was.</p>
<p>The research aimed to understand whether political differences extend beyond opinions and values to include behavior in everyday, nonpolitical activities. While political polarization is often described in terms of opposing beliefs, the study examined whether liberals and conservatives also live different kinds of lives—and whether others perceive those differences accurately.</p>
<p>“I’m really interested in everyday life,” said study author <a href="https://www.sanaztalaifar.com/" target="_blank">Sanaz Talaifar</a>, an assistant professor at Imperial College London. “Kenneth Craik has a great quote about the importance of studying the seemingly mundane. He says, ‘Lives are lived day by day, one day at a time, from day to day, day after day, day in day out … lives as we experience and observe them are inherently quotidian.’ I was interested in whether even the mundane, ostensibly non-political stuff of everyday life is politically polarized.”</p>
<p>“I also think that we, as researchers, live in really exciting times. The technological advancements that have transformed people’s lives have also transformed how we do research. People always have their smartphones with them, and we can use that fact to collect data about what they’re doing in everyday life with an unprecedented scope and granularity (with their consent, of course). I was really excited about using data collected from smartphones to study the everyday behavior of liberals and conservatives.”</p>
<p>The researchers conducted two related studies at the University of Texas at Austin. In the first study, they recruited over 1,200 undergraduates to track their daily behaviors over two weeks using a smartphone app. The app collected data from sensors (such as GPS and microphone) and activity logs (including calls and texts) alongside short daily surveys. Students also completed a one-time questionnaire reporting their political orientation and basic demographics. This combination of passive tracking and self-reports allowed the researchers to capture 61 different behaviors in four domains: social activity, physical movement, academic or work-related activity, and leisure time.</p>
<p>Political orientation was measured on a 7-point scale from “extremely liberal” to “extremely conservative.” The students’ behaviors were then statistically correlated with their political self-placement, with controls in place to account for other possible influences such as gender, ethnicity, personality traits, socioeconomic status, and whether students lived on campus.</p>
<p>Despite attending the same university and living under similar daily constraints, liberal and conservative students showed subtle but consistent differences in their patterns of behavior. The differences were strongest in the leisure domain. Conservative students, for instance, were more likely to spend time in noisy social environments, attend religious spaces, and be present at fraternities or sororities. They also showed slightly higher rates of physical activity, including walking and commuting.</p>
<p>Liberal students, on the other hand, tended to spend more time in transit and visited more varied locations, suggesting a more mobile lifestyle. They also spent more time at home and reported higher use of the internet and social media. In the work domain, conservatives were more likely to be studying or attending meetings, while liberals were more likely to report working and spending time with coworkers. </p>
<p>Interestingly, some of these differences also showed up at specific times of day or week—for example, liberals were more active in the mornings, while conservatives were more likely to rest during that time.</p>
<p>“We knew from prior research that liberals and conservatives have different cultural and consumer preferences,” Talaifar told PsyPost. “We’ve all heard the stereotypes about liberals drinking lattes and conservatives driving trucks. Maybe some of those differences seem obvious. But I don’t think I appreciated the extent to which everyday behaviors that seemingly have nothing to do with politics or cultural stereotypes could also be polarized.”</p>
<p>“Moreover, I don’t think we would necessarily expect those differences when we’re looking at conservatives and liberals who otherwise have so much in common otherwise — they’re all on the same campus, in the same city, roughly the same age, pursuing the same education, and living the same kind of student lifestyle. Even under those conditions, you see that liberals and conservatives behave differently in everyday life.”</p>
<p>These behavioral patterns were small in magnitude but statistically robust. On average, the differences were about the same size as those found between men and women or between different socioeconomic groups in the sample. Most of the associations remained significant even when controlling for potential confounds such as personality traits or religiosity.</p>
<p>“Something we don’t talk about much in the paper is that behavioral differences in everyday life weren’t limited to liberals and conservatives,” Talaifar said. “We found behavioral differences between women and men, upper and lower class students, as well as students of color and white students. So lately I’ve been thinking about how everyday life is bifurcated along all kinds of identity lines, not just political identity.”</p>
