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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/people-struggle-to-separate-argument-quality-from-their-own-political-opinions/" 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;">People struggle to separate argument quality from their own political opinions</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 5th 2025, 08:00</div>
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<p><p>A series of three experiments found that when people evaluate arguments on political topics, their prior beliefs about that topic are more important than the actual quality of those arguments. People do not evaluate arguments independently of the background beliefs held about them. The paper was recently published in <a href="https://doi.org/10.1016/j.cognition.2025.106257"><em>Cognition</em></a>.</p>
<p>Media literacy is the ability to access, analyze, evaluate, and create media messages while understanding how different media forms influence perception, beliefs, and behavior. It helps people navigate an information-saturated world more effectively. Media literacy teaches individuals to question the source, intent, and credibility of the information they encounter, rather than accepting it at face value.</p>
<p>A major part of media literacy is learning to identify biases, emotional manipulation, and persuasive techniques that appear in news, social media, advertising, and entertainment. To do this, people often need to evaluate the quality of arguments a media piece uses.</p>
<p>Evaluating the quality of arguments requires examining whether claims are backed by evidence, whether sources are reliable, and whether reasoning is logically consistent instead of relying on personal impressions or popularity.</p>
<p>In contrast to this approach, which often requires substantial effort, people often decide which arguments to trust based on cognitive shortcuts such as the credibility of the speaker, alignment with prior beliefs, emotional appeal, or social cues.</p>
<p>Media-literate individuals learn to slow down these automatic judgments and instead assess arguments based on facts, context, and method. This includes being able to differentiate between correlation and causation, understand basic statistical claims, cross-check claims with multiple independent sources, and recognize misleading visuals or headlines.</p>
<p>In their new study, <a href="https://profiles.ucl.ac.uk/84735-calvin-deansbrowne" target="_blank" rel="noopener">Calvin Deans-Browne</a> and Henrik Singmann wanted to explore how people evaluate the quality of everyday arguments about disputable political claims (e.g., “Abortions should be legal in the U.S.”).</p>
<p>“I started conducting research around this topic in 2020 during the COVID-19 pandemic. During this time we saw a proliferation of poor quality information, which unfortunately included misinformation about how COVID-19 is spread and how to keep ourselves safe from the virus,” explained Deans-Browne, a PhD student at University College London.</p>
<p>“Though the circulation of misinformation is not a new phenomenon, the COVID-19 pandemic highlighted that uncredible information both spreads easily and is persuasive to many. This got me interested in researching what it is that makes people persuaded by an argument. In this case, is it the quality of the argument people see, or how far the argument is in line with what they already believe?”</p>
<p>The study authors conducted a series of three experiments in which they manipulated argument quality by varying how well the information presented in each argument was connected to the argument’s central claim.</p>
<p>“Good arguments” contained evidence that provided strong support for the claim that was either statistical (e.g., “The United States’ gun-related homicide rate is 25 times higher than the average of 22 other comparable high-income nations”) or causal (e.g., “When we heat our homes, power our cars, and run our factories, the emissions released cause our planet to warm”).</p>
<p>Evidence for ‘bad’ arguments was substantially weaker, containing various flaws including circular reasoning (essentially restatements of the claim), appeals to authority, appeals to popularity, and appeals to tradition. In total, study authors prepared arguments about 10 different political claims (topics), with participants seeing 8 topics in each experiment.</p>
<p>A group of 49 participants pretested the materials used in the first two experiments. They were U.S. residents recruited through Prolific and mostly Democrats. The study authors used them to verify whether “good arguments” were really perceived as better than “bad arguments” when viewed side-by-side.</p>
<p>The first experiment consisted of two parts. In the first part, participants were introduced to the 8 political topics and asked to report their beliefs about them on a scale from “extremely false” to “extremely true.” In the second part of the experiment, they were shown arguments about those topics and asked to rate their quality.</p>
<p>The results showed that participants are able to distinguish between good and bad arguments. However, the difference in quality evaluations participants gave between good and bad arguments was much smaller than the difference in quality evaluations between arguments the participant agreed with and those they did not agree with. Quantitatively, the effect of belief consistency was roughly three times larger than the effect of argument quality.</p>
<p>The second experiment used the same materials but controlled the order in which participants reported their beliefs and rated argument quality. Half of the participants first evaluated the arguments and then reported their beliefs, while the other half first reported beliefs and then evaluated the arguments (like in Experiment 1).</p>
