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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/psychology-researchers-identify-a-burnout-to-extremism-pipeline/" 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;">Psychology researchers identify a “burnout to extremism” pipeline</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 15th 2025, 10:00</div>
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<p><p>When Luigi Mangione was arrested for the alleged murder of the CEO of UnitedHealthcare in December 2024, public reaction shocked observers. Far from universal condemnation, many people expressed support. This was especially true among younger people, with polls showing <a href="https://emersoncollegepolling.com/december-2024-national-poll-young-voters-diverge-from-majority-on-crypto-tiktok-and-ceo-assassination/">41% of young adults</a> viewed the murder as acceptable.</p>
<p>So what leads the average person to justify extreme violence? <a href="https://doi.org/10.1037/vio0000643">Our recently published research</a>, in the special issue <a href="https://www.apa.org/pubs/journals/vio/understanding-violent-extremism">“Understanding violent extremism”</a> of the APA <em>Journal Psychology of Violence</em>, locates the answer in one increasingly widespread phenomenon: workplace burnout.</p>
<p>Mangione’s <a href="https://www.kenklippenstein.com/p/luigis-manifesto">manifesto</a> cites “corruption and greed” as a source of frustration, a sentiment that resonates widely amid growing dissatisfaction with modern work environments. <a href="https://clinicalsocialwork.eu/wp-content/uploads/2024/06/cswhi_03_2024_02_butz_OPR_04.pdf">Recent research</a> shows that broader patterns of systemic frustration and perceived corruption are associated with burnout.</p>
<p>Our study, which took daily surveys from over 600 employees, suggests burnout may quietly fuel worrying attitudes – specifically, the potential justification of violent extremism – towards the perceived source of their distress.</p>
<h2>The burnout to extremism pipeline</h2>
<p>In our study, employees made daily notes of their burnout symptoms, emotional states, and violent extremist attitudes. On days when employees felt more burnt out, they reported significantly more sympathy toward extremist ideas, such as justifying violence against perceived injustices.</p>
<p>The daily grind of burnout produced negative feelings of fear, sadness, shame, and guilt. To alleviate these negative feelings – and regain a sense of purpose – some individuals appeared to find extremist ideologies more appealing.</p>
<p>This phenomenon can be explained through the combined lens of three established psychological theories. The first is <a href="https://oxfordre.com/criminology/display/10.1093/acrefore/9780190264079.001.0001/acrefore-9780190264079-e-249">General Strain Theory</a>, which suggests that daily frustrations lead to violent extremism through the experience of negative emotions.</p>
<p>The second is the <a href="https://www.taylorfrancis.com/chapters/edit/10.4324/9781315227979-4/burnout-existential-perspective-ayala-pines">existential model of burnout</a>, which links burnout to a failed existential quest when meaningfulness in work disappears. Last is <a href="https://journals.sagepub.com/doi/10.1037/gpr0000144">Significance Quest Theory</a>, which argues that when the sense of personal significance is eroded in people’s everyday lives, they might look elsewhere, including to radical beliefs, to restore meaning.</p>
<p>In combination, these ideas, particularly the existential and Significance Quest models, suggest that burnout reflects a failed search for meaning – one that may drive individuals toward violent extremism as a means of restoration. General Strain Theory further contributes by emphasising the emotional path involved in this process.</p>
<h2>Why burnout matters</h2>
<p>Our study does not suggest that individuals experiencing burnout will inevitably engage in extremist violence. Rather, it demonstrates how everyday experiences of burnout can subtly shift individuals toward violent extremist attitudes, thereby normalising the acceptance of violence.</p>
<p>This distinction is critical and is emphasised in the <a href="https://psycnet.apa.org/doiLanding?doi=10.1037%2Famp0000062">two-pyramids model</a>, which differentiates between radicalisation of opinion and radicalisation of action. While the link between the two may be weak, radicalisation of opinion alone can pose a <a href="https://www.ijcv.org/index.php/ijcv/article/view/3807">serious threat to democracies and open societies</a> by eroding social cohesion and fostering polarisation. For this reason, it warrants focused study in its own right.</p>
<p>Today, workplace burnout is alarmingly common, affecting approximately <a href="https://www.vanede.nl/media/2669/gallup-iii-employee-burnout.pdf">three in four employees</a>. This means a huge portion of the workforce experiences the emotional strain capable of fuelling extremist ideas.</p>