<p>The second study looked at how students perceived these behavioral differences. A new group of 156 undergraduates was asked to estimate how often liberal or conservative students on their campus engaged in the same 61 behaviors. Their task was to indicate whether they believed liberals or conservatives were more likely to engage in each behavior, or whether there was no difference. The researchers then compared these perceptions to the actual behavioral data from Study 1.</p>
<p>The results of Study 2 showed a strong disconnect between perception and reality. Most students significantly overestimated how much liberal and conservative students differed in their daily behaviors. When asked to guess which group did a particular activity more, students were incorrect about three out of every four behaviors. Most of the inaccuracies involved imagining partisan differences that did not exist. For example, students frequently assumed conservatives were more likely to commute, even though the data showed no such difference.</p>
<p>The researchers found that students were most accurate when judging leisure behaviors—the domain where real differences were most pronounced. But they were far less accurate in estimating partisan differences in social and work-related behaviors. This suggests that people may be more attuned to visible lifestyle cues, while underestimating—or misunderstanding—less observable daily patterns.</p>
<p>Together, these studies highlight a double layer of polarization: one that exists in behavior, and one that exists in perception. While political identity does shape some aspects of lifestyle, the belief that liberals and conservatives live in completely different worlds is an exaggeration. That misperception may itself contribute to political division. If people assume that those on the other side of the political spectrum live fundamentally different lives, they may be less inclined to interact, cooperate, or empathize with them.</p>
<p>“Liberals and conservatives behave differently in everyday life, but not to the extent that people assume,” Talaifar said.</p>
<p>The researchers argue that lifestyle polarization, even when subtle, can reduce the chances of cross-partisan contact. People who live different kinds of lives—working at different times, visiting different places, socializing in different settings—may have fewer chances to encounter one another. But even more damaging may be the belief that these differences are vast and unbridgeable.</p>
<p>“The behavioral differences were robust and mostly held when we accounted for demographic factors like socioeconomic status, gender, and ethnicity,” Talaifar noted. “But it’s important to remember that the behavioral differences were small overall. There were many behaviors liberals and conservatives engaged in to a similar degree, and other students on campus generally overestimated the degree to which liberals and conservatives behaved differently in everyday life.”</p>
<p>The researchers are now building on their findings by exploring how lifestyle polarization may relate to other important outcomes.</p>
<p>“Right now we’re looking at whether the behavioral differences we found can explain wellbeing differences between liberals and conservatives,” Talaifar explained. “Prior research generally finds that liberals are unhappier than conservatives, so we’re investigating whether their everyday behaviors can explain that. I’m also <a href="https://osf.io/preprints/psyarxiv/6mk2a_v1" target="_blank">working on a project</a> that maps the everyday behavioral patterns of individuals with authoritarian tendencies using data collected with smartphones.”</p>
<p>The study, “<a href="https://psycnet.apa.org/fulltext/2026-13129-001.html" target="_blank">Lifestyle Polarization on a College Campus: Do Liberals and Conservatives Behave Differently in Everyday Life?</a>,” was authored by Sanaz Talaifar email the author, Diana Jordan, Samuel D. Gosling, and Gabriella M. Harari.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/neuroscientists-shed-new-light-on-how-heroin-disrupts-prefrontal-brain-function/" 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 shed new light on how heroin disrupts prefrontal brain function</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 11th 2025, 14:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41386-025-02102-6" target="_blank">Neuropsychopharmacology</a></em> sheds light on how heroin exposure alters brain function related to social interaction and drug craving. Researchers found that a specific group of brain cells in the prefrontal cortex responded less to social cues but more strongly to heroin-related signals after abstinence, a change that may contribute to relapse risk.</p>
<p>The study was motivated by the observation that people with opioid use disorder often struggle with maintaining stable social connections, and that social difficulties may increase the likelihood of relapse. Previous animal studies and clinical reports have suggested that opioid use not only disrupts reward systems in the brain but also impairs social behaviors. Since the prefrontal cortex is involved in both drug-seeking behavior and social cognition, the researchers wanted to explore how this region responds to social and drug-related cues after heroin use.</p>
<p>“People who are suffering from substance use disorders always values drug over any other rewards, such as social connection/interaction. We wanted to understand why this happens. How are drug users’ brains are different from healthy people?” explained study author Zi-Jun Wang, an assistant professor at the University of Kansas.</p>