<p>This was done because study authors suspected that stating their own beliefs before rating arguments might have made participants believe that their own beliefs were important for evaluating argument quality. The results of the second experiment replicated those of the first. The order of the arguments did not seem to affect the argument quality evaluations.</p>
<p>Finally, the third experiment was conducted with the goal of understanding which specific feature of a bad argument makes an argument bad. Unlike the first two experiments, this sample was balanced to include a nearly equal number of Democrats and Republicans.</p>
<p>The study authors systematically manipulated two elements of bad arguments: half the bad arguments had inconsistent evidence and the other half were based on appeals to authority. Inconsistent evidence arguments were constructed so that some of the evidence supported the claim made, while the rest of the evidence opposed it.</p>
<p>Surprisingly, the results indicated that people find arguments with inconsistent evidence to be better than arguments based on appeals to authority, though “good” arguments were still rated the highest overall.</p>
<p>To determine if this preference was based on the content of the argument or the participant’s bias, the researchers performed a critical check. For each topic, the “inconsistent” arguments for both the left and right leaning perspectives used essentially the same sentences, just in a different order and ending with different conclusions.</p>
<p>They found that left-leaning participants rated the left-leaning inconsistent argument higher, and right-leaning participants rated the right-leaning version higher. Since the text was essentially identical, this confirmed that the rating was driven by the participant’s prior beliefs, not the argument itself.</p>
<p>“The inconsistent arguments we had in our study did not make much sense if you read them carefully, as an argument cannot simultaneously support opposing perspectives,” Deans-Browne told PsyPost. “We were therefore surprised to find that the people in our study thought these inconsistent arguments were better than the arguments based on the appeal to a well-known figure that were much easier to follow.”</p>
<p>So what are the primary takeaways? “Arguments with better evidence are usually judged as better arguments. However, arguments that are in line with what an individual believes are also more likely to be judged as better arguments,” Deans-Browne explained.</p>
<p>“When we compare these two factors, how far the argument is in line with what an individual believes has a greater effect than how good the evidence presented in the argument is. This highlights that two individuals can see the same argument and interpret it very differently depending on their pre-existing beliefs on the topic.”</p>
<p>The study contributes to the scientific understanding of the way humans reason and interpret arguments. However, all three experiments were conducted on groups of Prolific users. Results on other demographic groups might differ, though the authors noted that results replicated even when the education level of the sample dropped significantly in Experiment 2.</p>
<p>“The long term goal of this line of research is to get a better idea of what makes an argument persuasive,” Deans-Browne said. “I am particularly interested in the role of people’s existing beliefs and how far this predicts how an argument is received. Our immediate next step following this paper is to see whether we can change how people evaluate an argument by manipulating their beliefs directly.”</p>
<p>“I want to highlight that while people tend to perceive arguments positively when in line with what they believe as an individual, people also perceive arguments more positively when presented with good quality evidence,” he added. “While we highlight the limitations of trying to persuade people with good evidence alone, we do not want to give the impression that presenting arguments with good quality evidence is a fruitless endeavour or something that should not be done.”</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.cognition.2025.106257">For everyday arguments prior beliefs play a larger role on perceived argument quality than argument quality itself,</a>” was authored by Calvin Deans-Browne and Henrik Singmann.</p></p>
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<td><a href="https://www.psypost.org/neuroscientists-find-evidence-that-brain-plasticity-peaks-at-the-end-of-the-day/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Neuroscientists find evidence that brain plasticity peaks at the end of the day</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 5th 2025, 06:00</div>
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<p><p>New research provides evidence that the brain’s ability to process signals and adapt to new information fluctuates rhythmically over a 24-hour cycle. A study published in<em> <a href="https://doi.org/10.1016/j.neures.2025.104981" target="_blank">Neuroscience Research</a></em> reveals that while fatigue appears to suppress immediate neural activity at the end of the active phase, this same period may heighten the brain’s capacity for learning and memory formation. These findings suggest that the brain creates specific temporal windows that are optimized for different types of neural processing.</p>
<p>Biological systems differ significantly from mechanical circuit boards because they do not always produce the same output from the same input. An electrical circuit is hard-wired to respond consistently. A brain, however, operates within a constantly changing internal environment. Factors such as metabolism, hormonal cycles, and sleep pressure shift throughout the day and night.</p>
