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<td><a href="https://www.psypost.org/parenting-stress-alters-the-link-between-attachment-avoidance-and-sexual-satisfaction-in-couples-with-children/" 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;">Parenting stress alters the link between attachment avoidance and sexual satisfaction in couples with children</a>
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<p><p>Higher levels of attachment avoidance in both mothers and fathers were associated with lower sexual satisfaction in themselves, as reported in <a href="https://doi.org/10.3138/cjhs-2022-0053"><em>The Canadian Journal of Human Sexuality</em></a>.</p>
<p>Romantic attachment and sexual satisfaction are closely interconnected, with attachment security fostering intimacy and satisfaction, while attachment insecurity (anxiety or avoidance) undermines these outcomes. Parenting stress, a chronic stressor tied to the demands of child-rearing, often results in decreased attention to romantic relationships. Mariève Vandervoort and colleagues examined parents with school-aged children to explore how parenting stress moderates the link between attachment orientations and sexual satisfaction.</p>
<p>This study included 103 mixed-sex couples from two Canadian provinces, all of whom had at least one child between the ages of 6-11 years. Participants were recruited through community advertisements, and data were collected during a home visit, where both parents completed self-report questionnaires independently. The study drew on data from the second wave of a longitudinal project, conducted approximately 4.5 years after the first wave.</p>
<p>Romantic attachment was assessed using the short-form Experiences in Close Relationships scale (ECR-12), which measures attachment anxiety (e.g., fear of rejection, excessive reassurance-seeking) and attachment avoidance (e.g., reluctance to depend on others, emotional withdrawal). Sexual satisfaction was measured using the Global Measure of Sexual Satisfaction (GMSEX), which evaluates the overall quality of sexual experiences on dimensions such as pleasure, fulfillment, and positivity.</p>
<p>Parenting stress was assessed with the Parenting Stress Index (PSI), which measures stress related to parenting responsibilities, including perceived difficulty in managing child-related demands. By analyzing responses from both partners, the study examined how each parent’s attachment style and stress levels influenced their own and their partner’s sexual satisfaction.</p>
<p>Higher attachment avoidance in both mothers and fathers was linked to lower sexual satisfaction in themselves. Fathers’ attachment avoidance also negatively affected mothers’ sexual satisfaction, suggesting that emotional withdrawal may undermine intimacy and fulfillment for their partners. However, attachment anxiety in either parent was not significantly associated with sexual satisfaction, contrasting with some previous research findings.</p>
<p>A key finding was that fathers’ parenting stress moderated the link between their attachment avoidance and their partner’s sexual satisfaction. Surprisingly, as fathers’ parenting stress increased, the negative effect of their attachment avoidance on mothers’ sexual satisfaction weakened. This suggests that, in higher-stress situations, fathers’ avoidant tendencies may become less relevant, either because stress elicits greater empathy from their partners or because parenting demands overshadow the influence of attachment styles.</p>
<p>Of note is that the sample consisted primarily of well-functioning, high-income, heterosexual couples, limiting generalizability to diverse populations.</p>
<p>The study, “<a href="https://doi.org/10.3138/cjhs-2022-0053">The moderating role of parenting stress when it comes to romantic attachment and sexual satisfaction</a>,” was authored by Mariève Vandervoort, Michelle Lonergan, Marie-France Lafontaine, and Jean-François Bureau.</p></p>
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<td><a href="https://www.psypost.org/gamers-with-lower-social-skills-are-more-likely-to-make-impulsive-in-game-purchases/" 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;">Gamers with lower social skills are more likely to make impulsive in-game purchases</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 2nd 2025, 06:00</div>
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<p><p>A new study published in <em><a href="https://doi.org/10.1016/j.chb.2024.108479" target="_blank" rel="noopener">Computers in Human Behavior</a></em> explores how competitive attitudes influence in-game impulse purchases, focusing on the psychological mechanisms that drive spending in gaming environments. The study found that while competitiveness alone does not directly lead to impulsive purchases, the desire for popularity acts as a key motivator, and the effect is especially strong for players with lower social competence. These findings offer important insights into the psychology of gamers and have implications for game developers and marketers.</p>
<p>The rise of in-game purchases has transformed the gaming industry, generating billions in revenue. As digital economies continue to expand, researchers have become increasingly interested in understanding the psychological factors that drive impulsive spending in games. While past studies have explored emotional triggers, game mechanics, and player engagement, little attention has been given to personality traits such as competitiveness, the desire for social recognition, and social competence.</p>