<p>To do this, they conducted a series of experiments in mice using advanced imaging technology to observe real-time brain activity. The focus was on excitatory neurons in a subregion of the prefrontal cortex called the prelimbic cortex. These neurons are known to play a role in decision-making, impulse control, and processing of social information. The researchers used genetically modified mice that express a fluorescent indicator in these neurons, allowing them to monitor activity levels during specific behaviors.</p>
<p>The experimental procedure involved training mice to self-administer heroin by poking their noses into a designated port, which delivered a small dose of the drug. Control mice received saline instead. After 10 days of this self-administration phase, the researchers imposed a 14-day abstinence period. During and after this abstinence, the researchers tracked drug-seeking behavior, brain activity, and social interaction.</p>
<p>The first finding confirmed that the mice trained to self-administer heroin displayed drug-seeking behavior after abstinence. When placed back into the testing chamber where they had previously received heroin, these mice made significantly more nose-poke attempts to trigger heroin-associated cues—even though no drug was delivered—than the control group. This demonstrated that the heroin-exposed mice retained a strong memory of the drug environment and remained motivated by drug-related signals.</p>
<p>In contrast, when these same heroin-abstinent mice were tested in a social setting, they spent significantly less time engaging with another mouse compared to control animals. This reduction in social behavior was observed in both male and female mice.</p>
<p>What made this study distinctive was the simultaneous measurement of neural activity during these behaviors. Using a method called fiber photometry, the researchers tracked calcium signals in the prelimbic cortex—signals that reflect neuronal activity. During the social interaction test, mice in the heroin group showed a lower level of activation in these excitatory neurons compared to the control group. But during the drug-seeking test, the same neurons showed heightened responses to heroin-associated cues.</p>
<p>“The prefrontal cortex is one of the key brain regions that malfunction after repeated drug exposure,” Wang told PsyPost. “This brain region gets over-activated by drug-associated cues/environments but get under-activated by social cues.” </p>
<p>The study also included recordings of baseline brain activity in the home cage, away from any stimuli. Mice in the heroin group showed reduced spontaneous activity in these neurons during resting conditions, suggesting that the overall functional state of the prefrontal cortex had shifted. These results imply that heroin exposure may leave the brain in a state where it is less responsive to social stimuli but more responsive to drug cues, even after a period of abstinence.</p>
<p>To probe the underlying causes of these changes, the researchers performed electrophysiological recordings of the same neurons. They found that synaptic inputs to these neurons—measured through specific types of electrical currents—were weaker in the heroin group. This suggests that long-term heroin exposure may reduce the strength of connections that normally keep these neurons active during rest and social exploration.</p>
<p>Interestingly, the researchers found a partial relationship between drug-seeking behavior and reduced social interaction in some mice. In particular, mice that made fewer drug-seeking attempts showed a stronger link between low social engagement and previous drug exposure. This may indicate that certain individuals are more vulnerable to the social consequences of drug use, which could in turn influence their risk of relapse.</p>
<p>The researchers also uncovered an unexpected correlation: mice with lower baseline neuronal activity in the prefrontal cortex tended to show stronger activation in response to heroin cues. While it’s unclear why lower resting activity would amplify responses to drug-related signals, the authors suggest it may involve compensatory mechanisms or changes in how inhibitory signals in the brain operate. </p>
<p>“We were surprised to see that although prefrontal activity is diminished at baseline and during social interaction, it is heightened in drug-related environments,” Wang said. “We were also surprised that this pattern in mice is similar to humans. Brain imaging studies focusing on cortical area show that people with substance abuse disorders have higher neuronal response to drug-associated cues, but lower response to other cues.”</p>
<p>Both male and female mice showed the same broad pattern of results, although some differences emerged. For example, the decline in brain activity during social interaction was slightly more pronounced in female mice, hinting at possible sex-specific vulnerabilities. Past studies have noted that female rodents may be more sensitive to social stress, which could interact with drug effects in ways that increase relapse risk.</p>
<p>While this research was conducted in mice, the authors believe the findings may help explain some of the social challenges faced by individuals recovering from opioid addiction. In particular, a brain that is less responsive to positive social cues might be less motivated to seek out healthy relationships, leaving individuals more susceptible to the lure of drug-associated environments.</p>