<p>“Neural circuits do not operate like fixed electronic systems,” explained study authors <a href="http://www.ims.med.tohoku.ac.jp/matsui/" target="_blank">Yoko Ikoma</a> and <a href="http://www.ims.med.tohoku.ac.jp/matsui/" target="_blank">Ko Matsui</a>, who are both professors at Tohoku University. “Even when viewing the same scene, what we perceive or remember depends strongly on our internal state at that moment. These fluctuations in responsiveness and metaplasticity are thought to arise from daily shifts in ions and neuromodulatory molecules surrounding neurons.”</p>
<p>“Among the factors shaping this internal environment are physiological rhythms that follow a 24-hour cycle, controlled by the interplay between the circadian clock and the external light–dark cycle. Although these rhythms are known to affect many biological processes, how they influence brain chemistry, neuronal excitability, and plasticity has remained largely unclear.”</p>
<p>“Our study directly examined how time of day alters neural responsiveness in the brains of nocturnal rats. These findings help explain why perception, learning, and fatigue vary across the day in both animals and humans.”</p>
<p>To investigate these daily rhythms, the research team focused on the primary visual cortex. They utilized a specialized technique called optogenetics. This method involves the use of transgenic rats that express a light-sensitive protein named channelrhodopsin-2 in specific neurons.</p>
<p>By delivering precise pulses of blue light directly to the brain, the investigators could activate these neurons without using electrical current. This allowed them to avoid the electrical interference that often complicates traditional recording methods. They implanted electrodes to record local field potentials, which are electrical signals that represent the collective activity of groups of neurons.</p>
<p>The study employed a sample of male Wistar rats housed under a controlled 12-hour light and 12-hour dark cycle. Since rats are nocturnal animals, their active phase occurs during the dark hours. The researchers defined “sunrise” as the end of the rat’s active period and “sunset” as the beginning of their wakefulness.</p>
<p>The researchers delivered identical pulses of light to the visual cortex at various times over several days. They recorded the resulting neural activity to measure excitability. The data indicated a clear diurnal pattern in how the neurons reacted.</p>
<p>Despite the stimulus intensity remaining constant, the neural response varied depending on the time of day. The neural signals were strongest just before sunset, which corresponds to the time when the rats were waking up and feeling refreshed. On the other hand, the signals were weakest just before sunrise, after the rats had been active all night.</p>
<p>This fluctuation suggests that the visual cortex is less excitable and less responsive to immediate stimuli after a prolonged period of wakefulness. To understand the chemical mechanism driving this suppression, the team investigated the role of adenosine. </p>
<p>Adenosine is a neuromodulator that accumulates in the brain the longer an organism stays awake. It is widely recognized as a chemical signal for sleep pressure. As adenosine levels rise, an animal feels more tired. The researchers hypothesized that high levels of adenosine at the end of the night were responsible for dampening neural activity.</p>
<p>To test this, they administered a drug called DPCPX to the rats. This drug acts as an antagonist to adenosine A1 receptors, effectively blocking adenosine from binding to neurons. The team administered this blocker just before sunrise and recorded the neural responses again.</p>
<p>When the action of adenosine was blocked, the suppression of neural activity disappeared. The signals at sunrise became as strong as they were at other times of day. This experiment provides evidence that the natural buildup of adenosine during wakefulness acts as a brake on neural excitability.</p>
<p>“Our results show that daily rhythms fine-tune the balance between excitability and plasticity in the cortex,” Ikoma and Matsui told PsyPost. “Because adenosine levels and sleep pressure fluctuate with circadian and behavioral cycles, the brain’s adaptability appears to be aligned with these internal rhythms. This work provides new insight into how the brain coordinates energy use, neural signaling, and learning capacity over the course of the day.”</p>
<figure aria-describedby="caption-attachment-229939" class="wp-caption aligncenter"><img fetchpriority="high" decoding="async" src="https://www.psypost.org/wp-content/uploads/2025/12/Low-Res_Figure-1.jpg" alt="" width="700" height="445" class="size-full wp-image-229939" srcset="https://www.psypost.org/wp-content/uploads/2025/12/Low-Res_Figure-1.jpg 700w, https://www.psypost.org/wp-content/uploads/2025/12/Low-Res_Figure-1-300x191.jpg 300w" sizes="(max-width: 700px) 100vw, 700px"><figcaption class="wp-caption-text">©Yuki Donen, Yoko Ikoma, Ko Matsui</figcaption></figure>
<p>The investigation then shifted focus to metaplasticity. This term refers to the brain’s potential to undergo changes in synaptic strength. The researchers used a different stimulation pattern consisting of rapid, repetitive light pulses to mimic a learning event.</p>
<p>They applied this “train stimulation” at both sunrise and sunset to see if it would induce long-term potentiation. Long-term potentiation describes a persistent strengthening of synapses that is thought to underlie memory storage. The results revealed an unexpected paradox regarding brain function and fatigue.</p>