<p>“I’ve been researching maladaptive consumption behaviors for many years. People often engage in impulsive or otherwise irrational purchasing when they feel especially highly positive or negative emotions, and these behaviors can lead to unfavorable outcomes for them,” said study author <a href="http://www.hakancengiz.biz/" target="_blank" rel="noopener">Hakan Cengiz</a>, a full professor of Marketing at Karabuk University.</p>
<p>“Video games, in particular, have become a major part of younger individuals’ leisure time and often involve substantial spending. The competitive environment and the drive for social recognition in these games sparked my curiosity about how factors like the need for popularity and competitive spirit might trigger impulsive in-game purchases.”</p>
<p>The researchers conducted an online survey of 234 participants recruited from the popular gaming platforms Discord and Twitch. These platforms were chosen due to their large, active gaming communities and the prevalence of live streaming, which can foster competition and encourage in-game purchases. Participants were eligible for the study if they had been actively playing games on Steam for at least three months and had made prior in-game purchases.</p>
<p>The survey included questions about demographics, gaming habits, social competence, the need for popularity, in-game impulse purchase tendencies, and competitive attitudes. Social competence was assessed using items like “I am good at making friends.” The need for popularity was measured with items such as “I have done things to make me more popular, even when it meant doing something I would not usually do.” In-game impulse purchasing tendencies were measured using items such as “I have a desire to buy things that do not pertain to my specific shopping goal when browsing the Steam website.” Finally, competitive attitudes were measured through items like “It is important to me to do better than others on a task.”</p>
<p>The findings of the study revealed an important distinction: competitive attitudes alone did not directly lead to in-game impulse purchases. This suggests that simply being competitive does not necessarily drive impulsive spending. However, competitiveness did significantly increase the need for popularity, meaning that highly competitive players were more likely to seek social validation through their gaming achievements.</p>
<p>In turn, the need for popularity strongly predicted in-game impulse purchases. Players who valued social recognition were more likely to make impulsive purchases, possibly as a way to gain status or approval within their gaming communities. This supports the idea that in-game purchases serve not only a functional purpose—such as enhancing performance—but also a social one, helping players maintain a desirable image among their peers.</p>
<p>“Overall, our results aligned closely with our hypotheses,” Cengiz told PsyPost. “The main surprise was that purely competitive feelings didn’t independently prompt in-game impulse purchases, even though we initially assumed they might. It turns out that the need for popularity plays a pivotal role in turning competitive drive into impulsive buying.”</p>
<p>The study also found that social competence played a key moderating role. Players with lower social competence were more susceptible to making impulsive purchases when driven by the need for popularity. In contrast, those with higher social competence were less influenced by these pressures. This suggests that individuals who struggle with social interactions in real life may be more likely to seek validation through in-game purchases, whereas those with stronger social skills rely less on virtual goods for social approval.</p>
<p>“One of the most important findings is that young people with higher levels of social competence tend to avoid impulsive in-game purchases, even when they desire to be popular,” Cengiz explained. “Conversely, those who perceive themselves as lacking social skills are more prone to spontaneous purchases if they feel a strong need for popularity. Another key insight is that competitive attitudes on their own don’t necessarily lead to impulsive purchases, but when combined with a heightened desire for popularity, they can drive more frequent impulse buying in gaming contexts.”</p>
<p>The study has some limitations that should be considered. First, the sample was drawn from users of Discord and Twitch, which may not be representative of all gamers. These platforms attract a specific type of gamer, often those who are highly engaged and participate in live streaming and online communities. Future research should include participants from a wider range of gaming platforms and demographics to improve the generalizability of the findings.</p>
<p>Second, the study focused on in-game item purchases, but other types of gaming expenditures, such as buying games directly or subscribing to gaming services, were not examined. Future research could explore these different types of purchases to provide a more complete picture of spending behaviors within gaming.</p>
<p>“Many variables are still worth exploring in the realm of impulsive in-game purchases,” Cengiz said. “Moving forward, I plan to investigate how different personality types influence or interact with in-game impulsive buying behavior. Expanding the scope, I hope we can better understand how various personal and situational factors shape these purchasing habits.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.chb.2024.108479" target="_blank" rel="noopener">Linking gamers’ competitive spirit and in-game impulse purchase: The need for popularity as a mediator and social competence as a moderator</a>,” was authored by Hakan Cengiz, Arezoo Pouyan, and Hasan Azdemir.</p></p>