<p>The study does have limitations. One major question that remains is why the same brain region can show reduced responses to social cues while simultaneously showing increased responses to drug-related ones. The researchers plan to investigate the specific molecular pathways and neural circuits that drive this contrast in future studies. Understanding these mechanisms could help identify new targets for treatments aimed at restoring healthy social motivation and reducing the risk of relapse.</p>
<p>The researchers also note that the current imaging technique, while powerful, cannot distinguish among different groups of neurons within the prelimbic cortex. More refined imaging methods will be needed to tease apart how different cell populations contribute to the behaviors observed.</p>
<p>In the long term, the researchers aim to uncover how the brain’s reward system processes both social and drug-related stimuli after exposure to opioids. Their goal is to find ways to restore balanced activity in the prefrontal cortex, potentially reducing the motivation to seek drugs and improving social functioning in people recovering from addiction.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41386-025-02102-6" target="_blank">Prefrontal cortex excitatory neurons show distinct response to heroin-associated cue and social stimulus after prolonged heroin abstinence in mice</a>,” was authored by Yunwanbin Wang, Junting Liu, Shuwen Yue, Lu Chen, Archana Singh, Tianshi Yu, Erin S. Calipari, and Zi-Jun Wang.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/new-research-identifies-four-distinct-health-pathways-linked-to-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;">New research identifies four distinct health pathways linked to 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;">Jul 11th 2025, 12:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A large study of electronic health records has uncovered four common patterns of medical conditions that tend to unfold in the years leading up to an Alzheimer’s disease diagnosis. These patterns—centered on mental health issues, brain disorders, cognitive decline, and vascular problems—emerged as distinct routes that people often follow before developing Alzheimer’s, offering new insights into how the disease may take shape over time.</p>
<p>The research, published in the journal <em><a href="https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(25)00275-0/fulltext" target="_blank">eBioMedicine</a></em>, suggests that combinations of health problems and the order in which they appear may carry more predictive power than any one condition alone. By identifying the most common multi-step pathways that precede Alzheimer’s, the study provides a new framework for recognizing who may be at elevated risk earlier and more accurately than existing models.</p>
<p>Alzheimer’s disease is a progressive brain disorder that affects memory, thinking, and behavior. It is the most common form of dementia and typically strikes older adults, gradually eroding their ability to live independently. More than 6.7 million people in the United States currently live with Alzheimer’s, and that number is expected to nearly double by 2050. Despite decades of research, there is still no cure, and current treatments only modestly slow progression. Much of the effort to reduce Alzheimer’s burden has focused on identifying people at high risk early enough to intervene—before major cognitive damage occurs.</p>
<p>Scientists have long known that certain conditions like depression, heart disease, and diabetes are associated with greater Alzheimer’s risk. But many past studies looked at these risk factors in isolation, without considering how they might unfold together across time. This new research takes a different approach by examining the sequences in which diseases appear in people’s medical records before they are diagnosed with Alzheimer’s. Rather than just focusing on single conditions, the researchers tried to map out the typical paths people follow, step by step, on the way to Alzheimer’s.</p>
<p>“We were interested in understanding the healthcare pathway people have before a diagnosis of Alzheimer’s disease. Electronic health records help us identify these pathways over time,” said study author Tim Chang, an assistant professor and Augustus S. Rose Chair in Neurology at UCLA.</p>
<p>The researchers analyzed longitudinal health data from nearly 25,000 patients in the University of California Health Data Warehouse, which collects records from six academic medical centers. These patients were between the ages of 65 and 90 and had multiple medical visits across several years. Alzheimer’s diagnoses were identified using standardized billing codes. The researchers then used statistical modeling and advanced techniques from data science to align and compare the sequences of conditions that occurred before Alzheimer’s onset.</p>
<p>They found that 5762 of the Alzheimer’s patients had at least one multi-step disease pathway made up of three or more health conditions that led up to their diagnosis. Using clustering methods to group similar sequences, they identified four major trajectory types. Each one was defined by a central condition and showed distinct patterns of progression.</p>
<p>One of the pathways centered on mental health, particularly depression. People in this group often had anxiety, high blood pressure, diabetes, or cholesterol issues before being diagnosed with depression. Depression then tended to occur several years before Alzheimer’s. This group was more likely to include women and Hispanic individuals, and their records often showed memory-related symptoms appearing one to three years before Alzheimer’s onset.</p>