<p>At sunset, when the rats were fresh and neural excitability was high, the repetitive stimulation failed to induce significant plasticity. The brain circuits remained relatively stable. However, at sunrise, when the rats were tired and excitability was low, the same stimulation triggered a robust long-term potentiation effect.</p>
<p>“We examined whether the brain’s metaplastic potential—the ease with which synapses can be modified—changes with time of day,” the researchers explained. “Surprisingly, repetitive optical stimulation produced LTP-like enhancement at sunrise but not at sunset. Although sleep pressure and fatigue peak at sunrise, the brain’s capacity for reorganizing its networks was greatest at this time. This suggests that metaplasticity itself follows a daily rhythm, with distinct windows that favor learning and adaptation.”</p>
<p>For humans, who are diurnal, these findings imply a different optimal schedule than for nocturnal rats. The equivalent of the rat’s “sunrise” is the human evening, just before sleep. This is the time when human adenosine levels are typically highest following a day of activity.</p>
<p>The study suggests that the human brain might be most adaptable during the twilight period approaching bedtime. While a person might feel tired and less alert in the evening, their brain could be in a prime state to consolidate new information.</p>
<p>“Because rats are nocturnal, sunrise corresponds to the end of their active phase and the onset of their rest period,” Ikoma and Matsui noted. “In humans, the comparable window is likely before bedtime, near sunset. Thus, these findings do not imply that learning is best immediately after waking. Rather, they indicate that the brain may enter a state more conducive to memory formation as fatigue accumulates toward the end of the active period.”</p>
<p>The researchers propose that the daily rhythm fine-tunes the balance between stability and flexibility in the cortex. During the start of the day, the brain is excitable and ready to react to the environment. By the end of the day, the brain shifts into a state that favors internal reorganization and memory saving.</p>
<p>As with all research, there are limitations to consider. The research was conducted on the visual cortex, and it is not yet clear if the same rhythms govern other areas like the hippocampus or motor cortex. “Human studies will be required to determine whether daily fluctuations in fatigue and circadian timing also modulate learning capacity,” the researchers said.</p>
<p>Understanding these rhythms could have practical applications for education and rehabilitation. If the brain has specific windows for adaptability, therapies involving brain stimulation or skills training could be timed to coincide with these peaks.</p>
<p>“In experimental animals, shifts in brain chemistry and excitability can be measured precisely across the day,” Ikoma and Matsui said. “By selectively modifying these factors, we aim to identify which components are most critical in shaping daily fluctuations in neural activity. Future studies will also incorporate various behavioral tests to determine which aspects of information processing are most sensitive to time-of-day effects.”</p>
<p>“In humans, determining whether comparable patterns exist could deepen our understanding of how energy metabolism, neural signaling, and learning capacity are coordinated over the day. Ultimately, these insights could guide strategies for optimizing training, rehabilitation, and cognitive performance.</p>
<p>The study, “<a href="https://doi.org/10.1016/j.neures.2025.104981" target="_blank">Diurnal modulation of optogenetically evoked neural signals</a>,” was authored by Yuki Donen, Yoko Ikoma, and Ko Matsui.</p></p>
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<td><a href="https://www.psypost.org/noninvasive-brain-stimulation-increases-idea-generation-and-originality/" 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;">Noninvasive brain stimulation increases idea generation and originality</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 4th 2025, 18:00</div>
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<p><p>An experimental study in China found that study participants who received alpha frequency transcranial alternating current stimulation to the parieto-occipital region of their brain exhibited significantly greater levels of novelty, flexibility, fluency, originality, and elaboration compared to when they received a sham stimulation. The paper was published in <a href="https://doi.org/10.1186/s40359-025-03492-4"><em>BMC Psychology</em></a>.</p>
<p>Alpha-frequency transcranial alternating current stimulation (alpha tACS) is a noninvasive brain-stimulation technique that applies a weak electrical current to the scalp at the brain’s natural alpha rhythm, typically around 8–12 Hz. The goal is to entrain or synchronize neuronal oscillations in the alpha band, which are associated with relaxed wakefulness, attention, and inhibitory control.</p>
<p>By rhythmically modulating cortical activity, alpha tACS can influence cognitive functions such as memory, perception, and attention. Alpha tACS is generally safe, produces only mild sensations like tingling or itching, and uses very low-intensity currents. It is studied both as a neuroscience research tool and as a potential clinical method for modulating mood, anxiety, sleep, and cognitive control.</p>
<p>Study author Runze Zhou and his colleagues wanted to explore whether alpha tACS applied to the parieto-occipital cortex region of the brain could improve creative performance and creative thinking. They hypothesized that applying alpha-frequency tACS to the parieto-occipital cortex might enhance creative thinking by increasing alpha oscillations, which reduce habitual thinking patterns and promote flexible, internally directed idea generation.</p>
