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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/this-specialized-cognitive-training-triggers-neurobiological-changes-and-lowers-cortisol/" 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;">This specialized cognitive training triggers neurobiological changes and lowers cortisol</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 8th 2026, 08:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1017/S0033291725102535" target="_blank">Psychological Medicine</a></em> has found that a specific type of cognitive training can reduce biological markers of stress. The training, focused on modifying memory biases, appeared to lower daytime cortisol levels and reduce the tendency to recall negative self-relevant information. These findings suggest that targeting how the brain retrieves memories could offer a preventative strategy for individuals prone to anxiety and depression.</p>
<p>Mental health conditions like depression and anxiety are often characterized by a cognitive pattern known as negative memory bias. This involves a tendency for individuals to preferentially remember negative information about themselves while forgetting or overlooking positive experiences. </p>
<p>For example, a person might dwell on a single criticism received at work while failing to recall several compliments received the same day. While therapies aimed at shifting attention away from negative stimuli exist, interventions specifically targeting memory retrieval remain understudied.</p>
<p>The authors of the current study aimed to fill this gap by developing a comprehensive training program. They sought to determine if explicitly practicing the recall of positive autobiographical memories could alter both psychological symptoms and biological stress responses. </p>
<p>“This study was motivated by an unaddressed issue in the clinical setting: no intervention directly targets the automated information- processing framework underpinning distorted memory. Our goal was to address it to break vicious cycles of lingering anxiety and depression,” said study author Yuko Hakamata, a professor at Toyama University School of Medicine and certified clinician at The Beck Institute for Cognitive Behavior Therapy.</p>
<p>Additionally, they intended to observe changes in brain connectivity associated with these improvements. The researchers hypothesized that modifying these memory habits could lead to measurable changes in how the body and brain handle stress.</p>
<p>To test this hypothesis, the research team recruited fifty-eight participants from the Tokyo area. All participants exhibited elevated levels of anxious or depressive personality traits. These elevated traits placed the participants at a higher risk for developing mood disorders in the future. The researchers utilized a randomized controlled trial design, which is considered a high standard for experimental evidence.</p>
<p>Participants were randomly assigned to one of two groups. The first group received Cognitive Bias Modification for Memory, or CBM-M. The second group received a sham training program to serve as a control. Both groups were unaware of which condition they were assigned to, ensuring a double-blind procedure. The intervention consisted of eight web-based sessions completed over the course of one month.</p>
<p>The training tasks were designed to look similar but functioned differently. In the CBM-M group, participants memorized lists containing positive, negative, and neutral words. Specifically, when they encountered positive words, they were instructed to vividly recall a specific personal memory related to that word. For instance, if the word was “competent,” they might recall a time they successfully completed a difficult project.</p>
<p>The sham group performed similar memorization tasks with the same lists of words. However, they did not receive the instruction to link positive words to personal memories. This distinction allowed the researchers to isolate the effect of actively engaging with positive autobiographical memories. The researchers monitored compliance to ensure all participants stayed engaged with the web-based program.</p>
<p>Before and after the one-month period, the researchers administered a battery of psychological and biological tests. They assessed personality traits using the NEO Personality Inventory and measured symptoms of psychological distress. </p>
<p>To gauge physiological stress, they collected saliva samples at five different times across two days. This allowed them to measure cortisol levels throughout the day, providing a comprehensive picture of the body’s stress response.</p>
<p>In addition to surveys and saliva samples, the team utilized functional magnetic resonance imaging. This brain scanning technique allowed them to observe changes in intrinsic functional connectivity. They were specifically interested in how different regions of the brain communicated with one another while the participants were at rest.</p>
<p>The study yielded several distinct findings regarding psychological changes. Both the active training group and the sham group reported reductions in general anxiety and depressive traits after the one-month period. This suggests that the act of engaging in a structured daily task may have some general beneficial effects, or it may reflect a placebo response.</p>
<p>However, specific differences emerged between the groups that highlight the unique effects of the CBM-M training. Participants in the CBM-M group showed a significant reduction in explicit memory bias. This means they became less likely to recall negative words describing themselves compared to the control group. This shift suggests that the training successfully altered their cognitive processing of self-relevant information.</p>