<p>Another large group followed a pattern marked by brain disorders classified under encephalopathy—broadly defined as disorders of brain function. Conditions like encephalopathy and cerebrovascular disease appeared more quickly before Alzheimer’s diagnosis in this group, and these individuals had the shortest time between their central diagnosis and the onset of Alzheimer’s. This cluster was also associated with higher mortality, meaning patients tended to die sooner after their Alzheimer’s diagnosis than those in other groups.</p>
<p>The third trajectory was dominated by people who had previously been diagnosed with mild cognitive impairment or other degenerative nervous system diseases. This group largely followed what might be considered the classic path of cognitive decline that eventually meets the threshold for an Alzheimer’s diagnosis. These patients had longer medical histories, and their diagnoses often included minor neurological or systemic problems years before Alzheimer’s was identified.</p>
<p>The final group followed a vascular pathway. These patients tended to have cardiovascular-related conditions such as hypertension, cerebrovascular disease, and anemia, as well as musculoskeletal issues like joint pain. They also had the longest medical records and the highest number of comorbidities, indicating a high overall disease burden. Many of them followed stepwise trajectories that included hypertension, then cerebrovascular problems, and finally dementia.</p>
<p>To determine whether these trajectories actually predicted Alzheimer’s risk better than individual conditions, the researchers tested their findings in a separate control group that did not have Alzheimer’s. They found that people who followed any of the multi-step trajectories were significantly more likely to eventually be diagnosed with Alzheimer’s than people who had one or two of the same conditions but not in that specific sequence. In many cases, the increased risk from following a particular path was higher than the risk conferred by any single condition in the path.</p>
<p>The researchers also examined whether these pathways were likely to reflect causal relationships. Using a machine learning method called causal structural learning, they estimated the directionality of links between conditions. Some pathways showed stronger evidence of step-by-step progression. For instance, in the encephalopathy cluster, diagnoses like kidney failure were often followed by brain disorders, which in turn were followed by Alzheimer’s. This suggests that systemic health issues may contribute to neurological decline.</p>
<p>To ensure that these findings were not specific to the University of California dataset, the researchers repeated the analysis in the All of Us Research Program, a national study with a more diverse population. They applied the same methodology and found that the four clusters were largely replicable in this independent sample. Nearly 90% of the Alzheimer’s patients in the All of Us cohort could be assigned to one of the previously identified disease trajectories. Most of the stepwise sequences were again found to be predictive of future Alzheimer’s diagnoses.</p>
<p>The findings provide evidence that “the order or pattern of when diagnoses are made may influence a person’s risk for Alzheimer’s disease,” Chang told PsyPost.</p>
<p>Although the results are promising, the researchers caution that their study has limitations. The data came from electronic health records, which can miss diagnoses made outside the health system or be affected by variations in how doctors code conditions. The team used strict inclusion criteria to improve accuracy, but it’s possible that some cases were missed or misclassified. </p>
<p>Also, because the dataset excluded people over 90, the findings may not generalize to the oldest adults, who are at the highest risk of Alzheimer’s. Finally, the study relied on observed associations rather than biological markers, so while the trajectories are informative, they don’t prove that one condition causes another.</p>
<p>However, the findings still have important implications for public health and clinical care. By identifying common patterns that lead up to Alzheimer’s, doctors may be able to spot people at higher risk earlier and target them for screening or interventions. For instance, someone with a history of depression followed by metabolic issues might be more closely monitored for signs of cognitive decline. The study also highlights the need to treat chronic conditions—such as cardiovascular disease and diabetes—not just in isolation, but in light of how they may interact and evolve over time to affect brain health.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.ebiom.2025.105831" target="_blank">Identifying common disease trajectories of Alzheimer’s disease with electronic health records</a>,” was authored by Mingzhou Fua, Sriram Sankararaman, Bogdan Pasaniuc, Keith Vossel, and Timothy S. Chang.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<table style="font:13px Helvetica, sans-serif; border-radius:4px; -moz-border-radius:4px; -webkit-border-radius:4px; background-color:#fff; padding:8px; margin-bottom:6px; border:1px solid #adadad;" width="100%">
<tbody>
<tr>