<p>The study participants were 28 undergraduate students from Qufu Normal University in China. Their average age was 20 years, and 19 of them were women.</p>
<p>The researchers employed a within-participant design, meaning every student underwent both experimental conditions. Participants completed two sessions separated by 24 to 48 hours to prevent carry-over effects. The order of the sessions was randomized: one session involved active alpha tACS delivered using the NeuStim transcranial electrical stimulation system (developed by Neuracle), while the other was a sham (placebo) session.</p>
<p>The active stimulation lasted for 20 minutes. The sham treatment consisted of 10 seconds of alpha tACS stimulation at the start and the end of the session to mimic the sensation, while the equipment was turned off (without participants knowing) for the rest of the period.</p>
<p>After the stimulation, participants completed a creative thinking task called the Alternative Uses Task (AUT), while wearing electroencephalography (EEG) equipment that recorded their brain activity. The total duration of the task phase was approximately 30 minutes.</p>
<p>Results showed that when participants received the active alpha tACS, they exhibited significantly greater levels of novelty, flexibility, fluency, originality, and elaboration compared to their performance in the sham condition.</p>
<p>Further analyses revealed that alpha tACS treatment significantly increased alpha power in the parieto-occipital regions compared to the sham condition. Alpha power refers to the strength or amplitude of neural oscillations in the brain’s alpha frequency range (about 8–12 Hz). It reflects how prominently this rhythm is expressed in cortical activity.</p>
<p>“These findings suggest that α-tACS [alpha tACS] applied to the parieto-occipital cortex, with an inter-session interval of 24 to 48 h, enhances creative thinking performance. This supports the potential of α-tACS as a neuromodulatory technique for facilitating creative cognitive processes,” the study authors concluded.</p>
<p>The study contributes to the scientific understanding of the effects of non-invasive brain stimulation. However, it should be noted that the study was conducted on a small group of students. Results on larger groups and groups with different demographic characteristics might differ.</p>
<p>The paper, “<a href="https://doi.org/10.1186/s40359-025-03492-4">Enhanced creative thinking performance: the role of alpha frequency transcranial alternating current stimulation in the parieto‑occipital region,</a>” was authored by Runze Zhou, Jinqian Wang, Xiaotong Man, Xinying Huang, An’ning Zhan, Chunlei Liu, and Jiaqin Yang.</p></p>
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<td><a href="https://www.psypost.org/boosting-a-regulatory-protein-allows-brain-cells-to-clear-alzheimers-plaques-in-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;">Boosting a regulatory protein allows brain cells to clear Alzheimer’s plaques in mice</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 4th 2025, 16:00</div>
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<p><p>A new study identifies a biological process that empowers specific brain cells to eliminate harmful proteins associated with Alzheimer’s disease. By increasing the levels of a specific regulatory protein in mice, scientists successfully cleared existing brain plaque and halted memory loss. These findings appear in the journal <em><a href="https://www.nature.com/articles/s41593-025-02115-w" target="_blank" rel="noopener">Nature Neuroscience</a></em>.</p>
<p>The brain relies on a vast network of cells to maintain its daily function. While neurons often receive the most attention for their role in transmitting signals, they are supported by a population of star-shaped cells called astrocytes. These cells were once viewed merely as a glue that held the nervous system together. Modern science now recognizes them as active participants in brain health. They facilitate communication between neurons and assist in memory storage.</p>
<p>Astrocytes undergo significant physical and functional changes as the brain ages. The relationship between these age-related shifts and neurodegenerative conditions has been a subject of intense study. A team of researchers at Baylor College of Medicine sought to understand this connection. The group included lead author Dong-Joo Choi and senior author Benjamin Deneen. They investigated how these cellular changes might influence the progression of diseases like Alzheimer’s.</p>
<p>The researchers focused their attention on a protein known as Sox9. This protein acts as a master regulator within the cell. It controls the activity of multiple genes responsible for astrocyte function during the aging process. The team hypothesized that manipulating this protein could alter how the brain responds to the toxic accumulation of proteins.</p>
<p>Alzheimer’s disease is characterized by the buildup of amyloid beta plaques. These are clumps of toxic proteins that accumulate between nerve cells. They disrupt cell function and are a hallmark of the disease’s pathology. The researchers wanted to see if astrocytes could be coaxed into removing these deposits.</p>
<p>To test this, the team designed an experiment using mouse models of Alzheimer’s disease. They specifically selected mice that had already developed signs of the condition. These animals displayed memory deficits and possessed established amyloid plaques in their brains.</p>