<p>The CBM-M group also demonstrated a significant decrease in scores for fatigability. In the context of this study, fatigability refers to a trait associated with tiring easily and recovering slowly from stress or illness. A reduction in this score implies an improved resilience or capacity to handle daily demands.</p>
<p>Most notably, physiological data showed a specific reduction in daytime cortisol levels for the CBM-M group. Cortisol is often referred to as the stress hormone, and chronically high levels are associated with various negative health outcomes. </p>
<p>The analysis indicated that the reduction in negative memory bias was statistically correlated with the reductions in both fatigability and cortisol. This link provides evidence that changing how one remembers information can have direct biological consequences.</p>
<p>Brain imaging revealed changes in neural connectivity for those who underwent the active training. The researchers observed increased connectivity between the right amygdala and the anteromedial orbitofrontal cortex. The amygdala is a region central to emotional processing and the detection of threats. The orbitofrontal cortex is often associated with decision-making and the processing of social rewards.</p>
<p>The strengthening of the connection between these two areas suggests improved regulation or processing of emotional memories. Previous research has linked these circuits to the retrieval of positive autobiographical memories. The authors propose that this neural change may underlie the observed behavioral and physiological improvements.</p>
<p>Despite the positive outcomes, the study has some limitations that affect how the results should be interpreted. The sample size was relatively small, which limits the statistical power to detect smaller effects. The study relied on a comparison with a sham training group rather than a waitlist control group. While this controls for the activity itself, it makes it harder to rule out general placebo effects entirely.</p>
<p>The researchers also noted a complex result regarding autobiographical memory specificity. While individuals with high anxiety traits maintained their ability to recall specific positive memories, those with high depressive traits showed a decrease in this ability after training. This suggests that the intervention might need to be tailored differently for individuals with severe depression. It appears that simply prompting positive recall may not be sufficient for everyone.</p>
<p>Future research is needed to identify which personality profiles respond best to this type of training. It would be beneficial to investigate whether these effects persist over a period longer than one month. </p>
<p>Larger studies are also necessary to confirm the neurobiological mechanisms underlying the observed changes. Understanding the precise brain circuits involved could help refine the training to be more effective.</p>
<p>The study provides a promising step toward non-pharmaceutical interventions for stress and mood vulnerability. By showing that a computerized memory task can lower stress hormones, the research highlights the deep connection between cognitive habits and physical health. It suggests that training the brain to focus on positive personal history can build resilience against stress.</p>
<p>“We can have non-conscious information-processing patterns that distort reality in the processes of perception and memory, which trap us in anxiety and depression,” Hakamata told PsyPost. “Although challenging, we can still change these automated processing patterns by viewing and approaching them from new perspectives beyond imagination.”</p>
<p>The study, “<a href="https://doi.org/10.1017/S0033291725102535" target="_blank">The effectiveness and neurobiological actions of memory bias modification: a randomized controlled trial</a>,” was authored by Yuko Hakamata, Shinya Mizukami, Shuhei Izawa, Mie Matsui, Yoshiya Moriguchi, Takashi Hanakawa, Hiroaki Hori, Yusuke Inoue, and Hirokuni Tagaya.</p></p>
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<td><a href="https://www.psypost.org/scientists-find-eating-refined-foods-for-just-three-days-can-impair-memory-in-the-aging-brain/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists find eating refined foods for just three days can impair memory in the aging brain</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 8th 2026, 06:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.bbi.2025.106220" target="_blank">Brain, Behavior, and Immunity</a></em> provides evidence that consuming refined diets for as little as three days can lead to memory impairments in the aging brain. The research suggests that the removal of dietary fiber, a common characteristic of refined foods, may trigger rapid disruptions in brain cell energy production and inflammatory signaling, particularly in the the amygdala, a brain region central to processing fear and emotional memories.</p>
<p>The motivation behind this investigation stems from a need to disentangle the specific nutritional components that contribute to cognitive decline. Previous experiments have frequently utilized high-fat diets to model poor nutrition.</p>
<p>But these experimental diets often differ from standard control diets in multiple ways, including sugar content, protein sources, and fiber levels. Consequently, it remained unclear whether dietary fat, added sugar, or a combination of both drives the memory deficits observed in earlier work.</p>
<p>“Previous research, including our own, has shown that so-called ‘high-fat diets’ can impair memory very quickly, within just a few days, especially in older animals and people. The problem is that the term ‘high-fat diet’ is vague,” explained study authors Ruth M. Barrientos, an associate professor, and Kedryn K. Baskin, an assistant professor, both at The University of Ohio.</p>
<p>“These diets often differ not just in fat, but also in how much sugar and other nutrients they contain. Because of this, it hasn’t been clear whether fat, sugar, or some combination of the two is actually responsible for the memory deficits that have been reported.”</p>