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<td><a href="https://www.psypost.org/how-brain-connectivity-differs-in-healthy-aging-and-semantic-dementia/" 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 brain connectivity differs in healthy aging and semantic dementia</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 1st 2025, 14:00</div>
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<p><p>A new study published in the journal <em><a href="https://doi.org/10.1016/j.cortex.2024.11.013" target="_blank" rel="noopener">Cortex</a></em> sheds light on how brain network organization differs in healthy aging and semantic dementia. Researchers found that older adults experience changes in the balance between structural and functional brain connectivity, which are linked to cognitive performance. These changes appear more widespread and diffuse in healthy aging, while semantic dementia is associated with more localized alterations, particularly in the temporal and parietal regions. The study suggests that the brain undergoes a dynamic process of adaptation in response to aging and disease, with some changes helping to preserve cognitive function and others contributing to decline.</p>
<p>Semantic dementia is a progressive neurodegenerative disorder that primarily affects the ability to understand and recall meanings of words, objects, and concepts. It is classified as a subtype of frontotemporal lobar degeneration and is distinct from other forms of dementia, such as Alzheimer’s disease, because it mainly targets the anterior temporal lobes rather than causing widespread memory loss. Patients with semantic dementia often struggle with word-finding difficulties and may eventually lose the ability to recognize familiar objects and faces, even though their memory for recent events and their ability to carry out day-to-day tasks may remain relatively intact in the early stages.</p>
<p>The study was motivated by the need to better understand how aging and neurodegenerative diseases like semantic dementia alter brain connectivity and how these changes affect cognitive function. Normal aging is known to bring about widespread changes in both structural and functional networks, with the frontal regions of the brain being particularly affected. In contrast, semantic dementia leads to more localized damage, particularly in the temporal and parietal areas. These differences raise important questions about whether the brain compensates for structural decline by reorganizing its functional networks and whether this reorganization is beneficial or detrimental to cognitive abilities.</p>
<p>“We all experience cognitive and brain changes with advancing age, but these changes are mixed with the impacts of neurodegeneration in patients suffering from age-related disease like Alzheimer’s disease or semantic dementia. It is critical to distinguish the specificities associated with physiological aging and pathologies to identify early markers of neurodegeneration,” said study author <a href="https://thomashinault.wordpress.com/" target="_blank" rel="noopener">Thomas Hinault</a>, a research associate at INSERM.</p>
<p>The brain functions as a vast network of interconnected regions that communicate with one another to support thought, memory, and behavior. This network is often studied in terms of <em>structural connectivity</em>, which refers to the physical connections between different brain areas through white matter pathways, and <em>functional connectivity</em>, which describes how different brain regions work together based on patterns of activity.</p>
<p>The study included 14 younger adults (ages 20–30), 19 older adults (ages 51–75), and 12 individuals with semantic dementia (ages 56–80). All participants underwent brain imaging using two different techniques: diffusion-weighted imaging (DWI) to map structural brain connections and functional magnetic resonance imaging (fMRI) to measure brain activity. Participants also completed cognitive tests assessing memory, executive function, and language abilities.</p>
<p>The researchers used a technique called multiplex brain network analysis, which allowed them to examine how well structural and functional networks were aligned. Two key measures were used to assess network organization: the multiplex participation coefficient, which indicates how integrated a brain region is across structural and functional networks, and the multiplex clustering coefficient, which reflects how isolated or segregated certain brain regions are.</p>
<p>The study revealed distinct patterns of brain connectivity changes in healthy aging and semantic dementia.</p>
<p>Among healthy older adults, the researchers observed a reduction in the similarity between structural and functional networks, particularly in the frontal regions. This suggests that as people age, brain activity patterns become more independent of structural pathways. Interestingly, this reduced similarity was associated with better cognitive performance, indicating that the brain may adapt by reorganizing functional connections to compensate for structural decline. However, at the same time, the older adults also showed increased network clustering in the frontal regions, which was linked to poorer cognitive performance. This suggests that while some network changes may be beneficial, others could contribute to cognitive decline.</p>
