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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/could-this-natural-protein-be-the-key-to-reversing-age-related-memory-loss/" 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;">Could this natural protein be the key to reversing age-related memory loss?</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 17th 2025, 10:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1111/acel.14493" target="_blank" rel="noopener">Aging Cell</a></em> has identified a promising molecule that may help reverse cognitive decline associated with both normal aging and Alzheimer’s disease. Scientists found that increasing the levels of a protein called Hevin—secreted by astrocytes, a type of support cell in the brain—improved memory and learning in middle-aged mice. The intervention worked in both healthy animals and those genetically modified to model Alzheimer’s disease, and it did so without affecting the buildup of amyloid plaques, a hallmark of the condition.</p>
<p>The researchers, based at the Federal University of Rio de Janeiro and the University of São Paulo in Brazil, were motivated by growing evidence that astrocytes play an underappreciated role in brain health. Historically, Alzheimer’s research has focused heavily on neurons and the accumulation of amyloid beta plaques. But in recent years, studies have shown that astrocytes help regulate synapse formation and stability, and their dysfunction may contribute to cognitive impairment. This research aimed to explore how one astrocyte-secreted protein, Hevin, might influence the aging brain.</p>
<p>“I have dedicated most of my life to studying how the brain works at the molecular level, which drove me to question: what happens there as we get older that impacts its normal function? That question dictates most of my projects today,” said study author Felipe Cabral-Miranda, a staff scientist at the Federal University of Rio de Janeiro.</p>
<p>To test this, the researchers examined Hevin expression in brain tissue from both Alzheimer’s patients and healthy controls. They found that Hevin levels were significantly lower in the brains of people with Alzheimer’s, particularly within astrocyte subtypes linked to the disease. These findings were mirrored in a mouse model of Alzheimer’s known as APP/PSEN, which shows memory loss and plaque accumulation. In both humans and mice, Hevin appeared to be reduced in areas of the brain important for memory.</p>
<p>Building on this observation, the researchers designed an experiment to increase Hevin production specifically in the hippocampal astrocytes of mice. They used a type of viral vector—adeno-associated virus (AAV)—to deliver the gene for Hevin under a promoter that activates only in astrocytes. The gene was injected directly into the hippocampus, the brain region critical for memory. This was done in both wild-type mice and the APP/PSEN Alzheimer’s model mice at middle age.</p>
<p>After either one or six months of Hevin overexpression, the mice underwent a battery of behavioral tests designed to assess different forms of memory. These included the novel object recognition test, the Barnes maze for spatial learning, and the novel object location task. In all cases, mice with elevated astrocytic Hevin levels performed significantly better than controls. They were better at remembering object placements and navigating to specific locations, and they showed more engagement with new stimuli.</p>
<p>“Initially, we tested if an artificial genetic manipulation in the brain could prevent the negative features in Alzheimer’s disease using an animal model,” Cabral-Miranda told PsyPost. “To our surprise, those interventions could also benefit aged animals without Alzheimer’s disease! In other words, we found a molecule target that could impact both pathological and also normal brain aging in mammals.”</p>
<p>These cognitive improvements occurred even though the amyloid plaque burden in the brains of the Alzheimer’s model mice remained unchanged. Using immunofluorescence imaging, the researchers confirmed that Hevin did not reduce the number or size of beta-amyloid plaques. This suggests that the improved cognition came from other mechanisms, most likely involving synaptic structure and function.</p>
<p>“We found that our treatment ameliorated age-associated cognitive decline but did not impact the appearance of beta-amyloid plaques, which are one of the ‘hallmarks’ of Alzheimer’s disease<br>
and is believed to be one of its primary causes,” Cabral-Miranda said. “Our data indicate that we can improve cognitive decay in the disease by alternative mechanisms.”</p>
<p>To understand those mechanisms, the team conducted a proteomic analysis of the hippocampus in treated and untreated mice. They found that Hevin overexpression altered the levels of numerous proteins involved in synaptic signaling, dendritic development, and cytoskeletal dynamics. In Alzheimer’s model mice, Hevin increased the expression of proteins related to chemical synapse modulation, such as Shank3, Cask, and Ntrk2—key players in maintaining and stabilizing synapses. In wild-type mice, the affected proteins were more involved in actin filament organization and neurotransmitter release.</p>
<p>Confocal microscopy revealed increased colocalization of presynaptic and postsynaptic proteins in the hippocampus of mice with elevated Hevin. This suggests stronger or more mature synapses, which aligns with the observed behavioral improvements. Interestingly, the sets of proteins influenced by Hevin differed between the Alzheimer’s model and the wild-type mice, implying that the protein exerts its beneficial effects through different biological pathways depending on the brain’s condition.</p>
<p>To assess whether these findings have relevance for humans, the researchers analyzed gene expression data from Alzheimer’s patients and found that Hevin levels in brain tissue correlated positively with the expression of several key synaptic genes. This reinforces the idea that Hevin supports healthy brain function by regulating synaptic components.</p>
<p>The study introduces Hevin as a promising candidate for therapies targeting cognitive decline. Because Hevin is secreted by astrocytes and can influence neurons indirectly, it may be possible to develop drugs that stimulate its production or mimic its effects. One of the challenges will be designing compounds that can cross the blood-brain barrier and maintain Hevin’s beneficial actions without unwanted side effects.</p>
<p>The findings provide evidence that “it is possible to ameliorate some aspects of brain aging pharmacologically and in the near future we will be able to delay cognitive decay using those strategies,” Cabral-Miranda told PsyPost.</p>
<p>“Hevin is a well-known molecule involved in neural plasticity. It’s naturally secreted by cells in the central nervous system that support the functioning of neurons and are known as astrocytes. We found that the overproduction of hevin is capable of reversing cognitive deficits in aged animals by improving the quality of synapses in these rodents,” added Flávia Alcantara Gomes, the head of the Cellular Neurobiology Laboratory the Institute of Biomedical Sciences.</p>