<p>“To address this gap, we designed a study that allowed us to isolate these nutrients more precisely. We used carefully controlled, refined diets that contained specific amounts of fat, sugar, and protein, without the extra components normally found in standard diets. This allowed us to directly compare the effects of high versus low saturated fat and sugar, both alone and together, against a typical low fat, low sugar grain-based diet.” </p>
<p>The researchers utilized male rats at two distinct life stages: young adults at three months old and aged rats at twenty-four months old. The sample size included groups of four to eight animals per condition for various biological and behavioral assays. The animals were assigned to one of several dietary groups for a period of three days.</p>
<p>One group received standard laboratory chow, which is high in fiber and complex carbohydrates. Other groups received purified, refined diets that varied in their composition. These included a low-fat low-sugar diet, a low-fat high-sugar diet, and a high-fat low-sugar diet. A critical feature of all the refined diets was the exclusion of dietary fiber.</p>
<p>To assess memory function, the team employed a fear conditioning procedure. After three days on their respective diets, the rats were placed in a specific chamber where they heard a tone followed by a mild foot shock. This created an association between the environment, the tone, and the negative stimulus.</p>
<p>The researchers tested the rats’ memory four days later. They placed the animals back in the original chamber to test “contextual fear memory,” which relies heavily on the hippocampus. They also placed the rats in a new environment but played the tone to test “cued-fear memory,” which relies heavily on the amygdala.</p>
<p>“By testing both young and aged rats and examining different types of memory, we aimed to better understand which parts of the diet matter most for brain health, and whether age makes the brain more vulnerable to certain nutrients,” Barrientos and Baskin explained.</p>
<p>The behavioral assessments revealed a clear distinction between age groups. Young rats maintained intact memory function across all diet types, showing no significant deficits in freezing behavior when exposed to the context or the tone. In contrast, the aged rats displayed significant vulnerabilities.</p>
<p>The results indicated that aged rats fed the high-fat, low-sugar refined diet exhibited impairments in hippocampal-dependent memory. This group showed reduced freezing behavior when returned to the original chamber compared to those fed standard chow. However, the results regarding the amygdala were even more broad.</p>
<p>Aged rats across all refined diet groups showed significant impairments in amygdala-dependent memory. Regardless of whether the diet was high in fat or high in sugar, the animals failed to freeze in response to the tone as effectively as the control group. This suggests that the aged amygdala is sensitive to the general composition of refined diets rather than a single macronutrient like fat.</p>
<p>“We were surprised at how quickly these effects were observed (3 days) after eating these diets, suggesting that reaching a state of obesity isn’t necessary to see significant effects to brain health and function.”</p>
<p>Beyond behavior, the investigators examined the biological machinery within the brain cells. They extracted mitochondria, the energy-producing powerhouses of the cell, from the hippocampus and amygdala tissues. Using a technique called respirometry, they measured how much oxygen the mitochondria consumed to produce energy.</p>
<p>The analysis showed that mitochondria in the amygdala of aged rats functioned less efficiently after consuming any of the refined diets. These organelles exhibited reduced oxygen consumption at baseline and when stimulated with specific energy substrates. This metabolic suppression mirrored the behavioral deficits observed in the cued-fear tasks.</p>
<p>Similar mitochondrial dysfunction was observed in the hippocampus of aged rats. While the behavioral deficits in this region were limited to the high-fat group, the metabolic data indicated that refined diets generally compromised mitochondrial respiration in this area as well. Young rats, however, showed preserved mitochondrial function, suggesting their brains possess compensatory mechanisms that protect them from short-term dietary stress.</p>
<p>Further investigation focused on specific types of brain cells isolated from the tissue. The researchers examined microglia, the brain’s primary immune cells, and astrocytes, which support neuronal health. The data revealed that microglia from aged rats were particularly susceptible to the dietary challenge.</p>
<p>Microglia isolated from aged rats on refined diets exhibited a widespread suppression of mitochondrial respiration. They appeared metabolically rigid and unable to adapt to changing energy demands. In contrast, microglia from young rats retained metabolic flexibility, showing the ability to increase activity when necessary.</p>
<p>Astrocytes from aged rats showed more specific impairments. While they maintained baseline energy production, they exhibited deficits when their maximal capacity was tested. Interestingly, the data suggested that aged astrocytes might increase their reliance on glycolysis, an alternative method of energy production, potentially as a coping mechanism.</p>
<p>The researchers also analyzed the contents of the rats’ guts and blood to explore potential causes for these brain changes. A common characteristic of all the refined diets used in the experiment was a deficiency in dietary fiber. Fiber is fermented by gut bacteria to produce short-chain fatty acids, such as butyrate.</p>