<p>“An important point of our experimental design is that we worked with mouse models of Alzheimer’s disease that had already developed cognitive impairment, such as memory deficits, and had amyloid plaques in the brain,” Choi said. “We believe these models are more relevant to what we see in many patients with Alzheimer’s disease symptoms than other models in which these types of experiments are conducted before the plaques form.”</p>
<p>This approach differs from many standard preclinical studies. Often, treatments are tested on animals before they show symptoms to see if prevention is possible. Testing on animals with established impairment better mimics the clinical reality for human patients. Most people receive a diagnosis only after significant biological changes have occurred.</p>
<p>The scientists manipulated the expression of the Sox9 gene in these mice. They created two distinct experimental groups to observe the effects. In one group, they eliminated the gene responsible for producing Sox9. In the second group, they induced the astrocytes to overproduce the protein.</p>
<p>The team then monitored the animals for a period of six months. They evaluated the cognitive health of individual mice using standard behavioral assessments. These tests measured the animals’ ability to recognize specific objects or remember distinct locations. Such tasks are commonly used to gauge memory and learning in rodents.</p>
<p>Following the behavioral testing, the researchers examined the brains of the mice. They utilized imaging techniques to quantify the amount of plaque deposition. This allowed them to correlate the physical state of the brain with the behavioral results.</p>
<p>The results revealed a distinct divergence between the two groups. Reducing Sox9 expression had detrimental effects on the brain tissue. The removal of this regulator accelerated the formation of amyloid plaques. It also resulted in astrocytes that were less structurally intricate.</p>
<p>Conversely, increasing Sox9 levels produced a beneficial outcome. The astrocytes in the overexpression group displayed greater complexity and activity. This heightened state triggered the cells to actively remove the amyloid deposits. The presence of Sox9 essentially instructed the astrocytes to clean the surrounding tissue.</p>
<p>“We found that increasing Sox9 expression triggered astrocytes to ingest more amyloid plaques, clearing them from the brain like a vacuum cleaner,” Deneen said.</p>
<p>This biological clearance translated directly to cognitive preservation. The mice with elevated Sox9 levels did not suffer the same memory loss as their counterparts. Their ability to recognize objects and places remained intact. This suggests that the physical removal of plaques by astrocytes can halt the cognitive decline associated with neurodegeneration.</p>
<p>The study also mapped the specific molecular pathway responsible for this cleaning process. The researchers found that Sox9 regulates a receptor called MEGF10. This receptor sits on the surface of the astrocyte. It enables the cell to perform phagocytosis, a process where the cell engulfs and digests foreign substances.</p>
<p>When Sox9 levels are high, the production of MEGF10 increases. This equips the astrocyte with the necessary machinery to consume the amyloid plaques. The researchers confirmed that this specific signaling pathway is sufficient to preserve cognitive function.</p>
<p>“Most current treatments focus on neurons or try to prevent the formation of amyloid plaques,” Deneen said. “This study suggests that enhancing astrocytes’ natural ability to clean up could be just as important.”</p>
<p>The findings represent a shift in potential therapeutic strategies. Many existing drug development efforts target neurons directly. Others attempt to stop the production of amyloid beta before it aggregates. This research points toward a different approach: harnessing the brain’s innate immune and maintenance systems to repair damage.</p>
<p>There are caveats to consider when interpreting these results. The study was conducted in mouse models, which do not perfectly replicate human biology. The timeframe of the study, while significant for a mouse, is short compared to the decades over which Alzheimer’s develops in humans.</p>
<p>The specific mechanisms of Sox9 in the human brain require further verification. Human astrocytes are larger and more diverse than those found in rodents. It is necessary to determine if the Sox9-MEGF10 pathway functions identically in human tissue.</p>
<p>The authors also note that the long-term effects of overexpressing Sox9 need investigation. While beneficial in the context of this study, the permanent alteration of a master regulator could have other physiological consequences. Future research will likely focus on how to transiently activate this pathway or target the MEGF10 receptor directly.</p>
<p>This work opens the door to a new class of astrocyte-based therapies. By understanding how these support cells change with age, scientists can identify new targets for intervention. The goal is to restore the brain’s youthful capacity for self-maintenance.</p>
<p>Deneen, Choi, and their colleagues emphasize that this is a step toward a broader understanding of neurodegeneration. The interplay between different cell types in the brain dictates the progression of disease. Focusing solely on neurons provides an incomplete picture of brain health.</p>
<p>The research highlights the importance of non-neuronal cells in the fight against dementia. As the global population ages, the prevalence of Alzheimer’s disease continues to rise. Novel approaches that address the underlying cellular dysfunction are urgently needed. This study provides a strong foundation for exploring how to turn the brain’s support cells into active defenders against disease.</p>