<p>But the researchers emphasize that this is early-stage work in mice, and there is a long road ahead before any human applications become available. Still, their findings challenge the dominant narrative that reducing amyloid plaques is the key to reversing Alzheimer’s symptoms. Instead, their work highlights the potential of glial-targeted therapies and a broader approach to treating age-related cognitive decline.</p>
<p>Some limitations of the study include its reliance on animal models and invasive gene delivery techniques. While the APP/PSEN mouse model captures several aspects of Alzheimer’s disease, it does not replicate the full complexity of the human condition. Moreover, the AAV method used to increase Hevin is not yet practical for clinical use. Future research will need to explore whether Hevin-based therapies can be delivered systemically, whether Hevin levels in the blood or cerebrospinal fluid could serve as biomarkers for cognitive decline, and how the molecule behaves across different stages of aging and neurodegeneration.</p>
<p>“We performed an analysis that showed that the molecules impacted by our treatment were also observed in human brain samples, which indicates that it is strongly associated with human brain cognitive decline as well,” Cabral-Miranda noted. “However, it is important to highlight that our preclinical data arises from animal models (mice) and further studies must be performed using human cohorts to confirm them. It is also important to highlight that the molecule Hevin is a bit hard to be converted in an efficient drug, although our study indicated a path to generate more efficient drugs for dementia.”</p>
<p>The researchers are currently investigating whether Hevin levels change in the blood of older adults and whether such changes might help predict cognitive decline or Alzheimer’s disease. They also hope to understand how astrocytes differ across brain regions and how this diversity affects synaptic health.</p>
<p>“We aim to study if the levels of this molecule are changed in the blood of aged individuals as a means to determine if it can be used as a more accurate test for Alzheimer’s and other forms of dementia,” Cabral-Miranda said.</p>
<p>“Of course, in the future it’ll be possible to develop drugs that have the same effect as hevin. For now, however, the fundamental benefit of this work is a deeper understanding of the cellular and molecular mechanisms of Alzheimer’s disease and the aging process. The originality lies in understanding the role of the astrocyte in this process. We’ve taken the focus away from neurons, shedding light on the role of astrocytes, which we’ve shown could also be a target for new treatment strategies for Alzheimer’s disease and cognitive impairment,” Gomes said.</p>
<p>The study, “<a href="https://doi.org/10.1111/acel.14493" target="_blank" rel="noopener">Astrocytic Hevin/SPARCL-1 Regulates Cognitive Decline in Pathological and Normal Brain Aging</a>,” was authored by Felipe Cabral-Miranda, Ana Paula Bergamo Araujo, Danilo Bilches Medinas, and Flávia Carvalho Alcantara Gomes.</p></p>
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<td><a href="https://www.psypost.org/inhaled-dmt-produces-rapid-and-lasting-antidepressant-effects-in-treatment-resistant-depression/" 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;">Inhaled DMT produces rapid and lasting antidepressant effects in treatment-resistant depression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 17th 2025, 08:00</div>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41386-025-02091-6" target="_blank" rel="noopener">Neuropsychopharmacology</a></em> has found that inhaled N,N-dimethyltryptamine (DMT), a fast-acting psychedelic compound, produced rapid and sustained antidepressant effects in people with treatment-resistant depression. Participants reported major reductions in depression and suicidal thoughts within a day of dosing, with benefits lasting up to three months. The therapy was safe, well-tolerated, and may offer a more accessible alternative to existing treatments.</p>
<p>DMT is a naturally occurring psychedelic compound found in certain plants and also produced in small amounts in the human body. It is best known as the main psychoactive ingredient in the Amazonian brew ayahuasca, but unlike ayahuasca, which requires co-administration of substances that prolong its effects, vaporized DMT acts quickly and clears the system within about 20 minutes. Because of its short duration and inhalation delivery, DMT has attracted interest as a potentially more scalable and less disruptive option for psychedelic therapy. The researchers aimed to investigate whether this compound could offer fast, lasting relief for people with depression who have not responded to traditional treatments.</p>
<p>“My team and I have been studying psychedelics, especially ayahuasca and DMT, for almost 20 years now,” said study author Draulio Barros de Araujo, a professor of neuroscience at the Brain Institute at Federal University of Rio Grande do Norte and director of the Center for Advanced Medical Psychedelics.</p>
<p>“What caught our attention with vaporized DMT is how it offers such a deep and intense psychedelic experience in a very short window of time. We were curious to see whether such a brief intervention, when supported properly, could still make a meaningful difference for people struggling with treatment-resistant depression.”</p>
<p>The study focused on individuals with treatment-resistant depression—a severe form of depression that does not improve after trying at least two different antidepressant medications. Fourteen adults were recruited through online ads, clinician referrals, and word-of-mouth. All met criteria for moderate to severe depression and had failed to respond to multiple prior medications. Participants received two doses of inhaled DMT in a controlled hospital setting: a lower dose of 15 milligrams followed by a higher dose of 60 milligrams about 90 minutes later. Both sessions occurred on the same day and were accompanied by preparation and integration support from trained clinicians.</p>
<p>Participants inhaled DMT using a medical-grade vaporizer. During the experience, they lay back in a quiet room with dim lighting and calming music while being monitored by a psychiatrist, psychologist, and nurse. The team measured participants’ vital signs, mood, and subjective experience before, during, and after the sessions. Clinical assessments took place immediately after dosing, then at 1 day, 1 week, 2 weeks, 1 month, and 3 months later.</p>
<p>The researchers found that depression symptoms, measured by the Montgomery-Åsberg Depression Rating Scale (MADRS), dropped significantly within 24 hours of treatment. On average, scores fell by 21 points—enough to shift many patients from a range of severe depression to mild or even minimal symptoms. About 79% of participants responded to the treatment by day 1, and 71% achieved full remission. By day 7, the response rate rose to nearly 86%, and more than half of participants remained in remission. Even after three months, 57% still showed a meaningful response and 36% remained in remission, despite receiving no further DMT.</p>
<p>“One of the most surprising aspects was just how consistently strong the clinical response was, even though the DMT experience itself only lasts about 10 to 20 minutes,” De Araujo told PsyPost. “Many participants not only reported emotional breakthroughs during the session, but also experienced lasting changes in mood and outlook from just a single dose. That’s not something we typically see with most psychiatric interventions.”</p>