<p>While the vast majority will never resort to violence, a society that becomes increasingly tolerant of extremist attitudes risks normalising destructive behaviours and undermining both democratic values and workplace cohesion. Moreover, even if only a small minority ultimately engage in violence, the consequences can still be profound.</p>
<h2>Organisational support can help</h2>
<p>Our findings also reveal an effective form of protection: <a href="https://citeseerx.ist.psu.edu/document?repid=rep1&type=pdf&doi=b6e9be0e81ee13424f7140685a689bd2d85d7d3c">perceived organisational support</a>. Employees who felt that their organisations genuinely valued their contributions and cared about their wellbeing were less likely to gravitate toward extremist ideologies, even when experiencing burnout symptoms.</p>
<p>However, there’s a critical caveat to this: organisational support is most effective at mitigating the harmful effects of burnout before negative emotions take hold. Once employees have crossed that emotional threshold, additional support alone has limited power to prevent the escalation toward violent extremist attitudes.</p>
<p>Employers therefore hold the key to addressing burnout before it escalates into something more serious. Organisations must proactively invest in burnout prevention, not merely as a health initiative, but as a vital strategy for preserving stability, both in the workplace and in society at large.</p>
<p>This means promoting fairness and transparency in the workplace, ensuring employees feel recognised and valued, training managers to identify early signs of burnout and respond proactively, and establishing open, safe channels for employee feedback.</p>
<p>Concerns about fairness don’t stop at the office door. Broader perceptions of injustice in society may also fuel extremist sympathies, especially when individuals are already mentally exhausted. For instance, efforts to pursue the <a href="https://www.justice.gov/opa/pr/attorney-general-pamela-bondi-directs-prosecutors-seek-death-penalty-luigi-mangione">death penalty against Mangione to serve President Trump’s political agenda</a> may deepen perceptions of systemic unfairness, which will only exacerbate radical views.</p>
<h2>The broader implications</h2>
<p>Burnout is more than just workplace exhaustion or disengagement. It signals a deeper and more dangerous existential vulnerability. A workplace that ignores employee burnout doesn’t just risk lower productivity – it creates a breeding ground for ideological radicalisation.</p>
<p>As both workplaces and societies confront a surge in extremist sentiment, including support for violent acts framed as resistance to corporate greed, it is crucial that we learn to recognise the underlying psychological triggers. Burnout is one of them, and employees don’t just need support to do their jobs better – they need it to maintain a sense of meaning, stability, and connection in their lives.</p>
<p>A burnt-out mind will seek meaning wherever it can find it. If the workplace fails to offer that, extremist ideologies are often ready to fill the void, with consequences that reach far beyond the office walls.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/261123/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/burnt-out-and-radicalised-how-workplace-exhaustion-breeds-extremist-thinking-new-study-261123">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/cognitive-ability-becomes-increasingly-stable-after-age-3-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;">Cognitive ability becomes increasingly stable after age 3, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 15th 2025, 08:00</div>
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<p><p>An analysis of data from the Colorado Longitudinal Twin Study suggests that general cognitive ability tends to be highly stable across the lifespan, but this stability only emerges after about age 3. Measures of cognitive ability taken during infancy were associated with cognitive ability in adulthood, but only weakly. The study was published in <a href="https://doi.org/10.1073/pnas.2426531122"><em>PNAS</em></a>.</p>
<p>Cognitive ability refers to a person’s capacity to acquire knowledge, think, reason, solve problems, and adapt to new situations. Individuals differ in these abilities, and such differences are meaningful even in early childhood, as they are linked to academic achievement. Higher cognitive ability is generally associated with better school outcomes. It also contributes to job performance, particularly in roles that require complex reasoning, quick learning, or problem-solving.</p>
<p>People with higher cognitive ability tend to make more informed decisions, as this capacity helps them weigh options and anticipate consequences more effectively. Cognitive ability also influences health-related behaviors, since individuals with higher ability are typically better at understanding medical guidance and managing long-term conditions. Research indicates that cognitive ability correlates with income, occupational status, and career advancement, making it a significant factor in socioeconomic mobility. It also shapes social interactions by supporting communication skills, perspective-taking, and conflict resolution.</p>