<p>The study, “<a href="https://www.nature.com/articles/s41593-025-02115-w" target="_blank" rel="noopener">Astrocytic Sox9 overexpression in Alzheimer’s disease mouse models promotes Aβ plaque phagocytosis and preserves cognitive function</a>,” was authored by Dong-Joo Choi, Sanjana Murali, Wookbong Kwon, Junsung Woo, Eun-Ah Christine Song, Yeunjung Ko, Debosmita Sardar, Brittney Lozzi, Yi-Ting Cheng, Michael R. Williamson, Teng-Wei Huang, Kaitlyn Sanchez, Joanna Jankowsky & Benjamin Deneen.</p></p>
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<td><a href="https://www.psypost.org/neurodiverse-youth-may-regulate-overwhelming-stimuli-by-turning-brain-activity-inward/" 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;">Neurodiverse youth may regulate overwhelming stimuli by turning brain activity inward</a>
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<p><p>Researchers have identified a distinct pattern of brain activity in neurodiverse children who experience sensory over-responsivity. The findings suggest that children who are highly sensitive to everyday stimuli may unknowingly regulate their neural networks to cope with overwhelming sights and sounds. The study was published in the <em><a href="https://doi.org/10.1186/s11689-025-09656-y" target="_blank" rel="noopener">Journal of Neurodevelopmental Disorders</a></em>.</p>
<p>Sensory processing challenges are a frequent concern for parents and clinicians. These issues often manifest as sensory over-responsivity. Children with this condition experience intense physical or emotional reactions to stimuli that others might find harmless or mundane.</p>
<p>Common triggers include the texture of clothing seams, the sound of a vacuum cleaner, or bright fluorescent lights. While these reactions are often observed in children with autism or attention deficit hyperactivity disorder, they also occur in children without a specific diagnosis.</p>
<p>The biological mechanisms behind these intense reactions have remained largely elusive. Diagnosis currently relies on caregiver reports and clinical observations rather than biological markers. To address this gap, a team of researchers sought to map the neural underpinnings of sensory over-responsivity. They aimed to understand how different brain systems interact when a child processes sensory information.</p>
<p>The study was conducted by a multidisciplinary team. The lead investigators included Pratik Mukherjee, a professor of radiology and biomedical imaging, and Elysa Marco, a pediatric neurologist. Both are affiliated with the University of California, San Francisco. They collaborated with researchers from Cortica Healthcare and other institutions.</p>
<p>The investigators based their analysis on a framework of two opposing brain systems. They categorized these as exogenous and endogenous systems. The exogenous system involves brain networks that face outward. It includes regions responsible for processing vision, touch, and movement. This system helps the brain interpret raw data coming from the external environment.</p>
<p>In contrast, the endogenous system focuses inward. It includes networks responsible for attention, decision-making, and emotional regulation. This system handles higher-level cognitive tasks. It allows an individual to plan actions, control impulses, and attribute meaning to experiences. The researchers hypothesized that the balance between these two systems might look different in children who struggle with sensory regulation.</p>
<p>To test this hypothesis, the team recruited 83 children between the ages of 8 and 12. All participants were recruited from a community neurodevelopment center. They screened the children to ensure they were neurodiverse, meaning they had a high likelihood of a developmental condition such as ADHD or learning differences. However, the researchers specifically excluded children with a confirmed autism diagnosis to reduce variability in the sample.</p>
<p>Clinicians assessed the children using a structured evaluation called the Sensory Processing 3 Dimensions Assessment. Based on this direct observation, the children were divided into two groups. One group consisted of 39 children who exhibited sensory over-responsivity. The second group consisted of 44 neurodiverse children who did not show these specific sensory sensitivities.</p>
<p>The researchers used magnetic resonance imaging to scan the brains of all participants. They employed a technique known as resting-state functional MRI. This method measures spontaneous fluctuations in brain activity while the subject is at rest. It allows scientists to see which brain regions are communicating with each other.</p>
<p>The imaging results revealed a striking divergence between the two groups. In the children with sensory over-responsivity, the researchers observed a reduction in connectivity within the exogenous networks. Specifically, the areas of the brain dedicated to vision and motor control showed lower levels of local synchronization. It appeared as though the brain was dampening its connection to the sensory world.</p>
<p>Simultaneously, these same children showed elevated connectivity within the endogenous networks. The brain regions associated with attention and cognitive control were highly active and synchronized. This pattern created a distinct neural signature. The inward-facing systems were dialed up, while the outward-facing systems were dialed down.</p>
<p>The neurodiverse children without sensory issues displayed the exact opposite pattern. In this group, the exogenous sensory networks were highly connected. Conversely, their endogenous regulation networks showed lower levels of connectivity. This created a clear “double dissociation” between the two groups. The functional organization of their brains appeared to be diametrically opposed depending on their sensory responsiveness.</p>