<p>In addition to easing depressive symptoms, inhaled DMT also sharply reduced suicidal thoughts. Nearly 90% of participants had suicidal ideation at the start of the study, with almost half considered to be at severe risk. One day after treatment, no participants showed severe suicidal ideation. Improvements in suicidality were maintained in most participants through the 3-month follow-up. Notably, the reduction in suicidal thoughts closely tracked with improvements in mood, suggesting that the antisuicidal effect was related to the overall antidepressant impact.</p>
<p>Subjective reports indicated that the DMT experience was intense but generally positive. Participants described vivid imagery, altered perception, and insightfulness, with most rating the experience as pleasant. Physiological measurements showed temporary increases in blood pressure and heart rate shortly after dosing, similar to what might occur during moderate exercise, but no serious adverse events were reported. The most common side effects were throat irritation and coughing from inhalation, which resolved quickly. Headaches and mild discomfort were reported by some participants the following day.</p>
<p>Interestingly, the intensity of the psychedelic experience did not predict treatment outcome. While some participants had mystical or highly visual experiences, the researchers found no strong statistical links between specific features of the trip and clinical improvements. This suggests that the therapeutic effects of DMT might not depend on achieving a particular type of altered state. However, one measure—complex visual imagery—did show a trend toward association with better outcomes, echoing past research on psychedelics like ayahuasca and psilocybin.</p>
<p>One of the most promising aspects of this treatment is its practicality. Unlike longer-acting psychedelics like psilocybin or LSD, which require several hours for each session, vaporized DMT produces its effects in about 20 minutes. The entire protocol—including screening, preparation, dosing, and integration—can be completed in a single day. This has important implications for making psychedelic-assisted therapy more affordable and scalable, especially in public health systems with limited resources.</p>
<p>“The main takeaway is that even an ultra-short psychedelic experience, when delivered in a safe and supportive setting, can lead to rapid and sustained improvements in depression,” De Araujo said. “Perhaps most importantly, we saw a significant reduction in suicidal ideation in many participants within 24 hours, and those effects were still present months later. This suggests that DMT-assisted therapy might offer fast-acting relief, which could be especially valuable in urgent clinical situations.”</p>
<p>While these results are encouraging, the study has limitations. It was open-label, meaning both participants and researchers knew they were receiving DMT, which raises the possibility of placebo effects. The sample size was small, and the findings need to be confirmed in larger randomized controlled trials. In addition, the researchers did not collect pharmacokinetic data to measure how much DMT was actually absorbed, which limits conclusions about dose-response relationships. Some participants had minor fluctuations in symptoms over time, and one experienced a relapse in suicidality, underscoring the need for follow-up care.</p>
<p>“This was a Phase 2a open-label study, without a placebo group, and the number of participants was small,” De Araujo noted. “We have to be cautious in how we interpret the results.”</p>
<p>Future studies will need to compare DMT directly with placebo or other treatments, test repeated dosing regimens, and examine how integration sessions contribute to long-term outcomes. Better understanding how individual differences—such as prior psychedelic use, expectations, or co-occurring medication—affect results will also help tailor treatments. Monitoring for rare but serious side effects, including cardiovascular changes, will be essential as researchers scale up trials.</p>
<p>“From the beginning, our goal has been to develop a model of psychedelic-assisted therapy that fits within clinical, ethical, and economic boundaries,” De Araujo explained. “We believe that treatments that are overly long or expensive will face serious obstacles when it comes to integration into health systems, especially in countries like Brazil, where resources are limited and access is a real concern. In that sense, the vaporized DMT protocol we designed seems to strike a promising balance: it’s efficient, potentially scalable, and still therapeutically meaningful. Going forward, we aim to refine this model and test it in larger, controlled trials, always with a focus on safety, accessibility, and real-world feasibility.”</p>
<p>“This work is part of a larger movement, one that’s challenging old assumptions and inviting us to reimagine mental health care through the lens of altered states of consciousness. Psychedelics are not a magic bullet, but they can offer powerful tools when approached with scientific rigor, cultural sensitivity, and genuine care for the human experience. It’s been incredibly meaningful to witness how these experiences can reconnect people with themselves, and sometimes even bring hope back into view.”</p>
<p>The study, “<a href="https://doi.org/10.1038/s41386-025-02091-6" target="_blank" rel="noopener">Rapid and sustained antidepressant effects of vaporized N,N-dimethyltryptamine: A phase 2a clinical trial in treatment-resistant depression</a>,” was authored by Marcelo Falchi-Carvalho, Fernanda Palhano-Fontes, Isabel Wießner, Handersson Barros, Raynara Bolcont, Sophie Laborde, Sérgio Ruschi B. Silva, Daniel Montanini, David C. Barbosa, Ewerton Teixeira, Rodrigo Florence-Vilela, Raissa Almeida, Rosana K. A. de Macedo, Flávia Arichelle, Érica J. Pantrigo, José V. Costa-Macedo, João Arthur da Cruz Nunes, Luiz Antonio de Araújo Costa Neto, Luis Fernando Nunes Ferreira, Luísa Dantas Corrêa, Romária Bárbara da Costa Bezerra, Emerson Arcoverde, Nicole Galvão-Coelho, and Draulio B. Araujo.</p></p>
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<td><a href="https://www.psypost.org/new-study-upends-decades-old-narrative-about-democrats-and-the-white-working-class/" 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 study upends decades-old narrative about Democrats and the white working class</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 17th 2025, 06:00</div>
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<p><p>A new study published in <em><a href="https://journals.sagepub.com/doi/abs/10.1177/10659129241287503" target="_blank" rel="noopener">Political Research Quarterly</a></em> casts doubt a widely accepted view of American political history. For years, scholars and pundits have argued that the Democratic Party once held the strong support of the white working class—only to lose it starting in the 1960s due to the party’s embrace of civil rights and liberal social issues. But political scientist Jeffrey M. Stonecash finds that this story doesn’t match the historical data. His analysis suggests the white working class was never a consistently solid base for Democrats after the 1930s, and that its shift toward the Republican Party started much earlier than many assume.</p>