<p>Study author Daniel E. Gustavson and his colleagues aimed to examine the stability of general cognitive ability across the first 30 years of life. They assessed cognitive ability at five key time points: ages 1–2, 3, 7, 16, and 29. They hypothesized that cognitive ability would become increasingly stable after early childhood and that the predictive power of infant cognition for adult cognitive ability would be limited. The researchers also sought to quantify how early genetic and environmental influences on cognitive ability contribute to later cognitive outcomes by comparing data from twin participants.</p>
<p>The study analyzed data from 1,098 individuals in the ongoing Colorado Longitudinal Twin Study, including 552 females. While not every participant completed assessments at all five time points, the sample size remained substantial across waves: 640 completed infant cognition measures at 7 to 9 months of age as part of the Twin Infant Project; 814 completed one or more assessments between ages 1 and 2; 757 were assessed at age 3; 820 at age 7; 813 at age 16; and 684 participants completed the adult assessment at approximately age 29.</p>
<p>As expected, the results showed that two specific infant cognition measures—novelty preference (object novelty) and tester-rated task orientation—were modestly associated with adult cognitive ability, with correlation coefficients of approximately 0.16 and 0.18. These associations were statistically significant but weak. In contrast, cognitive ability scores from age 7 onward showed strong correlations with later measures, with coefficients ranging from 0.72 to 0.86. This indicates a pattern of increasing stability with age.</p>
<p>Analyses using twin models revealed that 22% of the variation in adulthood cognitive ability could be attributed to genetic influences that were already present by age 3 or earlier. An additional 10% was explained by shared environmental influences measured at ages 1 to 2, which may include factors such as the home, school, or neighborhood environments shared by siblings.</p>
<p>“Findings suggest that genetic and environmental influences on GCA [general cognitive ability] demonstrate considerable stability as early as age 3 y [years], but that measures of infant cognition are less predictive of later cognitive ability,” the study authors concluded.</p>
<p>The study sheds light on the stability of cognitive abilities from infancy to adulthood. However, it should be noted that participants all came from Colorado. Results on other populations and cultures might not be identical. Authors also note that the reliability of infant cognition measures is much lower than that of cognitive ability measures used at older ages.</p>
<p>The paper, “<a href="https://doi.org/10.1073/pnas.2426531122">Stability of general cognitive ability from infancy to adulthood: A combined twin and genomic investigation</a>,” was authored by Daniel E. Gustavson, Giulia A. Borriello, Mohini A. Karhadkar, Soo Hyun Rhee, Robin P. Corley, Sally-Ann Rhea, Lisabeth F. DiLalla, Sally J. Wadsworth, Naomi P. Friedman, and Chandra A. Reynolds.</p></p>
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<td><a href="https://www.psypost.org/cannabis-compounds-have-distinct-effects-on-brain-connectivity-and-blood-flow-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;">Cannabis compounds have distinct effects on brain connectivity and blood flow, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 15th 2025, 06:00</div>
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<p><p>A new study in rats provides evidence that tetrahydrocannabinol (THC) and cannabidiol (CBD) have opposing effects on brain function—and that combining the two produces more muted changes than THC alone. Published in the <em><a href="https://doi.org/10.1177/02698811251360745" target="_blank" rel="noopener">Journal of Psychopharmacology</a></em>, the research used advanced neuroimaging to compare how these cannabis-derived compounds alter patterns of communication and blood flow in the brain.</p>
<p>Cannabis contains a wide range of bioactive compounds, but two of its most studied constituents are THC and CBD. THC is primarily responsible for the euphoric high associated with cannabis use and exerts its effects through the cannabinoid type 1 receptor, found throughout the brain. It is also approved for medical use in treating symptoms such as nausea in chemotherapy patients, spasticity in multiple sclerosis, and chronic pain.</p>