<p>The data showed a rapid and significant depletion of butyrate in the cecum and blood serum of rats fed refined diets. This drop occurred within just three days. Aged rats had lower baseline levels of butyrate compared to young rats, and the dietary intervention exacerbated this deficiency.</p>
<p>Butyrate is known to support mitochondrial function and control inflammation. The statistical analysis revealed a correlation between low circulating butyrate levels and the severity of memory impairment in the aged animals. This provides a plausible link between the lack of dietary fiber and the observed cognitive deficits.</p>
<p>Finally, the researchers analyzed the protein composition within the brain regions using proteomic techniques. This analysis identified broad changes in protein expression in the aged amygdala and hippocampus following refined diet consumption. Specifically, proteins related to mitochondrial structure and synaptic signaling were altered.</p>
<p>In the hippocampus, the diets affected pathways involved in sirtuin signaling, which regulates cellular health and energy. In the amygdala, the refined diets influenced pathways related to axon guidance and the formation of synapses. These molecular changes align with the functional deficits seen in the mitochondrial assays and behavioral tests.</p>
<p>“Our study shows a few key things,” Barrientos and Baskin told PsyPost. “Older animals that ate the high-fat, low sugar refined diet showed problems with memory linked to the hippocampus, the part of the brain involved in things like navigation and remembering events. But even more striking, all of the refined diets we tested, regardless of fat or sugar content, impaired the aged rats’ emotional memory, memory linked to the amygdala, which helps us learn from fearful or dangerous experiences.” </p>
<p>“These findings suggest that eating these diets may make it harder for older adults to recognize and remember situations that could be harmful, which could increase the risk of physical accidents or even financial mistakes. The common thread across these refined diets was a lack of fiber, making them very similar to ultra-processed foods.” </p>
<p>“At a biological level, we found that these diets interfere with how mitochondria within brain cells of aged rats produce and manage energy,” the researchers explained. “The biggest effects were seen in microglia, the brain’s immune cells, which became less flexible to changing energy demands. Importantly, low-fiber diets caused a sharp drop in butyrate, a helpful substance produced by gut bacteria when we eat fiber. This suggests that fiber plays a crucial role in supporting brain energy use and memory, (but this still needs to be tested).”</p>
<p>While the study provides detailed insights into the effects of refined diets, there are limitations to consider. The experiments were conducted exclusively on male rats, meaning the results may not fully apply to females. Hormonal differences can influence metabolic and immune responses, warranting similar studies in female subjects.</p>
<p>Additionally, while the study establishes a strong association between low butyrate levels and memory loss, it does not definitively prove causation. Future research will need to determine if supplementing fiber or butyrate can prevent or reverse the memory impairments caused by refined diets. The current findings focus on short-term exposure, and longer-term studies would be necessary to see if these deficits persist or worsen over time.</p>
<p>“We still need to determine whether supplementing unhealthy refined diets with fiber or butyrate, the metabolite of fiber, is sufficient to restore memory function,” Barrientos and Baskin said.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.bbi.2025.106220" target="_blank">The aged amygdala’s unique sensitivity to refined diets, independent of fat or sugar content: A brain region and cell type-specific analysis</a>,” was authored by Michael J. Butler, Jade A. Blackwell, Andrew A. Sanchez, Hannah F. Sanders, Dominic W. Kolonay, Jeferson Jantsch, Stephanie M. Muscat, Maria Elisa Caetano-Silva, Akriti Shrestha, Casey Kin Yun Lim, Sabrina E. Mackey-Alfonso, Bryan D. Alvarez, Robert H. McCusker, Jacob M. Allen, Kedryn K. Baskin, and Ruth M. Barrientos.</p></p>
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<td><a href="https://www.psypost.org/how-genetically-modified-stem-cells-could-repair-the-brain-after-a-stroke/" 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;">How genetically modified stem cells could repair the brain after a stroke</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 7th 2026, 14:00</div>
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<p><p>Every year, millions of lives are suddenly, swiftly transformed by a stroke, which occurs when a blood vessel travelling towards the brain becomes obstructed, causing neurons to die off. Strokes are among the leading causes of disability in adults, and it is estimated that <a href="https://healthcare-in-europe.com/en/news/one-in-six-people-will-have-a-stroke-but-most-strokes-can-be-prevented.html">one in six people</a> will suffer one at some point in their lives.</p>
<p>The human brain is by far the most complex organ in our bodies. Its sophisticated cellular architecture and neural networks give us language, memory and abstract reasoning. But this complexity comes at a cost, as brain tissue has a very limited ability to regenerate. Unlike skin or liver tissue, <a href="https://doi.org/10.1523/JNEUROSCI.22-03-00612.2002">neurons that die are rarely replaced</a>.</p>
<p>This is why brain injuries are the root cause of so many age-related diseases. One of the most serious and common of these is ischaemic stroke, caused by the interruption of blood flow to an area of the brain. Although advances in emergency treatment have <a href="https://doi.org/10.1177/23969873251331482">improved survival rates</a>, there is currently no therapy capable of repairing the neuronal damage caused by a stroke.</p>