<p>In individuals with semantic dementia, the researchers found increased similarity between structural and functional networks, particularly in the temporal and parietal regions. Unlike in healthy aging, this increased similarity was associated with cognitive decline, particularly in executive function and problem-solving abilities. Additionally, these individuals showed increased clustering in the temporo-parietal regions, which was also linked to poorer cognitive performance. These findings suggest that in semantic dementia, the brain struggles to adapt functionally to structural damage, leading to more rigid and less flexible connectivity patterns.</p>
<p>“Across patients suffering from the same conditions, some will show a stronger decline in daily life autonomy than others,” Hinault told PsyPost. “This heterogeneity partly comes from how the disease is affecting the brain’s structure and whether this is compensated in the communications across brain regions.”</p>
<p>There are some limitations to consider. The sample size was relatively small, particularly for the semantic dementia group, which may limit the generalizability of the findings. Additionally, the study was cross-sectional, meaning it captured only a snapshot of brain connectivity at a single point in time. The researchers are currently conducting follow-up studies to investigate whether the structural and functional changes observed in this study can predict future cognitive decline.</p>
<p>“We are currently conducting longitudinal research to determine how much the changes we report at the brain’s structural or functional level are associated with cognitive changes (memory, reasoning) in the following years,” Hinault said. “This would have important implication to improve patients’ prognosis.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.cortex.2024.11.013" target="_blank" rel="noopener">Linking structural and functional changes during healthy aging and semantic dementia using multilayer brain network analysis</a>,” was authored by Gwendolyn Jauny, Marine Le Petit, Shailendra Segobin, Catherine Merck, Serge Belliard, Francis Eustache, Mickael Laisney, and Thomas Hinault.</p></p>
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<td><a href="https://www.psypost.org/large-scale-neuroimaging-study-finds-no-evidence-of-atypical-amygdala-connectivity-in-autism/" 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;">Large-scale neuroimaging study finds no evidence of atypical amygdala connectivity in autism</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 1st 2025, 12:00</div>
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<p><p>A neuroimaging study of over 200 individuals with autism found no evidence of atypical functional connectivity in the amygdala, a brain region critical for processing emotions, particularly fear, and for threat detection. The paper was published in the <a href="https://doi.org/10.1176/appi.ajp.20230249"><em>American Journal of Psychiatry</em></a>.</p>
<p>Autism, or autism spectrum disorder, is a neurodevelopmental condition characterized by challenges in social interaction, communication, and repetitive behaviors. The symptoms and severity of autism vary widely, which is why it is considered a spectrum disorder. Individuals with autism often have difficulty understanding social cues, forming relationships, and adapting to changes in routine.</p>
<p>Despite extensive research, the causes and neural basis of autism remain poorly understood. One long-standing and popular hypothesis suggests that individuals with autism exhibit reduced functional connectivity between various brain regions. Another hypothesis posits that autistic individuals have an atypical amygdala structure. Some researchers also suggest that structural brain atypicalities may depend on the autism subtype and vary between individuals. However, tests of these hypotheses have produced inconsistent findings so far.</p>
<p>Study author Dorit Kliemann and her colleagues sought to test these hypotheses comprehensively using a large sample of individuals with autism. They conducted a neuroimaging study examining functional connectivity between multiple pairs of brain regions using functional magnetic resonance imaging (fMRI). Functional connectivity refers to the temporal correlation of neural activity across different brain areas, indicating how they communicate and work together during various cognitive and behavioral processes.</p>
<p>The researchers analyzed data from the Autism Brain Imaging Data Exchange (ABIDE) datasets, publicly available collections of neuroimaging data from individuals with and without autism. ABIDE aims to advance research on the neural basis of autism through large-scale, multi-site collaborations. The study included data from 488 individuals between 16 and 50 years of age, of whom 212 had autism.</p>
<p>The results showed no evidence of reduced functional connectivity in individuals with autism. Although certain analytic approaches pointed to some regions with slightly lower functional connectivity, these findings varied depending on the analytic method used and were not consistent.</p>
<p>Similarly, analyses did not reveal any atypical connectivity patterns in the amygdala of individuals with autism. The individual differences in functional connectivity of the amygdala among participants with autism were no greater than those found in neurotypical participants.</p>
<p>Overall, the study did not find any consistent differences in amygdala functional connectivity between individuals with autism and neurotypical participants.</p>