<p>In contrast, CBD does not produce a high and has a very different pharmacological profile. It interacts with multiple systems in the body but does not strongly bind to cannabinoid receptors. Instead, it has shown promise as a treatment for conditions like epilepsy, anxiety, and psychosis. A pharmaceutical-grade form of CBD, known as Epidiolex, is already approved for certain seizure disorders. Research also suggests CBD may reduce neuroinflammation and protect brain cells in neurodegenerative diseases.</p>
<p>There is growing interest in how THC and CBD interact when used together. Products like nabiximols, which contain THC and CBD in roughly equal amounts, are already used to treat multiple sclerosis symptoms. These combination treatments are thought to allow for higher THC doses while limiting unwanted side effects, but the mechanisms behind these interactions remain unclear. The new study sought to shed light on this by examining how THC, CBD, and their combination affect brain connectivity and blood flow using non-invasive imaging.</p>
<p>“We were interested in directly comparing the effects of the two best-known cannabis constituents: cannabidiol (CBD) and tetrahydrocannabinol (THC),” said study author Diana Cash, an associate professor at King’s College London and director of <a href="https://brain-imaging.org/" target="_blank" rel="noopener">The Brain Centre</a>.</p>
<p>“CBD, which is non-psychoactive, is often promoted as a treatment for a wide range of issues—from inflammation to stress and insomnia—although the scientific evidence does not always support these claims. THC, on the other hand, is often stigmatized because it is the psychoactive component of cannabis, the one responsible for the ‘high,’ yet it also has recognized therapeutic benefits.”</p>
<p>“We wanted to investigate how these compounds act alone and in combination, as in ‘nabiximols,’ a licensed medication used to treat pain and spasticity in multiple sclerosis. We used rats as an experimental model but applied clinically relevant brain imaging techniques to measure neural connectivity and blood flow. These kinds of controlled studies are difficult to perform in humans due to ethical and practical challenges, such as prior recreational drug use, but of course, animal research also comes with limitations when translating findings to people.”</p>
<p>The researchers used 48 adult male Sprague Dawley rats divided into four groups. Each group received a single dose of either THC, CBD, a THC:CBD combination, or a placebo. The THC dose was 10 milligrams per kilogram, the CBD dose was 150 milligrams per kilogram, and the combination contained both THC and CBD in a ratio similar to that used in nabiximols. About two hours after administration, the rats were scanned using magnetic resonance imaging to assess two key brain functions: resting-state functional connectivity and cerebral blood flow.</p>
<p>Functional connectivity refers to the level of synchrony in activity across different brain regions. It is measured by analyzing patterns in blood oxygenation over time and provides insight into how different parts of the brain communicate. Cerebral blood flow, on the other hand, is a measure of how much blood is reaching different brain areas, serving as a proxy for neural activity and metabolic demand.</p>
<p>The imaging data were analyzed using a combination of graph theory and statistical modeling. This allowed the researchers to examine both overall brain-wide changes and effects within specific neural networks. They also analyzed tissue samples to measure the concentrations of THC, CBD, and their metabolites in the brain and plasma.</p>
<p>The most pronounced effects were seen in the THC group. Rats given THC showed widespread increases in functional connectivity across the brain, especially between cortical regions and between the cortex and the hippocampus and striatum. Graph theory analysis revealed that THC increased both the strength and clustering of connections, suggesting more tightly knit communication within and between brain networks. Cerebral blood flow was also significantly elevated in many regions, including the thalamus, striatum, and cingulate cortex.</p>
<p>The rats given CBD, in contrast, showed a general reduction in functional connectivity. This reduction was not localized to a specific area but was more diffuse across the brain. Unlike THC, CBD did not produce any significant changes in cerebral blood flow. These results suggest that CBD may have a dampening or calming effect on neural synchrony, which aligns with its potential use in treating anxiety and seizure disorders.</p>
<p>“We were somewhat surprised that CBD reduced brain connectivity,” Cash told PsyPost. “However, this is not necessarily a negative outcome—it’s possible that THC-induced hyperconnectivity reflects an overstimulated state, whereas CBD may allow the brain to “reset” or relax. This interpretation is speculative, especially since our work was conducted in rats rather than humans, but it is an intriguing possibility.”</p>