<td><a href="https://www.psypost.org/a-surprising-body-part-might-provide-key-insights-into-schizophrenia-risk/" 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 surprising body part might provide key insights into schizophrenia risk</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jul 11th 2025, 11:00</div>
<div style="font-family:Helvetica, sans-serif; color:#494949;text-align:justify;font-size:13px;">
<p><p>A new study published in <em><a href="https://www.nature.com/articles/s44220-025-00414-6" target="_blank">Nature Mental Health</a></em> has found that people with a higher genetic risk for schizophrenia tend to have thinner retinas, even if they do not have the disorder. Using data from nearly 35,000 healthy individuals, the researchers showed that this association was especially pronounced in areas of the retina involved in neural signaling and inflammation, raising the possibility that the eyes could serve as a subtle indicator of schizophrenia-related biology long before symptoms appear.</p>
<p>Schizophrenia is a severe psychiatric condition that affects how a person thinks, feels, and behaves. It often involves hallucinations, delusions, and social withdrawal. The disorder is thought to arise from a complex combination of genetic, developmental, and environmental factors, but researchers still don’t fully understand what biological processes lead to its onset. There are currently no reliable biological tests that can predict who will go on to develop schizophrenia, especially during early stages when interventions may be most effective.</p>
<p>One area that has recently drawn attention is the retina—the light-sensitive tissue at the back of the eye that is part of the central nervous system. Previous studies have found that people with schizophrenia tend to have thinner retinal layers and signs of degeneration. However, because those studies were conducted after diagnosis, it was unclear whether these changes were a result of the disease, the medication used to treat it, or other health complications. This left open the question of whether retinal thinning could be a sign of underlying risk before symptoms begin.</p>
<p>“Schizophrenia is a complex disorder, and we still lack reliable biological markers for early detection or risk stratification,” said study author <a href="https://homanlab.github.io/blog/2025/06/20/nmh/" target="_blank">Philipp Homan</a>, vice chair and chief physician at the Department of Adult Psychiatry and Psychotherapy at the University of Zurich.</p>
<p>“There has been increasing evidence linking immune pathways to schizophrenia, and we were interested in whether these immune-related genetic risks might show up as measurable changes in the body, particularly in the retina, which is accessible and reflects central nervous system processes.”</p>
<p>To address this, researchers at the University of Zurich and colleagues used genetic and retinal imaging data from the UK Biobank, a large database of health information from more than 500,000 volunteers in the United Kingdom. They focused on 34,939 adults of British or Irish ancestry who had no known history of schizophrenia or related disorders. They excluded anyone with eye diseases, diabetes, or other conditions that could affect retinal health, as well as individuals taking antipsychotic medications. This allowed the team to isolate the effects of genetic risk for schizophrenia in a healthy population.</p>
<p>For each participant, the team calculated a polygenic risk score for schizophrenia. This score represents a person’s overall genetic risk based on many small variations in their DNA that have been linked to the disorder in previous studies. They then examined retinal images collected using optical coherence tomography, a noninvasive technique that creates detailed cross-sectional images of the retina. The researchers focused on the macula, a central part of the retina that is densely packed with nerve cells and plays a key role in vision.</p>
<p>After adjusting for factors such as age, sex, smoking status, blood pressure, and image quality, the researchers found that individuals with higher polygenic risk scores had thinner retinas. Specifically, each standard deviation increase in genetic risk for schizophrenia was associated with a reduction of 0.17 microns in macular thickness. While this is a very small change—less than one-tenth of one percent of the average retinal thickness—it was consistent and statistically significant.</p>
<p>The researchers also explored whether genetic risk related to specific biological pathways might be linked to changes in particular retinal layers. The strongest association was found for genes involved in neuroinflammation, or immune system activity in the brain. People with higher genetic risk for schizophrenia within this pathway had thinner ganglion cell inner plexiform layers—regions of the retina responsible for early-stage neural signal processing. Further analysis suggested that this relationship may be partly explained by elevated levels of C-reactive protein, a marker of systemic inflammation, though the effect was modest.</p>
<p>“We were somewhat surprised by the specificity of the association,” Homan told PsyPost. “The genetic risks linked to immune function, rather than schizophrenia risk in general, seemed to be more clearly associated with retinal thinning. This points toward a more targeted biological pathway.”</p>
<p>These findings suggest that retinal thinning, especially in certain inner layers of the retina, could be an early marker of genetic vulnerability to schizophrenia. Importantly, this thinning was observed in people without any diagnosis or treatment for the disorder, suggesting it reflects underlying risk rather than consequences of illness or medication.</p>