<p>“A preregistered set of analyses found no reliable evidence for atypical functional connectivity of the amygdala in autism, contrary to leading hypotheses. Future studies should test an expanded set of hypotheses across multiple processing pipelines, collect deeper data per individual, and include a greater diversity of participants to ensure robust generalizability of findings on amygdala FC [functional connectivity] in ASD [autism spectrum disorder],” the study authors concluded.</p>
<p>The study contributes to the scientific understanding of the neural basis of autism. However, the analysis was based on resting-state functional connectivity data, meaning it examined brain activity while participants were at rest—that is, not engaged in any specific tasks. It is possible that the brains of individuals with and without autism function similarly in a resting state but exhibit differences when engaged in specific activities, particularly those that highlight the distinctions between autistic and neurotypical individuals.</p>
<p>The paper, “<a href="https://doi.org/10.1176/appi.ajp.20230249">Resting-State Functional Connectivity of the Amygdala in Autism: A Preregistered Large-Scale Study,</a>” was authored by Dorit Kliemann, Paola Galdi, Avery L. Van De Water, Brandon Egger, Dorota Jarecka, Ralph Adolphs, and Satrajit S. Ghosh.</p></p>
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<td><a href="https://www.psypost.org/scientists-uncover-a-new-mechanical-pathway-linked-to-alzheimers-disease/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists uncover a new mechanical pathway linked to Alzheimer’s disease</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Feb 1st 2025, 10:48</div>
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<p><p>A newly published study in <em><a href="https://doi.org/10.1098/rsob.240185" target="_blank" rel="noopener">Royal Society Open Biology </a></em>provide new insight into the potential mechanical underpinnings of Alzheimer’s disease. Researchers have identified a previously unknown interaction between two proteins in the brain—amyloid precursor protein and talin—that may be fundamental to memory formation and maintenance. Their findings suggest that disruptions in this interaction could contribute to the progression of Alzheimer’s disease by impairing the brain’s ability to maintain synaptic stability, ultimately leading to cognitive decline.</p>
<p>Alzheimer’s disease is a progressive neurodegenerative disorder that primarily affects memory, thinking, and behavior. It is the most common cause of dementia, accounting for 60 to 80 percent of cases worldwide. The disease is characterized by the accumulation of amyloid plaques and tau tangles in the brain, which contribute to the breakdown of neural connections and the loss of cognitive function. Despite extensive research, the precise mechanisms driving Alzheimer’s disease remain poorly understood, and effective treatments remain elusive.</p>
<p>Previous studies have focused heavily on the toxic buildup of amyloid plaques, but this approach has yet to yield successful treatments. Researchers sought to explore an alternative explanation—whether mechanical forces within the brain play a role in disease progression</p>
<p>“The research in our lab is focused on how the cells in our body can sense and respond to mechanical forces. We work on the protein, talin, each of which contain tiny force-dependent binary switches that turn on and off different cellular functions, acting as a mechano-sensitive signalling hub,” said study authors <a href="https://www.liverpool.ac.uk/people/ben-goult" target="_blank" rel="noopener">Ben Goult</a> of the University of Liverpool and Charles Ellis of the University of Southampton.</p>
<p>“We recently discovered a complex meshwork of these talin proteins within the scaffold protein networks that organise the synapses (neuronal connections) in our brain. As these binary switches are built into the scaffolding of every synapse in our brain, it led me to propose <a href="https://www.frontiersin.org/journals/molecularneuroscience/%20articles/10.3389/fnmol.2021.592951/full" target="_blank" rel="noopener">the MeshCODE theory</a>. Building upon this work, we then focussed on understanding how talin and its switches control the brain, its activity and any potential dysfunction is this network that leads to disease.”</p>
<p>“Consequently, we recently discovered that one of the proteins that talin attaches to is the amyloid precursor protein (APP),” the researchers explained. “APP itself is known for its central role in the devastating Alzheimer’s disease, where it has been suggested that incorrect processing of the APP protein can lead to the formation of amyloid plaques seen in the brains of Alzheimer’s disease patients. This discovery led us to study precisely how talin and APP are connected, leading to a radical new view of Alzheimer’s disease.”</p>
<p>“In our work, we suggest that the APP-talin interaction is vital for the maintenance of healthy synaptic connections, where APP misprocessing leads to mechanical dyshomeostasis (via talin) at the synapse. We postulate that this mechanical impairment leads to the synaptic dysfunction seen in Alzheimer’s disease.”</p>
<p>The researchers utilized a combination of structural biology techniques, biochemical assays, and cellular experiments to explore the relationship between these two proteins and how their interaction might contribute to memory formation and maintenance.</p>