<p>When THC and CBD were given together, the effects were intermediate. Functional connectivity and cerebral blood flow were both elevated compared to the placebo group, but not to the same degree as with THC alone. Seed-based analyses showed that the combined treatment produced some of the same patterns as THC, such as increased connectivity between the striatum and sensorimotor cortex, but the effects were less robust.</p>
<p>Importantly, the researchers observed that CBD seemed to moderate some of THC’s impact on brain activity. This was evident in both the graph theory metrics and the regional analyses. Increases in connectivity and blood flow were smaller in the combination group than in the THC-only group, even though THC levels in the brain were actually higher in the combination condition. This finding supports the idea that CBD can alter THC’s effects, not just by reducing its absorption or metabolism but by actively influencing brain function.</p>
<p>The researchers also used a multivariate statistical approach to identify distinct neural signatures associated with each treatment. This analysis revealed that THC, CBD, and the combination treatment each produced unique patterns across connectivity and blood flow measures. These signatures were consistent enough to differentiate the drug groups and could be useful in future efforts to classify how other cannabis-based compounds affect the brain.</p>
<p>“We found that THC strongly increased both brain connectivity and blood flow, while CBD had no effect on blood flow but significantly reduced connectivity,” Cash explained. “The combination produced an effect somewhat similar to THC, but much weaker—suggesting that CBD can dampen or modulate the effects of THC. This could help explain why traditional cannabis, which contains both compounds, is often reported to produce milder effects compared to newer strains bred for very high THC content.”</p>
<p>“Our results are broadly consistent with several previous studies in both animals and humans, though the literature is quite mixed. One striking aspect we noticed is just how heterogeneous the findings in this field are—likely reflecting differences in methods, models, and populations studied.”</p>
<p>While the findings offer insight into how cannabis compounds affect brain function, there are limitations to consider. The study was conducted in healthy, anesthetized male rats, which means the results may not fully translate to human users or to individuals with medical conditions. The use of anesthesia, although necessary for high-quality imaging, may interact with cannabinoid signaling and affect brain activity in ways that do not occur in awake brains.</p>
<p>Additionally, the study only examined the short-term effects of a single dose. Longer-term studies are needed to understand how repeated use of THC, CBD, or their combination might reshape brain networks over time. There is also a need to study female animals and include disease models to better assess the therapeutic potential of these compounds.</p>
<p>Future research may build on these findings by incorporating additional brain imaging techniques, testing different doses and delivery methods, or examining how other cannabinoids and non-cannabinoid components of cannabis influence brain activity. The researchers note that they are working toward creating a comprehensive database of brain imaging profiles for different drugs. Such a resource could aid in drug development by linking specific brain signatures to therapeutic or side effect profiles.</p>
<p>“The biggest limitation is that our experiments were conducted in animals, and the rats were lightly sedated during imaging to minimize stress,” Cash said. “These factors limit direct generalization to humans. Still, one of our main goals was to establish a framework for comparing the brain effects of different compounds, including synthetic cannabinoids and other psychoactive drugs. In that sense, the study provides a valuable blueprint for future work.”</p>
<p>“We are currently extending this work by profiling a range of drugs that affect the brain. Ultimately, we aim to build a database of brain signatures using advanced imaging techniques, combined with AI and machine learning, to support drug discovery and the development of new therapeutics.”</p>
<p>“We would like to emphasize the importance of using comparable brain imaging approaches in both animal and human studies, to make results more directly translatable,” Cash added. “Standardization of imaging analysis methods across research groups would also help the field move forward more effectively.”</p>
<p>The study, “<a href="https://doi.org/10.1177/02698811251360745" target="_blank" rel="noopener">Acute cannabidiol (CBD), tetrahydrocannabinol (THC) and their mixture (THC:CBD) exert differential effects on brain activity and blood flow in rats: A translational neuroimaging study</a>,” was authored by Eilidh MacNicol, Michelle Kokkinou, Maria Elisa Serrano Navacerrada, Donna-Michelle Smith, Jennifer Li, Camilla Simmons, Eugene Kim, Michel Mesquita, Loreto Rojo Gonzalez, Tierney Andrews, Sally Loomis, Royston A Gray, Volker Knappertz, Benjamin J Whalley, Andrew C McCreary, Steven CR Williams, David Virley, and Diana Cash.</p></p>