<p>Stonecash undertook this study after encountering surprising results during research for his recent book <a href="https://amzn.to/4dmo8at"><em>The Transformation of the Republican Party</em></a>. While exploring how Republicans gained political strength in the postwar era, he tested the popular belief that Democrats lost the white working class in the 1960s and 1970s because of racial and cultural backlash. Expecting to find evidence for that theory, he instead discovered that white working-class support for Democrats had already eroded by the late 1940s. That contradiction led him to a deeper investigation using data from Gallup surveys, the American National Election Studies, and historical voting records.</p>
<p>“This focus on the voting of the white working class emerged as of result if research on another issue. I was writing a book on how the Republican Party has changed over time,” said Stonecash, distinguished professor emeritus at Syracuse University. “A conventional explanation of their resurgence in presidential and congressional elections is that they drew the white working class away from the Democratic Party after the 1960s because Democrats became too liberal on race and social issues.”</p>
<p>The dominant narrative in political science and media describes a dramatic realignment that began in the 1960s. According to this view, white working-class voters in northern cities had long been a bedrock of Democratic support thanks to the New Deal programs of the 1930s. But as the Democratic Party shifted toward civil rights, feminism, and other progressive causes, the story goes, those voters felt alienated and began voting Republican. Political shifts under presidents like Lyndon Johnson and Ronald Reagan are often described as pivotal turning points in this transformation.</p>
<p>“To verify that, I ran the American National Election Studies time series and was most surprised to find it remarkably inaccurate,” Stonecash explained. “I ran the analysis multiple times because the results are so at odds with the standard explanation. I then acquired Gallup poll data and realized Democrats received strong white working-class support only in 1936 and 1940 and then it faded.”</p>
<p>To investigate, Stonecash began by reexamining the supposed baseline of Democratic support: the New Deal coalition of the 1930s. Using Gallup polls from 1936 to 1948, he tracked how white working-class voters outside the South supported Democratic presidential candidates. The data showed a surge in 1936 and 1940, but that support fell steadily over the next decade. By 1948, only about half of white lower-class voters were backing Democrats, and that number remained flat in subsequent decades. The idea that Democrats had solid working-class backing through the 1950s and then lost it in the 1960s simply didn’t hold up.</p>
<p>Stonecash also analyzed long-term voting trends from 1952 to 2020, focusing on presidential and House elections. He defined the white working class using three measures: education (those without a college degree), income (those in the bottom two-thirds of earners), and self-identification as working class. Across all indicators, Democratic support was modest—typically hovering around 50 percent or lower. Contrary to the belief that the white working class abandoned Democrats after 1964, the data show that Democrats only won a majority of their votes in one presidential election: Lyndon Johnson’s landslide in 1964.</p>
<p>For House elections, Democrats performed slightly better, with white working-class support reaching or exceeding 50 percent in many years. But the patterns showed no dramatic drop tied to race or cultural issues in the 1960s or 1980s. Instead, white working-class support for Democrats was already soft by the early 1950s and remained relatively stable until a sharper decline occurred after 2008.</p>
<p>“The basic findings are a great surprise,” Stonecash told PsyPost. “There is a voluminous literature focused on how race and social issues transformed American politics. They have been important, but it is not as simple as portrayed. It also means that the portrayal of the white working class as reactionary is too simple.”</p>
<p>Stonecash also examined party composition to see whether the Democratic Party had historically depended more on the white working class than the Republican Party. Using presidential election data, he calculated what share of each party’s vote came from non-college white voters or low-income whites. In the 1950s and 1960s, both parties drew similar portions of their support from the white working class. Over time, Democrats became less reliant on these voters, not because they defected in large numbers, but because the party grew its base among nonwhite voters and college-educated whites. Republicans, by contrast, remained anchored in white working-class support.</p>
<p>The study highlights a key methodological point: party identification can lag behind actual voting behavior. For decades, many white working-class voters continued to call themselves Democrats even as they voted Republican in presidential elections. Stonecash argues that relying on identification rather than actual votes can distort assessments of partisan change. His data show that defections—Democrats voting for Republican presidential candidates—have been a persistent feature since the 1950s.</p>
<p>“Two matters are important,” Stonecash explained. “First, Republicans have been winning a majority of the white working class in presidential elections since 1952. The story that the rise of racial and social issues pushed the white working class to Republicans has problems. We need a serious reexamination of the consistency of white working-class support for Republicans.”</p>
<p>“Second, Donald Trump did not engineer a dramatic shift of the white working class to Republicans. A majority was already supporting Republicans. He attracted roughly five percent more support than recent candidates but not more than Reagan. He is less the transformative vote attractor than many have suggested.”</p>
<p>At the same time, Stonecash acknowledges the limits of his analysis. Aggregating white working-class voters into a single group obscures important differences among them. While some may vote Republican for cultural or religious reasons, others might prioritize economic concerns. Unfortunately, political surveys often provide little insight into how this group thinks about the economy and how they view their long-term prospects.</p>
<p>“Focusing on the white working class as an aggregate, even as I do in these comments, is too simple,” Stonecash noted. “They are a diverse collection of people and the bases of their support for Republicans differ. Some is due to conservative positions on social issues. But we do not know enough about how the white working class thinks about economic issues and how they can survive and prosper in society. We have lots of survey data about racial and social issues, but nearly enough about how they think about the economy and how they should function. I hope this work sets off more research about that.”</p>
<p>He also cautions against using outdated assumptions to guide political strategy or public discourse. Both major parties have used the narrative of working-class realignment to advance competing moral arguments—either celebrating their support as a sign of authenticity or blaming progressive activists for electoral losses. But if that foundational story is flawed, the conclusions drawn from it may be misleading.</p>