<p>One of the key methodologies involved X-ray crystallography and nuclear magnetic resonance spectroscopy, which allowed the researchers to determine the molecular structure of the interaction between APP and talin. They focused on a specific region within the intracellular portion of APP, known as the NPxY motif, which is known to bind to adhesion-related proteins. By mapping the binding sites of these two proteins, the researchers were able to confirm that talin directly interacts with APP, forming a mechanical link that connects the cytoskeleton to the extracellular environment at synapses.</p>
<p>“We were surprised that despite the billions of dollars of funding for Alzheimer’s research, there was very little literature on the full-length molecule or what it looked like,” Goult and Ellis told PsyPost. “When we modeled the APP protein in full, it was immediately obvious that APP might be (a) part of a mechanical linkage in cells and (b) might connect to the mechanosensitive machinery on both sides of the synapse. When APP is considered to be part of the force-sensitive machinery of the brain, it immediately indicates a novel role for APP in healthy brain function.”</p>
<p>The study also involved experiments in cultured cells to analyze the functional impact of this interaction. Using gene silencing techniques, the researchers selectively removed talin from cells and observed how this affected the processing of APP. Their findings revealed that when talin was absent, the processing of APP was altered, leading to an increase in the production of amyloidogenic fragments. These fragments are known to contribute to the formation of amyloid plaques, which are a hallmark of Alzheimer’s disease. This suggests that a loss of mechanical stability at synapses may lead to the misprocessing of APP, potentially triggering the early stages of neurodegeneration.</p>
<p>Furthermore, the study provided evidence that APP may function as a mechanosensor, helping neurons maintain synaptic integrity by responding to mechanical forces. In a healthy brain, this interaction likely plays a crucial role in stabilizing synapses and ensuring efficient communication between neurons. However, in Alzheimer’s disease, disruptions in this mechanical signaling pathway could weaken synaptic connections, leading to memory loss and cognitive decline. The researchers proposed that the misprocessing of APP, caused by altered mechanical forces, might be one of the driving factors behind synaptic degeneration.</p>
<p>One of the most exciting implications of the study is the potential for new therapeutic approaches. The researchers suggested that drugs known to stabilize focal adhesions—protein complexes that anchor cells to their surroundings—could be repurposed to restore mechanical stability at synapses. Although this idea remains theoretical, it opens the possibility of developing treatments that target the mechanical aspects of Alzheimer’s disease rather than focusing solely on amyloid plaque accumulation.</p>
<p>“In our work, we present a novel interaction between a key Alzheimer’s-linked protein, APP, and a mechanically sensitive synaptic scaffolding protein, talin,” Goult and Ellis explained. “From this, we suggest the APP-talin interaction is central in a pathway that leads to synaptic dysfunction, which is central to the development of Alzheimer’s disease. We end our work with six testable hypotheses, the most notable of which speculates on a potential repurposing of currently available cancer drugs, suggesting a possible treatment route to restore mechanical integrity at synapses and prevent symptomatic presentation.”</p>
<p>The researchers plan to investigate whether APP forms an extracellular meshwork that mechanically couples the two sides of the synapse, ensuring stability in healthy neuronal communication. They also hope to explore whether the processing of APP functions as a mechanical signaling pathway that helps maintain synaptic homeostasis and whether disruptions to this process contribute to the progression of Alzheimer’s disease.</p>
<p>Another key focus will be determining if altered mechanical cues lead to the misprocessing of APP, ultimately triggering synaptic degeneration and memory loss. Additionally, they aim to test whether the spread of Alzheimer’s disease results from a breakdown in mechanical stability that propagates through neural networks. Finally, the researchers are interested in whether existing drugs that stabilize focal adhesions could be repurposed to restore synaptic integrity and slow disease progression. These investigations could lead to a deeper understanding of Alzheimer’s disease and open new avenues for potential treatments.</p>
<p>“We hope to continue to work on the six testable hypotheses we present, with the focus on finding a novel approach to slow the progression and speed up the diagnosis of Alzheimer’s disease,” the researchers said. “We are developing mechanobiology approaches to exert forces onto these proteins, to hopefully prove that force is playing a central role in APP processing. We are currently working with clinicians to test whether cancer drugs that stabilize talin complexes in cells in culture alter APP processing in neurons to potentially slow down the spread of Alzheimer’s disease.”</p>
<p>The study, “<a href="https://doi.org/10.1098/rsob.240185" target="_blank" rel="noopener">The structure of an amyloid precursor protein/talin complex indicates a mechanical basis of Alzheimer’s disease</a>,” was authored by Charles Ellis†, Natasha L. Ward†, Matthew Rice†, Neil J. Ball, Pauline Walle, Chloé Najdek, Devrim Kilinc, Jean-Charles Lambert, Julien Chapuis, and Benjamin T. Goult.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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