<p>Rehabilitation helps restore some function, but in many cases stroke survivors live with permanent motor and cognitive impairments, as well as an <a href="https://doi.org/10.3233/JAD-160527">increased risk</a> of depression, dementia and other neurodegenerative diseases. However, this could soon change thanks to the development of stem cell-based therapies.</p>
<h2>A new therapeutic horizon</h2>
<p>In recent decades, cell therapies have opened the door to a new generation of treatments in <a href="https://theconversation.com/topics/regenerative-medicine-9282">regenerative medicine</a>. These are therapies that seek to replace or repair damaged tissue by introducing new cells capable of surviving, maturing and ultimately performing the functions that have been lost.</p>
<p>This is especially important for conditions that affect the brain. Despite its high potential, regenerative medicine has developed relatively slowly because it needs to comply with legislation in different regions. It also requires large financial investments.</p>
<p>A crucial precedent took place in the late 1980s at Lund University Hospital in Sweden, where a team led by Anders Björklund and Olle Lindvall successfully <a href="https://doi.org/10.1126/science.2105529">transplanted neural stem cells into the brains of patients with Parkinson’s disease</a>. Parkinson’s is a neurodegenerative disorder characterised by the progressive loss of dopaminergic neurons, which are essential for controlling body movement.</p>
<p>The results were extraordinary: by replacing damaged neurons, many patients regained motor function for more than a decade. These experiments provided the first solid evidence that the human brain can be repaired using living cells.</p>
<p>Since then, research has advanced, techniques have been refined, and European regulations have established strict frameworks to ensure the safety and quality of these treatments, which are now classed as <a href="https://www.ema.europa.eu/en/human-regulatory-overview/advanced-therapy-medicinal-products-overview">advanced therapy medicinal products</a>. Currently, various <a href="https://www.nature.com/articles/d41586-025-00688-x">clinical trials</a> are underway around the world that continue Björklund and Lindvall’s work, and offer hope to patients with Parkinson’s and many other diseases that affect the brain.</p>
<h2>The unique challenge of strokes</h2>
<p>Although this story inspired many studies, strokes present a different challenge to Parkinson’s disease. Ischemic damage is usually more extensive. It also does not affect just one cell type, but multiple populations of neurons, glial cells and blood vessels.</p>
<p>Furthermore, it is not enough for transplanted cells to merely survive in the patient’s brain – they have to integrate functionally. This means they need to send out their axons (the extensions that transmit nerve impulses) and establish synapses or appropriate connections with the surviving neurons, becoming part of the brain circuits.</p>
<p>It is comparable to rebuilding both a collapsed bridge and the traffic that crosses it: connections must be established in the right way for information to flow. Therefore, in addition to adding new cells, the challenge of strokes is to effectively <a href="https://doi.org/10.3389/fcell.2021.662636">reconnect the brain</a>.</p>
<h2>The promise of genetic engineering</h2>
<p>This is where genetic engineering, one of the most transformative technologies in modern biology, comes into play. This discipline allows cells to be modified to make them more effective, more resistant, or better able to integrate into damaged tissue.</p>
<p>In our case, we have incorporated into the transplanted cells the gene that encodes the BDNF (Brain-Derived Neurotrophic Factor) protein, a neurotrophic factor that aids brain development and promotes axon growth and synapse formation. The aim is to <a href="https://doi.org/10.3390/ijms26157262">facilitate the functional integration</a> of new neurons into the injured brain, a key step in ensuring that the transplant not only fills a gap, but also restores neuronal communication.</p>
<h2>A question of ethics</h2>
<p>Genetic manipulation <a href="https://theconversation.com/researchers-have-grown-human-embryos-from-skin-cells-what-does-that-mean-and-is-it-ethical-157228">also raises ethical dilemmas</a>, especially regarding the limits of its application and its possible long-term effects. The aforementioned transplants in Parkinson’s patients, for instance, were performed with cells from foetal tissue.</p>
<p>Today, thanks to the work of Japanese researcher Shinya Yamanaka, winner of the <a href="https://www.nobelprize.org/prizes/medicine/2012/yamanaka/facts/">2012 Nobel Prize in Medicine</a>, and his <a href="https://doi.org/10.1016/j.cell.2007.11.019">discovery of induced pluripotent stem cells (iPS)</a>, it is possible to generate stem cells from the patient’s own adult cells. It is now very common to generate iPS cells in a laboratory from skin biopsies.</p>
<p>This avoids many of the ethical conflicts associated with the use of embryos, and reduces the risk of immune rejection. Therefore, the question is no longer whether we can modify cells to repair the brain, but rather what criteria to use, under what regulations, and with what responsibility.</p>
<p>The history of medicine is made up of small victories against the impossible. Just a few decades ago, the idea of healing a stroke-damaged brain would have seemed completely unthinkable. Today, thanks to the combination of biology, genetic engineering and regenerative medicine, it is beginning to take shape in laboratories. Many challenges are yet to be solved, but each new advance reminds us of something essential: not only can the brain learn, it can also be repaired.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/269829/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/how-stem-cell-therapy-can-regenerate-brain-tissue-after-a-stroke-269829">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/psychologists-identify-a-potential-bridge-between-narcissism-and-ocd/" 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;">Psychologists identify a potential bridge between narcissism and OCD</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 7th 2026, 12:00</div>