<p>“There is much research necessary expand on the issue of white working class voting,” Stonecash said. “To analyze it more, I have spent the last year or so working on a book entitled <em>The Myth that Democrats Lost the White Working Class</em>. t is an effort to build on the article and ask how did a conventional wisdom develop if the data do not support it and what do we make of all the theories and analyses about how race and social issues moved people to the Republican Party. I also make a stab at trying to explain why a majority of the white working class has voted for Republican presidential candidates.”</p>
<p>“I have always been fascinated by how conventional wisdoms develop that are inaccurate,” he concluded. “I have researched some prior ones. This issue demonstrates how powerful a conventional wisdom can be in structuring how we think about change in American politics.”</p>
<p>The study, “<a href="https://doi.org/10.1177/10659129241287503" target="_blank" rel="noopener">The Democrats Loss of the White Working Class: Another Look at the Evidence</a>,” was published September 26, 2024.</p></p>
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<td><a href="https://www.psypost.org/loss-of-empathy-in-frontotemporal-dementia-traced-to-weakened-brain-signals/" 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;">Loss of empathy in frontotemporal dementia traced to weakened brain signals</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 16th 2025, 18:00</div>
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<p><p>Frontotemporal dementia has gained significant attention in recent years after the family of actor Bruce Willis announced in 2023 that he had been <a href="https://www.theaftd.org/mnlstatement23/?utm_source=Instagram&utm_medium=Social&utm_campaign=MNL23">diagnosed with the condition</a>. A year later, it was revealed that US chat show host Wendy Williams had also been <a href="https://www.prnewswire.com/news-releases/wendy-williams-diagnosed-with-primary-progressive-aphasia-and-dementia-302068851.html">diagnosed with the condition</a>.</p>
<p>Yet despite all this recent attention, there’s still much we don’t know about frontotemporal dementia – including what mechanisms cause certain symptoms, and how we can better spot signs of the disease earlier on. But <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2827334">our research</a> has uncovered the brain processes that underlie one of the disease’s earliest symptoms. This finding brings us one step closer to better diagnosing and treating the condition.</p>
<p>Frontotemporal dementia accounts for <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10852906/">approximately 5% of dementia cases</a>. Symptoms typically begin in a person’s late sixties or seventies. The disease primarily affects behaviour, personality and language abilities.</p>
<p>A hallmark symptom of frontotemporal dementia, which sets it apart from other forms of dementia (such as Alzheimer’s disease), is early loss of empathy. This often manifests as diminished warmth and concern for loved ones. This symptom can be profoundly unsettling for family members and loved ones close with the patient. They may feel as though the patient’s personality has transformed – and that their efforts to help and support are met with indifference.</p>
<p>While <a href="https://www.sciencedirect.com/science/article/abs/pii/S0149763410001739?via%253Dihub">loss of empathy</a> has been the focus of <a href="https://psycnet.apa.org/fulltext/2020-82377-001.html">much research</a> from the scientific community, the precise brain mechanisms underlying the loss of empathy in frontotemporal dementia remain unclear.</p>
<p>Alongside colleagues from Karolinska Institute, Lund University and Umeå University in Sweden, we conducted a study which sought to <a href="https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2827334">understand how empathy diminishes</a> in frontotemporal dementia. We looked at 28 patients with frontotemporal dementia and compared them against 28 healthy people.</p>
<p>To conduct our study, we used a type of brain scan called functional magnetic resonance imaging (fMRI). While in the fMRI scanner, participants viewed images of hands being pricked by needles. These images were contrasted with those of hand being touched by a q-tip. This is a well-established neuroscience test that is designed to evoke feelings of concern and distress as witnessing another person in pain. We analysed the brain activity of the patients with frontotemporal dementia as they viewed the images.</p>
<p>In healthy volunteers, the anterior insula, anteria cingulate and thalamus are the brain regions responsible for monitoring internal bodily signals (such as pain). These brain systems became active when they observed the images of a person in pain.</p>
<p>But in the patients with frontotemporal dementia, activity in these crucial brain regions was significantly reduced. These reductions were strikingly related to the degree of empathy patients exhibited in their daily lives, as judged by questionnaires filled out by family members.</p>
<h2>Empathy and brain function</h2>
<p>Empathy is typically thought to be comprised of two dimensions. Emotional empathy is the ability to react to others’ feelings (such as their distress and concern). Cognitive empathy is the capacity to understand the intention of others.</p>
<p>Although the two are closely related, they’re not quite the same thing. It’s also possible for a person to possess one facet of empathy but not the other. The difference between <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3427869/">the two facets of empathy</a> can actually be exemplified by two psychiatric conditions, antisocial personality disorder and autism.</p>
<p>People diagnosed with antisocial personality disorder are typically good at understanding the intentions and motivations of other people (<a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC3427869/">cognitive empathy</a>), but cannot empathise emotionally. This can lead to a disregard for other people. On the other hand, a person with autism typically has emotional empathy skills but might not have the ability to infer other peoples’ intentions (<a href="https://link.springer.com/article/10.1007/s10803-025-06802-2">cognitive empathy</a>).</p>
<p>Our study revealed reduced activity in parts of the brain associated with the brain’s monitoring of bodily states, which are typically used when emotionally empathising with another person. These findings underscore the critical link between this brain system and our capacity to take others into consideration.</p>
<p>In light of these findings, the next step with our research is to explore if and how the in-flow of the bodily signals necessary for the brain to create an inner self is altered in frontotemporal dementia – and how this relates to empathy.</p>
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<p>Apart from <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC6647117/">about 30% of cases being genetic</a>, the causes of frontotemporal dementia remains unclear. Despite intense efforts from the community, there’s currently no cure. But thanks to courageous sufferers and their families coming forward, awareness is increasing. This is a crucial thrust forward.</p>