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<td><a href="https://www.psypost.org/genetically-modified-zebrafish-provide-new-clues-about-the-biology-of-aggression-and-anxiety/" 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;">Genetically modified zebrafish provide new clues about the biology of aggression and anxiety</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 14th 2025, 14:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1111/apha.70042" target="_blank" rel="noopener">Acta Physiologica</a></em> suggests that one gene may play a big role in how animals react to social situations. Researchers in Austria found that zebrafish missing a gene called lrrtm4l1 were less aggressive and more anxious than normal fish. This gene is similar to one found in humans, and the results suggest it may help shape how the brain handles emotions and social behavior. The study provides clues about how certain mental health traits might be linked to brain biology.</p>
<p>LRRTM4 has previously been associated with childhood aggression, autism spectrum disorders, and Tourette syndrome, but the mechanisms behind these links have remained unclear. By switching off the corresponding gene in zebrafish, the team was able to study its effects on behavior, brain chemistry, and gene expression. The results suggest that LRRTM4 may influence how threats are perceived and responded to, possibly by altering neurotransmitter systems such as dopamine and adenosine.</p>
<p>Florian Reichmann and his team at the Medical University of Graz were drawn to this line of research because of prior genetic studies linking LRRTM4 polymorphisms with aggression and neurodevelopmental disorders. While large genome-wide association studies have found correlations between variations in this gene and traits like aggression or autism, these studies do not reveal how the gene actually influences brain function.</p>
<p>“Our lab is very interested in behavioural neurogenetics to study the influence of genetic factors on behavior,” Reichmann told PsyPost.</p>
<p>LRRTM4 codes for a synaptic adhesion protein involved in shaping connections between neurons, especially in brain regions responsible for emotion and memory. Its role in organizing synaptic transmission makes it a promising candidate for investigating behavioral regulation. Despite this, no previous animal study had examined the behavioral consequences of knocking out LRRTM4 or its orthologues. Reichmann’s group aimed to close this gap using zebrafish, a model increasingly used in neuroscience due to their genetic similarity to humans and transparent, fast-developing embryos.</p>
<p>“When we started this work no detailed behavioral characterization in an animal model with disturbed Lrrtm4 function existed,” Reichmann explained. “We wanted to fill this gap by using zebrafish as a model system and try to understand the consequences of lrrtm4l1 deficiency, a zebrafish orthologue of the LRRTM4 gene, at the behavioral level.”</p>
<p>Zebrafish share about 70 percent of their genes with humans, and over 80 percent of disease-linked genes have a zebrafish equivalent. Their social nature, well-characterized behaviors, and ease of genetic manipulation make them well-suited for studying the neural and molecular basis of social traits.</p>
<p>The researchers began by mapping where the lrrtm4l1 gene was most active in the zebrafish brain. They found high expression in the telencephalon, inferior lobe, and optic tectum—regions associated with emotion regulation, sensory processing, and social decision-making. Notably, the gene was strongly expressed in the dorsal and medial zones of the telencephalon, which correspond to the hippocampus and amygdala in mammals. These structures are known to be involved in fear, memory, and threat detection.</p>
<p>Next, the researchers created a line of zebrafish with a disrupted version of the lrrtm4l1 gene. These mutant fish appeared physically normal, but their behavior differed significantly from that of wild-type fish. In multiple anxiety-related tests, the mutants showed signs of heightened nervousness. They moved less in open spaces, avoided the upper parts of a novel tank, and showed erratic swimming patterns—typical indicators of anxiety in zebrafish models.</p>
<p>In contrast, when tested for aggression using a mirror-based challenge, the mutant fish were less combative than their unaltered counterparts. They spent less time confronting their reflection, though they were just as quick to notice it. The researchers concluded that the lowered aggression was unlikely to be a side effect of anxiety alone. Importantly, other social behaviors such as shoaling and response to familiar versus unfamiliar groups were unaffected, suggesting that the gene specifically influences aggression without impairing social engagement more broadly.</p>