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<p><p>New psychological research suggests that the drive for perfection may be the dangerous bridge connecting narcissism to obsessive-compulsive symptoms. A study published in the journal <em><a href="https://doi.org/10.1016/j.paid.2025.113487" target="_blank">Personality and Individual Differences</a></em> identifies how the gap between an individual’s expectations and their actual achievements can trigger mental distress. The findings indicate that for people with narcissistic traits, the inability to meet their own lofty standards is a primary driver of intrusive thoughts and compulsive behaviors.</p>
<p>Psychologists classify narcissism into different categories. It is not simply a monolithic trait of vanity. There is grandiose narcissism, which is characterized by an inflated sense of superiority, aggression, and a need for admiration. There is also vulnerable narcissism. This second type involves a fragile self-esteem, deep insecurity, and a tendency to oscillate between feeling superior and feeling inferior. Both types involve a relentless pursuit of a “perfect” self-image.</p>
<p>Researchers have previously established links between narcissism and perfectionism. They have also seen connections between narcissism and obsessive-compulsive disorder (OCD). However, the specific psychological mechanisms that link these personality traits to clinical symptoms have remained unclear. The authors of this new paper sought to map the specific pathways that lead from a narcissistic personality to the distress of OCD.</p>
<p>The study was conducted by a team of researchers from the Universidade São Francisco in Brazil. The first author is Laís Costa dos Santos Pereira Reis. The corresponding author is Rafael Moreton Alves da Rocha. They collaborated with Ariela Raissa Lima-Costa. They focused on the concept of “maladaptive perfectionism.”</p>
<p>Perfectionism is not always harmful. Psychology distinguishes between adaptive and maladaptive forms. Adaptive perfectionism involves setting high standards and striving for excellence. This can be healthy and motivating. Maladaptive perfectionism involves a critical self-evaluation and a fixation on mistakes. The researchers utilized a framework known as the tripartite model of perfectionism. This model breaks the trait down into three parts: standards, order, and discrepancy.</p>
<p>The “standards” dimension refers to setting high goals. The “order” dimension relates to a preference for organization. The “discrepancy” dimension is the most psychologically volatile. It measures the extent to which a person feels they are failing to meet their own standards. It represents the painful gap between idealized expectations and reality.</p>
<p>The researchers recruited 214 participants from the general population in Brazil. The participants ranged in age from 19 to 78 years old. The majority of the sample identified as women. The team used an online survey method to collect data on personality traits and symptoms.</p>
<p>Participants completed three standardized psychological assessments. The first was the Almost Perfect Scale-Revised (APS-R). This instrument measured the three dimensions of perfectionism. The second was the Five-Factor Narcissism Inventory (FFNI). This tool assessed levels of grandiose and vulnerable narcissism. The third was the Yale-Brown Obsessive-Compulsive Scale (Y-BOCS). This scale measured the severity of obsessions and compulsions.</p>
<p>Obsessions are defined as intrusive, unwanted thoughts that cause anxiety. Compulsions are repetitive behaviors or mental acts performed to reduce that anxiety. The researchers hypothesized that the “discrepancy” aspect of perfectionism would be the key mediator. A mediator is a variable that explains the relationship between an independent variable and a dependent variable. It is the mechanism through which one thing influences another.</p>
<p>The researchers used statistical modeling to test their hypotheses. They analyzed the data to see if perfectionism explained why narcissistic individuals develop obsessive-compulsive symptoms. The results provided a detailed look at the internal world of narcissism.</p>
<p>The study found that grandiose narcissism was weakly associated with obsessive symptoms. However, the mediation analysis revealed a hidden pathway. Grandiose narcissism was linked to the “discrepancy” factor of perfectionism. This sense of discrepancy then led to obsessions. The data suggests that for grandiose narcissists, the trouble begins when reality does not match their inflated self-view.</p>
<p>When a grandiose individual feels a gap between their entitlement and their actual life, they experience distress. This distress manifests as obsessive thoughts. The researchers found that the discrepancy factor explained most of the relationship between grandiose narcissism and obsessions. The direct link between the personality trait and the symptom was not statistically significant once perfectionism was taken into account. This means the perfectionism is the necessary vehicle for the symptoms to emerge.</p>
<p>The results for vulnerable narcissism were more extensive. Vulnerable narcissism showed a stronger connection to overall distress. These individuals were more likely to experience both obsessions and compulsions. The statistical models showed that maladaptive perfectionism played a central role here as well.</p>
<p>Vulnerable narcissists tend to view the world as threatening. They are highly sensitive to criticism. The study showed they experience high levels of discrepancy. They feel they are constantly falling short. This feeling of failure was strongly linked to the development of obsessive thoughts. It was also linked to compulsive behaviors.</p>