<p>We hope that understanding how the brain processes empathy in frontotemporal dementia may not only help improve diagnosis but may, in the future, pave the way for potential treatments which mitigate some of the devastating effects of this disease.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/247402/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/loss-of-empathy-is-a-key-problem-in-people-with-frontotemporal-dementia-our-research-shows-whats-happening-in-the-brain-247402">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/single-dose-of-5-meo-dmt-alters-gene-expression-in-brain-and-reduces-anxiety-like-behavior-in-stressed-mice/" 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;">Single dose of 5-MeO-DMT alters gene expression in brain and reduces anxiety-like behavior in stressed mice</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 16th 2025, 16:00</div>
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<p><p>A new study published in <em><a href="https://www.nature.com/articles/s41380-024-02655-w" target="_blank">Molecular Psychiatry</a></em> suggests that the fast-acting psychedelic compound 5-MeO-DMT can reduce anxiety-like behavior in stressed mice while altering the expression of genes linked to neural activity in specific brain regions. The research found that a single dose of 5-MeO-DMT modified expression of immediate early genes and affected behavioral responses up to five days later, offering insights into how this compound might work at the molecular level.</p>
<p>5-MeO-DMT, short for 5-methoxy-N,N-dimethyltryptamine, is a powerful psychedelic substance structurally related to DMT. It occurs naturally in certain plants and the venom of the <em>Incilius alvarius</em> toad and has recently drawn attention for its rapid, intense, and short-lived psychological effects. In clinical settings, 5-MeO-DMT has been explored for its potential to treat depression, anxiety, and addiction.</p>
<p>The compound is known to engage serotonin receptors in the brain, but unlike other psychedelics such as LSD or psilocybin, it binds more strongly to the 5-HT1A receptor, which is commonly linked to anti-anxiety effects. Despite growing interest, little is known about the biological changes it induces in the brain.</p>
<p>To better understand how 5-MeO-DMT affects the brain and behavior, researchers at the Brain Institute of the Federal University of Rio Grande do Norte in Brazil administered a single high dose of 5-MeO-DMT to male mice and analyzed both their gene expression and behavioral responses. The team focused on brain regions involved in anxiety and emotion, including the anterior cingulate cortex, the basolateral amygdala, and the ventral hippocampus. These areas are part of a larger network that regulates fear, emotional responses, and stress.</p>
<p>The study involved multiple groups of mice. Some received a single dose of 5-MeO-DMT and were euthanized at different time points—one hour, five hours, or five days later—so their brain tissue could be analyzed using laser capture microdissection and quantitative PCR to measure levels of gene expression.</p>
<p>The researchers examined several genes known to be involved in synaptic plasticity and neural activity, including Arc, Zif268, BDNF, CREB, NR2A, mTORC1, TRIP8b, and NFkB. Another set of mice was tested for anxiety-like behaviors using two common experimental tools: the elevated plus maze and the open field test. A third group underwent a stressful restraint procedure to test how 5-MeO-DMT affects behavior under acute stress.</p>
<p>One of the main findings was that 5-MeO-DMT caused significant changes in the expression of immediate early genes—especially Arc and Zif268—in the anterior cingulate cortex, basolateral amygdala, and ventral hippocampus. These genes are rapidly activated in neurons and are involved in learning, memory, and synaptic remodeling. One hour after treatment, Arc expression increased in the anterior cingulate cortex and basolateral amygdala but decreased in the ventral hippocampus. Zif268 was upregulated only in the basolateral amygdala.</p>
<p>Five hours after treatment, the researchers observed a decrease in the expression of NR2A, a gene linked to glutamate signaling, in the ventral hippocampus. This was notable because NR2A has been associated with excitatory synaptic activity and learning processes. Interestingly, no significant changes were observed in the expression of several commonly studied plasticity-related genes, such as BDNF or CREB, at any time point. This suggests that 5-MeO-DMT may exert its effects through less conventional molecular pathways.</p>
<p>Five days after treatment, the only significant long-lasting change was an increase in the expression of TRIP8b in the ventral hippocampus. This gene helps regulate ion channels involved in controlling the excitability of neurons and has been implicated in mood regulation and antidepressant effects. No changes were seen in the dentate gyrus or for other genes at this later time point, suggesting that the effects of 5-MeO-DMT on gene expression are both region-specific and transient.</p>
<p>Behaviorally, mice treated with 5-MeO-DMT showed mixed results. In the elevated plus maze, which measures willingness to explore open, unprotected spaces, mice treated with 5-MeO-DMT five days earlier entered open arms more frequently than saline-treated mice, suggesting reduced anxiety. However, in the open field test, those same mice entered the exposed central area less often, a behavior typically associated with increased anxiety. This discrepancy raised questions about whether 5-MeO-DMT has context-dependent behavioral effects or whether it affects general locomotion.</p>
<p>To clarify these findings, the researchers examined mice subjected to a stress challenge. When mice received 5-MeO-DMT five days before undergoing a 20-minute restraint stress, they showed significantly lower baseline levels of corticosterone, the primary stress hormone in rodents. After stress, these mice spent more time in the open arms of the elevated plus maze and in the center of the open field arena—both considered signs of reduced anxiety-like behavior. These results suggest that 5-MeO-DMT can increase resilience to stress, possibly by modifying the stress hormone system and related neural pathways.</p>
<p>An additional behavioral analysis looked at specific exploratory actions, such as head dips over the edges of the maze. Across different groups, mice treated with 5-MeO-DMT showed more unprotected head dips and fewer protected ones, a pattern consistent with reduced anxiety. These effects were seen both in non-stressed mice and in those that had undergone stress, reinforcing the idea that 5-MeO-DMT influences anxiety-like behavior over an extended period.</p>
<p>The study has several limitations. It focused only on male mice, so it’s unclear whether the results apply to females. The researchers also measured only mRNA levels and not the actual proteins produced by the genes. Since many biological effects depend on protein activity, future studies will need to explore whether changes in gene expression translate into functional protein-level changes. Additionally, while the researchers chose a single high dose based on previous work, dose-response effects were not tested in this study.</p>