<p>“The most important findings are that zebrafish with lrrtm4l1 deficiency are more anxious and less aggressive,” Reichmann told PsyPost. “This suggests that the gene plays an important role for these behaviors.”</p>
<p>On a molecular level, deleting the gene caused widespread changes in brain activity. Transcriptomic analysis of the telencephalon revealed 126 genes that were either up- or down-regulated compared to controls. Many of these were involved in neural signaling and synaptic plasticity. For example, the researchers noted increased expression of genes involved in neurotransmitter regulation and reduced expression of genes linked to excitatory synapse function.</p>
<p>A particularly notable finding was increased dopamine turnover in the mutant fish. Dopamine is a neurotransmitter involved in reward, motivation, and aggression. The researchers found higher levels of homovanillic acid, a breakdown product of dopamine, suggesting faster dopamine metabolism. While dopamine itself was not elevated, the ratio of its metabolite to the original neurotransmitter pointed to a shift in how the brain was using this chemical.</p>
<p>The team also detected lower levels of adenosine, another neurotransmitter involved in regulating arousal and anxiety. Reduced adenosine has been linked to anxiety-like behavior in both fish and mammals. Additional changes were noted in serotonin and melatonin levels, though these did not reach statistical significance.</p>
<p>“Mechanistically, we found gene expression changes in the glutamatergic and serotonergic neurotransmitter systems as well as altered concentrations of homovanillinic acid, a dopamine metabolite and adenosine in the mutant brain, indicating strong effects on multiple major neurotransmitter systems,” Reichmann said.</p>
<p>In untargeted metabolomics, the researchers found reduced levels of a compound similar to methyl vanillate, a derivative of vanillic acid with reported antioxidant and neuroprotective properties. They also observed changes in molecules related to lipid metabolism and amino acid processing. These biochemical shifts add another layer of evidence that the gene influences brain function at multiple levels, from structural development to real-time neurotransmission.</p>
<p>Taken together, the findings suggest that lrrtm4l1 influences behavior by shaping how the brain responds to threats and social stimuli. The changes in neurotransmitter dynamics and synaptic signaling likely contribute to the behavioral differences seen in the mutant fish.</p>
<p>“The observed changes in the dopaminergic and serotonergic neurotransmitter system are surprising, because so far LRRTMs have been described as important regulators of excitatory glutamatergic synapses and inhibitory retinal GABAergic synapses only,” Reichmann explained. “This warrants further investigation. On the other hand our findings of reduced aggression in lrrtm4l1 mutants fits with the described association of aggression and LRRTM4 in humans.”</p>
<p>While the results provide new insight into how LRRTM4 may shape behavior, the authors caution against drawing direct conclusions about human conditions from zebrafish models. One limitation is that zebrafish have a second version of the LRRTM4 gene, known as lrrtm4l2, which was not examined in this study. It remains unclear whether this second gene compensates for the loss of lrrtm4l1 or has its own distinct role.</p>
<p>“This gene might have similar functions to lrrtm4l1, but also other functions/effects,” Reichmann said. “It would be interesting to study a double knockout mutant line for both of these genes.”</p>
<p>Another open question is whether the effects observed in zebrafish would be mirrored in mammals. “A next step could therefore also be to investigate the effects of Lrrtm4 deficiency on emotional-affective behaviour in another species such as the mouse,” Reichmann noted.</p>
<p>The study, “<a href="https://doi.org/10.1111/apha.70042" target="_blank" rel="noopener">Deficiency of the Synaptic Adhesion Protein Leucine-Rich Repeat Transmembrane Protein 4 Like 1 Affects Anxiety and Aggression in Zebrafish</a>,” was authored by Eva Tatzl, Giulia Petracco, Isabella Faimann, Marco Balasso, Agnes Anna Mooslechner, Thomas Bärnthaler, Giovanny Rodriguez-Blanco, and Florian Reichmann.</p></p>
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<td><a href="https://www.psypost.org/researchers-shed-light-on-how-personality-and-anxiety-relate-to-insomnia/" 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;">Researchers shed light on how personality and anxiety relate to insomnia</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 14th 2025, 12:00</div>
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<p><p>A recent study found that individuals with pronounced neuroticism and those who are less open to experience tend to report more severe insomnia symptoms. Anxiety appears to mediate the link between neuroticism and insomnia. The paper was published in the <a href="https://doi.org/10.1111/jsr.70003"><em>Journal of Sleep Research</em></a>.</p>