<p>The researchers suggest that vulnerable narcissists may use compulsions as a coping mechanism. They may engage in rituals to manage the anxiety caused by their perceived imperfections. The mediation effect was very strong. The discrepancy factor accounted for approximately 63 percent of the link to obsessions. It accounted for roughly 76 percent of the link to compulsions.</p>
<p>The “standards” dimension of perfectionism did not predict symptoms. Simply having high standards was not the problem. The “order” dimension also did not show a link to the symptoms in this context. The psychological damage came entirely from the discrepancy. This supports the idea that the “maladaptive” side of perfectionism is distinct from the drive to achieve.</p>
<p>The authors interpret these findings through the lens of self-regulation. Narcissistic individuals rely on external validation to maintain their self-esteem. They create an idealized image of themselves. When they cannot maintain this image, they experience a crisis.</p>
<p>For the grandiose narcissist, this crisis leads to ruminative, obsessive thinking. They may obsess over why they are not being recognized as superior. For the vulnerable narcissist, the crisis is more acute. They feel shame and fear. They may develop compulsive rituals to try to restore a sense of control or safety.</p>
<p>The study also included a sensitivity analysis. This is a statistical technique used to check the robustness of the results. It tests how easily the findings could be overturned by unmeasured variables. The analysis showed that the mediation effects were relatively stable. This gives the researchers more confidence that perfectionism is indeed a driving force.</p>
<p>There are several caveats to this research. The study was cross-sectional. This means the data was collected at a single point in time. Researchers cannot definitively prove causation with this type of data. It is theoretically possible that obsessive-compulsive symptoms lead to perfectionism, rather than the other way around. However, the authors argue that the theoretical models support the directionality they proposed.</p>
<p>The sample size was relatively small for this type of structural equation modeling. A larger sample would provide more statistical power. The sample was also recruited by convenience. This means it may not be perfectly representative of the general population. The high percentage of female participants is a potential bias. Men and women may experience narcissism and perfectionism differently.</p>
<p>The study relied on self-reported data. Participants answered questions about their own behavior. This can lead to bias, as people may not be fully aware of their own traits. This is particularly relevant for narcissism, as individuals may lack insight into their own arrogance or insecurity.</p>
<p>Future research is needed to confirm these findings. Longitudinal studies would be beneficial. These studies track participants over a long period. This would allow researchers to see if narcissistic traits in youth predict the development of OCD symptoms later in life.</p>
<p>The authors also suggest that future studies should look at clinical populations. This study used a general population sample. It is important to see if these patterns hold true for people diagnosed with Narcissistic Personality Disorder or Obsessive-Compulsive Disorder. The dynamics might be more extreme in a clinical setting.</p>
<p>The implications for therapy are relevant. The study suggests that treating the obsessive-compulsive symptoms of a narcissistic patient requires addressing their perfectionism. Therapists may need to focus on reducing the patient’s sense of discrepancy. Helping a patient accept that they do not need to be perfect could alleviate their obsessions.</p>
<p>This approach challenges the patient’s core beliefs. Narcissistic individuals often believe their perfectionism is a strength. They see it as the key to their superiority. The data indicates it is actually the source of their suffering.</p>
<p>The findings highlight the internal cost of narcissism. It is often viewed as a trait that harms others. This study shows it also inflicts damage on the self. The relentless pressure to be perfect creates a mental environment ripe for anxiety and ritualistic behavior.</p>
<p>By isolating the “discrepancy” factor, the researchers have pinpointed a specific target for intervention. Reducing the gap between expectation and reality may be the key to mental peace for these individuals. The authors conclude that understanding this dynamic is essential for comprehending the psychic life of narcissistic individuals.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.paid.2025.113487" target="_blank">The Mediating Role of Maladaptive Perfectionism Between Grandiose Narcissism, Vulnerable Narcissism, and Obsessive-Compulsive Symptoms</a>,” was authored by Laís Costa dos Santos Pereira Reis, Rafael Moreton Alves da Rocha, and Ariela Raissa Lima-Costa.</p></p>
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<td><a href="https://www.psypost.org/conversational-ai-can-increase-false-memory-formation-by-injecting-slight-misinformation-in-conversations/" 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;">Conversational AI can increase false memory formation by injecting slight misinformation in conversations</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 7th 2026, 10:00</div>
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<p><p>An experimental study in the United States found that having a conversational AI insert slight misinformation into conversations with users increased false memory occurrence and reduced memories of correct information. The research was published in <a href="https://doi.org/10.1145/3708359.3712112"><em>IUI ’25: Proceedings of the 30th International Conference on Intelligent User Interfaces</em></a>.</p>