<p>Despite these limitations, the findings contribute to a growing body of evidence that serotonergic psychedelics can produce long-lasting effects on brain function and behavior after just one administration. In particular, 5-MeO-DMT appears to act through non-traditional pathways, possibly involving its high affinity for the 5-HT1A receptor or its interactions with other targets like the sigma-1 receptor.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41380-024-02655-w" target="_blank">Serotonergic psychedelic 5-MeO-DMT alters plasticity-related gene expression and generates anxiolytic effects in stressed mice</a>,” was authored by Margareth Nogueira, Daiane C. Ferreira Golbert, Richardson Menezes, Raíssa Nóbrega de Almeida, Nicole L. Galvão-Coelho, Andressa N. Siroky, Thiago Z. Lima, Helton Maia, Katarina E. Leão, and Richardson N. Leão. </p></p>
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<td><a href="https://www.psypost.org/new-research-points-to-gut-serotonin-as-a-potential-way-to-treat-depression-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;">New research points to gut serotonin as a potential way to treat depression and anxiety</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 16th 2025, 14:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1053/j.gastro.2024.11.012" target="_blank" rel="noopener">Gastroenterology</a></em> provides evidence that serotonin in the gut lining may play a key role in regulating mood—and could open the door to safer antidepressant treatments, especially for pregnant women. In a series of experiments with mice and a large human birth cohort, researchers found that increasing serotonin in the intestinal lining reduced anxiety- and depression-like behaviors. But they also discovered that exposing developing babies to serotonin-targeting antidepressants in utero was linked to a much higher risk of constipation in early life.</p>
<p>The research team, led by Mark Ansorge at Columbia University and Kara Margolis at New York University, was motivated by a longstanding puzzle in mental health care. While drugs like Prozac and Zoloft are widely used and effective for many people with anxiety and depression, they can cause unwanted side effects—especially gastrointestinal issues. And when used during pregnancy, they cross the placenta and affect fetal brain and gut development. Despite this, exactly where in the body these medications work to improve mood has remained unclear.</p>
<p>To investigate whether the gut might be a key player in the antidepressant response, the researchers used genetic techniques to delete a specific serotonin transporter protein (SERT) only in the intestinal lining of mice. This transporter is responsible for clearing serotonin, a chemical that helps regulate mood, from the space between cells. Removing the transporter boosts serotonin levels in the gut. The team created two groups of mice: one with SERT removed from birth, and another where SERT was deleted only in adulthood using an inducible system.</p>
<p>The researchers then put these mice through a battery of behavioral tests designed to assess anxiety- and depression-like behaviors, including how much time they spent exploring new environments, their willingness to eat in unfamiliar situations, and how much time they spent immobile when suspended by the tail—a common sign of despair in rodents.</p>
<p>Mice lacking intestinal SERT, whether from birth or adulthood, showed less anxious and less depressive behaviors. They explored more, showed fewer signs of hesitation, and were more active than control mice. Importantly, this mood-improving effect depended on communication between the gut and brain. When the researchers surgically disrupted the vagus nerve—the main information highway between the gut and brain—the benefits disappeared. This suggested that serotonin in the gut lining influences mood by sending signals to the brain via the vagus nerve.</p>
<p>At the same time, the researchers wanted to understand whether reducing serotonin in the gut might have the opposite effect. In another set of experiments, they used genetically modified mice that couldn’t make serotonin in the gut and also tested a drug that blocks serotonin production without being absorbed into the bloodstream. In both cases, the animals showed more anxiety-like behavior. This further confirmed the role of gut serotonin in regulating mood.</p>
<p>Interestingly, targeting serotonin in the gut did not appear to harm cognition or gut motility, which are often affected by systemic antidepressant use. The researchers found no major changes in learning and memory tests, and gut function remained mostly normal—though there were subtle changes in the speed of intestinal movements when the transporter was deleted from birth.</p>
<p>The human part of the study involved over 400 mother-child pairs enrolled in a Canadian birth cohort. The researchers followed up with mothers who either used antidepressants during pregnancy, experienced depression without medication, or had no mental health issues. They found that babies exposed to antidepressants in the womb were about three times more likely to develop functional constipation in their first year of life compared to babies who were not exposed. Constipation is a common type of gut-brain interaction disorder, and the finding adds to concerns about how these drugs may affect the developing gut.</p>
<p>These results are consistent with earlier animal studies showing that systemic serotonin blockers can lead to abnormal development of the nervous system in both the brain and the gut. By focusing on the gut lining specifically, the new study offers a potential workaround: targeting serotonin only in the intestine may relieve symptoms of depression and anxiety without causing unwanted side effects or affecting fetal development during pregnancy.</p>
<p>“Antidepressants like Prozac and Zoloft that raise serotonin levels are important first-line treatments and help many patients but can sometimes cause side effects that patients can’t tolerate. Our study suggests that restricting the drugs to interact only with intestinal cells could avoid these issues,” said Ansorge, an associate professor of clinical neurobiology at Columbia University Vagelos College of Physicians and Surgeons.</p>
<p>While these findings are promising, the authors stress that pregnant individuals should not stop taking prescribed antidepressants without consulting a doctor. Untreated depression and anxiety can pose serious risks to both the mother and child. Instead, the researchers hope their findings will lead to new antidepressant medications that work only in the gut and avoid entering the bloodstream—especially during pregnancy.</p>
<p>Larissa Takser, a pediatrician and co-author based in Quebec, noted the implications: “At the age of one, 63% of children exposed to antidepressants during pregnancy experienced constipation, compared with 31% of children whose mothers did not take medication. This finding suggests a potential connection between serotonin levels in utero and gut development, and opens new doors to examine SSRI properties not previously studied.”</p>
<p>The researchers are already working on next-generation antidepressants that would be delivered in a way that keeps the drug in the intestine, reducing systemic exposure. “Our findings indicate that we may be able to treat a mother’s depression or anxiety effectively without exposing the child,” Ansorge said, “and we are working on drug delivery technology that will hopefully help us achieve that.”</p>