<p data-start="412" data-end="914">Insomnia is a common sleep disorder characterized by difficulty falling asleep, staying asleep, or waking too early and being unable to return to sleep. People with insomnia often feel unrefreshed upon waking and may experience reduced energy throughout the day. The condition can be acute, lasting a few days or weeks, or chronic, persisting for months or longer. Causes include stress, anxiety, depression, poor sleep habits, medical conditions, or the use of stimulating substances such as caffeine.</p>
<p data-start="916" data-end="1273">Insomnia affects both the quality and quantity of sleep, leading to problems with attention, concentration, and memory. It can also increase irritability and negatively impact mood, work performance, and relationships. Chronic insomnia raises the risk of various health problems, including hypertension, heart disease, obesity, and weakened immune function.</p>
<p data-start="1275" data-end="1678">Study author Bárbara Araújo Conway and her colleagues aimed to examine whether personality traits are associated with insomnia severity. They also explored whether anxiety and depression mediate or moderate the relationship between neuroticism and insomnia. The researchers hypothesized that individuals with insomnia would show higher levels of neuroticism compared to those without sleep difficulties.</p>
<p data-start="1680" data-end="1885">Participants were divided into two groups: those with insomnia and those without sleep-related complaints. The insomnia group included 353 individuals, while the comparison group included 242 participants.</p>
<p data-start="1887" data-end="2068">The average age of participants with insomnia was 40 years, compared to 37 years in the group without insomnia. Women made up 78% of the insomnia group and 86% of the control group.</p>
<p data-start="2070" data-end="2475">All participants completed an online survey that included assessments of insomnia severity (using the Insomnia Severity Index), personality traits (using the NEO-FFI-R), and symptoms of depression and anxiety (using the Hamilton Anxiety and Depression Rating Scales). The personality assessment measured five traits: neuroticism, extraversion, openness to experience, agreeableness, and conscientiousness.</p>
<p data-start="2477" data-end="2943">Neuroticism reflects a tendency to experience negative emotions such as anxiety, anger, or depression, and difficulty managing stress. Extraversion captures sociability, assertiveness, and the pursuit of positive emotions. Openness to experience reflects curiosity, creativity, and a preference for novelty. Agreeableness is associated with compassion, trust, and cooperativeness. Conscientiousness involves self-discipline, organization, and goal-directed behavior.</p>
<p data-start="2945" data-end="3186">The results showed that individuals who scored higher in openness to experience and conscientiousness tended to report less severe insomnia symptoms. In contrast, those with higher levels of neuroticism tended to report more severe symptoms.</p>
<p data-start="3188" data-end="3424">Symptoms of anxiety and depression were also linked to more severe insomnia. In fact, the associations between these emotional symptoms and insomnia were stronger than the associations between insomnia and any of the personality traits.</p>
<p data-start="3426" data-end="3704">The researchers tested a statistical model to examine the relationships between personality traits, insomnia, and emotional symptoms. After accounting for anxiety and depression, only openness to experience remained associated with insomnia severity—and this link was very weak.</p>
<p data-start="3706" data-end="3943">Further analysis suggested that anxiety may mediate the relationship between neuroticism and insomnia. That is, individuals high in neuroticism may be more prone to anxiety, which in turn is associated with more severe insomnia symptoms.</p>
<p>“The present study demonstrated that neuroticism and openness to experience personality traits are significant predictors of insomnia severity. In the case of neuroticism, the association is fully mediated by anxiety symptoms and moderated by depression symptoms,” the study authors concluded.</p>
<p>The study sheds light on the links between personality traits and insomnia. However, it should be noted that the design of the study does not allow any causal inferences to be derived from the results.</p>
<p>The paper, “<a href="https://doi.org/10.1111/jsr.70003">Personality traits and insomnia: direct and anxiety-mediated associations,</a>” was authored by Bárbara Araújo Conway, Marwin Machay Indio do Brasil do Carmo, Helder Sergio Lira Soares Filho, Andrea Cecília Toscanini, Rosa Hasan, Marcela Mansur Alve, and Renatha El Rafihi-Ferreira.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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