<p>The researchers note that their findings build on prior studies showing that schizophrenia can affect the brain’s physical structure, including reductions in gray matter volume. The retina, as an accessible part of the central nervous system, may offer a window into these changes.</p>
<p>“Our results suggest that some genetic risks for schizophrenia, especially those involving immune and inflammatory pathways, are associated with a thinner retina,” Homan said. “This implies that the retina could potentially serve as a non-invasive readout of the brain and its immune changes relevant for psychiatric risk, though this is still early-stage research.”</p>
<p>To test the robustness of their results, the researchers used a variety of statistical techniques, including robust regression models designed to handle data with outliers or uneven variance. They also ran analyses using multiple sets of genetic data to ensure their results were not dependent on a single model. Across these approaches, the association between higher genetic risk for schizophrenia and thinner retina remained consistent.</p>
<p>The study’s large sample size and rigorous exclusion criteria are major strengths. By focusing only on individuals without psychiatric diagnoses or eye diseases, the researchers were able to isolate subtle effects that might otherwise be masked by illness-related factors. They also included detailed information about health and lifestyle, allowing them to account for potential confounding variables.</p>
<p>Still, the researchers acknowledge some limitations. The UK Biobank is not fully representative of the general population. Participants tend to be healthier and less diverse than the broader public, and individuals with schizophrenia are underrepresented. This means the results may not apply equally to other groups, including non-European populations or people with more complex health histories.</p>
<p>“It’s important to realize that we studied healthy people, because we were interest in genetic risk, not manifest disorder,” Homan said.</p>
<p>The measured effect sizes were also extremely small. Although statistically significant, the differences in retinal thickness associated with genetic risk for schizophrenia are unlikely to have any practical effect on vision. At the same time, even small changes can be informative when studied across thousands of individuals, especially when they help uncover biological pathways involved in mental health.</p>
<p>Another important caveat is that polygenic risk scores, while useful for research, are not currently precise enough to predict whether any one person will develop schizophrenia. These scores capture only a portion of the total genetic risk, and they do not account for environmental influences, life stress, or early brain development, all of which are believed to contribute to the disorder.</p>
<p>“These findings are based on population-level data and do not immediately translate to individual diagnosis or prediction,” Homan explained. “The associations are statistical, and many other factors affect retinal thickness. More research is needed before this could inform clinical practice.”</p>
<p>The researchers suggest that future work should explore how environmental factors such as smoking, diet, and stress interact with genetic risk to influence retinal health. Longitudinal studies could help determine whether retinal thinning progresses over time in those at higher risk, or whether it stabilizes. Investigating these changes across different stages of development—from childhood to adulthood—could provide insight into how early in life these differences emerge.</p>
<p>“An interesting next step is to test whether these retinal changes actually help identify people at risk for schizophrenia before symptoms emerge, and whether interventions targeting immune pathways can modify these retinal or brain changes,” Homan said. “This work builds on a broader effort to find neural correlates of mental illness that can be measured easily and early. The retina is promising, but it will take larger and more diverse studies to establish its role.”</p>
<p>The study, “<a href="https://www.nature.com/articles/s44220-025-00414-6" target="_blank">Genetic susceptibility to schizophrenia through neuroinflammatory pathways associated with retinal thinness</a>,” was authored by Finn Rabe, Lukasz Smigielski, Foivos Georgiadis, Nils Kallen, Wolfgang Omlor, Victoria Edkins, Matthias Kirschner, Flurin Cathomas, Edna Grünblatt, Steven Silverstein, Brittany Blose, Daniel Barthelmes, Karen Schaal, Jose Rubio, Todd Lencz, and Philipp Homan.</p></p>
</div>
<div style="font-family:Helvetica, sans-serif; font-size:13px; text-align: center; color: #666666; padding:4px; margin-bottom:2px;"></div>
</td>
</tr>
</tbody>
</table>
<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
<p><strong>This information is taken from free public RSS feeds published by each organization for the purpose of public distribution. Readers are linked back to the article content on each organization's website. This email is an unaffiliated unofficial redistribution of this freely provided content from the publishers. </strong></p>
<p> </p>
<p><s><small><a href="#" style="color:#ffffff;"><a href='https://blogtrottr.com/unsubscribe/565/DY9DKf'>unsubscribe from this feed</a></a></small></s></p>