<p>Margolis emphasized that the study is not intended to change clinical practice today. Instead, it is a call for more research on how antidepressants affect the gut, especially during development. “These are not clinical guidelines,” she said. “Rather, they are a call that more research is needed on the connection between SSRIs, serotonin, and the gut. It’s recommended that mothers and providers together consider treatment options that have been shown to be successful, including medications and cognitive behavioral therapy.”</p>
<p>This research adds to growing interest in the gut-brain connection—a field that has revealed how gut bacteria, immune signals, and hormones interact with the nervous system. The idea that mood can be regulated from the gut opens new opportunities to improve mental health with fewer risks. If future clinical trials confirm these findings, we may see a new class of antidepressants designed to work where most of the body’s serotonin is made—not in the brain, but in the gut.</p>
<p>The study, “<a href="https://doi.org/10.1053/j.gastro.2024.11.012" target="_blank" rel="noopener">Intestinal epithelial serotonin as a novel target for treating disorders of gut-brain interaction and mood</a>,” was authored by Lin Y. Hung, Nuno D. Alves, Andrew Del Colle, Ardesheer Talati, Sarah A. Najjar, Virginie Bouchard, Virginie Gillet, Yan Tong, Zixing Huang, Kirsteen N. Browning, Jialiang Hua, Ying Liu, James O. Woodruff, Daniel Juarez, Melissa Medina, Jonathan Posner, Raquel Tonello, Nazli Yalcinkaya, Narek Israelyan, Roey Ringel, Letao Yang, Kam W. Leong, Mu Yang, Ji Ying Sze, Tor Savidge, Jay Gingrich, Robert J. Shulman, Michael D. Gershon, Annie Ouellet, Larissa Takser, Mark S. Ansorge, and Kara Gross Margolis.</p></p>
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<td><a href="https://www.psypost.org/childhood-adversity-linked-to-fear-overgeneralization-and-reduced-safety-learning-in-teens/" 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;">Childhood adversity linked to fear overgeneralization and reduced safety learning in teens</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">May 16th 2025, 12:00</div>
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<p><p>A study of adolescents who experienced childhood adversity found that they were less able to distinguish between signals of safety and threat in an experimental setting. This impaired threat-safety discrimination was associated with a tendency to overgeneralize their fear responses. The study was published in the <em><a href="https://doi.org/10.1111/jcpp.14092">Journal of Child Psychology and Psychiatry</a>.</em></p>
<p>Childhood adversity includes a range of stressful or traumatic experiences, such as abuse, neglect, household dysfunction, and exposure to violence. It is associated with disruptions in brain development, particularly in regions involved in emotional regulation and stress response, including the amygdala and prefrontal cortex. Chronic exposure to adversity can alter the functioning of the hypothalamic-pituitary-adrenal axis, resulting in heightened physiological reactivity to stress.</p>
<p>Children who face such adversity are at increased risk for developing mental health conditions such as anxiety, depression, and posttraumatic stress disorder. They may also experience difficulties with emotion regulation, social functioning, and cognitive performance. In adulthood, early adversity is linked to poor health outcomes, including cardiovascular disease, substance use disorders, and chronic inflammation.</p>
<p>Lead author Celine Samaey and her colleagues aimed to investigate how childhood adversity influences fear learning during adolescence—specifically, whether adolescents who had experienced adversity would show impairments in distinguishing safe from threatening cues and a greater tendency to generalize fear responses.</p>
<p>The study involved 119 adolescents between 12 and 16 years old, with an average age of 14. Sixty-five participants were girls, and 63 had been exposed to childhood adversity, as assessed by the abbreviated Juvenile Victimization Questionnaire – 2nd Revision.</p>
<p>Participants completed two key experimental tasks. In a fear conditioning task, they viewed circles of different sizes. One specific circle (designated CS+) was occasionally followed by a mild electric shock to the wrist, while another (CS–) was never followed by a shock. After learning this association, participants were shown additional circles of varying sizes and asked to rate how likely they thought it was that each circle would be followed by a shock. This allowed researchers to assess how broadly participants generalized fear to stimuli that resembled the threatening one.</p>
<p>Participants also completed a perceptual discrimination task, where they had to judge whether pairs of circles were the same or different in size. This test was used to determine whether generalization of fear might be due to difficulty distinguishing the visual stimuli.</p>
<p>As the fear conditioning task progressed, participants generally became more likely to expect an electric shock. Girls reported lower shock expectancy overall compared to boys.</p>
<p>Importantly, adolescents with greater exposure to childhood adversity were more likely to expect shocks, even for stimuli that were not followed by shocks. Boys who had experienced adversity gave higher threat ratings to the safe circle and to other generalization stimuli than boys without such experiences. Girls exposed to adversity showed elevated threat expectations for nearly all stimuli except the most extreme generalization stimulus.</p>
<p>This pattern suggests that adolescents who experienced childhood adversity were more prone to generalizing fear and had a reduced ability to distinguish between threatening and safe cues. Interestingly, those exposed to adversity were not worse at visually distinguishing the circles—in fact, they tended to perform better in the perceptual discrimination task. This indicates that their increased fear generalization was not due to perceptual confusion but rather to differences in emotional learning.</p>
<p>“The current study showed that CA [childhood adversity] is associated with reduced threat-safety discrimination and increased fear generalization during adolescence. As such, altered fear learning emerges as an important process through which adversity increases risk for the development of psychopathology,” the,” study authors concluded.</p>
<p>The study sheds light on the links between childhood adversity experiences and fear learning. However, it should be noted that the study used a very mild electric shock as the object of fear. The patterns of learning to respond to serious threats or dangers might not be the same.</p>
<p>The paper, “<a href="https://doi.org/10.1111/jcpp.14092">Childhood adversity is associated with reduced threat-safety discrimination and increased fear generalization in 12- to 16-year-olds,</a>” was authored by Celine Samaey, Aleksandra Lecei, Maarten Jackers, Lise Jennen, Koen Schruers, Bram Vervliet, Bart Boets, and Ruud van Winkel.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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