<p>Human memory works through three main processes: encoding, storage, and retrieval, i.e., processes during which information is transformed, maintained, and later accessed in the brain (respectively). Encoding depends on attention and meaning, so information that is emotionally salient or well-organized is remembered better. Stored memories are not exact recordings of events; they can change over time. Retrieval of stored memories is a reconstructive process, meaning that memories are rebuilt each time they are recalled rather than simply replayed.</p>
<p>In these processes, exploiting the reconstructive nature of memory, false memories can form. False memories are recollections of events or details that feel real but are inaccurate or entirely fabricated. They are formed through suggestion, imagination, repeated questioning, social influence, or confusion between similar experiences. During retrieval, the brain tends to fill in gaps using expectations, prior knowledge, or external information, which then becomes integrated into the memory. Over time, these altered details can feel just as vivid and real as true memories.</p>
<p>Study author Pat Pataranutaporn and his colleagues examined the potential for malicious generative chatbots to induce false memories by injecting subtle misinformation during interactions with users. Previous studies indicated that there is a rise in AI-driven disinformation campaigns, in which AIs using an authoritative tone, persuasive language, and targeted personalization contributed to users’ difficulties in distinguishing between true and false information. Earlier studies also showed that AI-generated content can influence people’s beliefs and attitudes.</p>
<p>Study participants were 180 individuals recruited via CloudResearch. Participants’ average age was 35 years. The numbers of female and male participants were equal.</p>
<p>Study authors randomly assigned each participant to read one of three information articles. One article was about elections in Thailand, another about drug development, and the third was about shoplifting in the U.K. This was followed by a short filler task. After this, participants were again randomly allocated to five different conditions. There were, in total, 36 participants per condition with 12 per article.</p>
<p>The experimental conditions were the control condition (no intervention) and four intervention conditions that included interaction with an AI (gpt-4o-2024-08-06, a large language model). Of these four conditions, two included reading an AI-generated summary of the article, while the other two included engaging in a discussion with the AI. In each pair of conditions, the AI was honest in one (i.e., correctly presenting facts from the articles) and misleading in the other (i.e., incorporating misinformation alongside factual points).</p>
<p>After undergoing their assigned intervention, participants answered questions, recalling whether specific points appeared in the original article. The questionnaire consisted of 15 questions, 10 of which were about key points from the article, while 5 were about misinformation. </p>
<p>For each question, participants could answer with Yes, No, or Unsure, and they also rated their confidence in the answer. Participants also self-reported their familiarity with AI, evaluated their own general memory performance, and rated their ability to remember visual and verbal information. Finally, participants rated the level of distrust they felt towards official information.</p>
<p>Results showed that participants who engaged in discussion with a misleading chatbot recalled the highest number of false memories compared to all the other conditions and recalled the lowest number of non-false memories. The number of false memories recalled by individuals who read a misleading summary was slightly higher compared to control and honest conditions, but the difference was not large enough to be sure that those were not just random variations. The situation was similar for non-false memories.</p>
<p>Similarly, participants who conversed with a misleading chatbot displayed lower confidence in their non-false memories compared to participants in honest conditions. Overall, participants who conversed with a misleading chatbot had the lowest confidence in their recalled memories compared to all the other treatment conditions.</p>
<p>“The findings revealed that LLM-driven [large language model-driven] interventions heighten false memory creation, with misleading chatbots generating the most pronounced misinformation effect. This points to a worrying capacity for language models to introduce false beliefs in their users. Moreover, these interventions not only fostered false memories but also diminished participants’ confidence in recalling accurate information,” the study authors concluded.</p>
<p>The study contributes to the scientific understanding of false memories. However, it should be noted that the study focused on immediate recall of memories with no particular personal relevance for study participants. </p>
<p>Also, their information came from just a single source, which was the article they read. This is profoundly different from real-world information acquisition, where individuals most often gather information from multiple competing sources, process them based on the level of trust they have in the sources and various other factors, and are able to verify points directly relevant to them.</p>
<p>The paper, “<a href="https://doi.org/10.1145/3708359.3712112">Slip Through the Chat: Subtle Injection of False Information in LLM Chatbot Conversations Increases False Memory Formation,</a>” was authored by Pat Pataranutaporn, Chayapatr Archiwaranguprok, Samantha Chan, Elizabeth F. Loftus, and Pattie Maes.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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