<p>This contrast was evident in both long-range and local brain connections. Long-range connectivity refers to communication between distant brain regions. Local connectivity refers to synchronization among neighboring neurons. The study found that children with sensory over-responsivity had generally weaker long-range connections across the brain. However, the local hyper-connectivity in their regulatory networks was a standout feature.</p>
<p>The researchers also examined the structural integrity of the brain’s white matter. White matter acts as the cabling that connects different brain regions. Using diffusion tensor imaging, the team found that children with sensory sensitivities had reduced structural integrity in specific pathways. These pathways included the posterior thalamic radiations, which carry visual information, and the internal capsule, which carries touch and motor signals.</p>
<p>To understand the practical implications of these brain patterns, the researchers looked at behavioral data. They assessed how well the children managed their emotions in daily life. They classified the children as either “resilient” or “dysregulated” based on parent reports. Resilient children were better at adapting to change and recovering from setbacks. Dysregulated children struggled more with anger and emotional control.</p>
<p>The study found that the distinct brain pattern—low sensory connectivity and high regulatory connectivity—was strongest in the resilient children with sensory over-responsivity. This suggests that the brain pattern may be an adaptive mechanism. A child who is easily overwhelmed by sensory input might subconsciously suppress their sensory networks to reduce the noise. At the same time, they may upregulate their cognitive control networks to maintain composure.</p>
<p>For the dysregulated children, this distinct separation of brain systems was less apparent. Their brain activity did not show the same clear compensatory shift. This implies that the ability to modulate these two systems is linked to better emotional and behavioral outcomes. The unique neural signature identified by the researchers seems to be a marker of successful coping in the face of sensory overload.</p>
<p>Pratik Mukherjee noted the logic behind this physiological response. He explained, “We think that when you are overstimulated by sensory input, you compensate by dialing up your brain’s inward-focused networks to gain self-control. You also dial down your outward-focused networks to minimize sensory input.” He added that children who are not overwhelmed do not need to employ this strategy.</p>
<p>The research team also tested whether these brain patterns could be used for diagnosis. They utilized machine learning algorithms to analyze the imaging data. By combining functional MRI data with structural white matter data, the algorithms could classify children with high accuracy. The model distinguished between children with and without sensory over-responsivity with nearly 90 percent accuracy.</p>
<p>This high level of classification suggests that sensory over-responsivity has a robust biological basis. It is not merely a behavioral preference or a symptom of other conditions. It involves measurable changes in how the brain is wired and how it functions. The ability to identify these markers could eventually lead to objective diagnostic tools.</p>
<p>There are several caveats to consider regarding this research. The sample size of 83 children is relatively small for a neuroimaging study. The findings will need to be replicated in larger, independent cohorts to ensure they are distinct and universal. Additionally, the study excluded children with autism. Since sensory issues are highly prevalent in autism, it remains unknown if these specific findings apply to that population.</p>
<p>The cross-sectional nature of the study also limits conclusions about cause and effect. The researchers looked at the children at a single point in time. It is not yet clear when these brain patterns emerge in development. Longitudinal studies following children from infancy through adolescence would be necessary to track how these networks develop. Such studies could determine if the brain patterns precede the sensory issues or develop as a response to them.</p>
<p>Future research directions include investigating how these brain networks respond to treatment. Occupational therapy is a common intervention for sensory processing challenges. Researchers could use these imaging techniques to see if therapy changes brain connectivity. If the brain pattern is indeed a coping mechanism, successful therapy might alter the need for such strong downregulation of sensory networks.</p>
<p>The study, “<a href="https://doi.org/10.1186/s11689-025-09656-y" target="_blank" rel="noopener">A neural substrate for sensory over-responsivity defined by exogenous and endogenous brain systems</a>,” was authored by Hannah L. Choi, Maia C. Lazerwitz, Rachel Powers, Mikaela Rowe, Jamie Wren-Jarvis, Amir Sadikov, Lanya T. Cai, Robyn Chu, LaShelle Rullan, Kaitlyn J. Trimarchi, Rafael D. Garcia, Elysa J. Marco & Pratik Mukherjee.</p></p>
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<td><a href="https://www.psypost.org/women-with-high-dark-triad-scores-exhibit-more-anhedonia-and-alexithymia/" 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;">Women with high Dark Triad scores exhibit more anhedonia and alexithymia</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 4th 2025, 12:00</div>
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<p><p>A study in Belgium found that high levels of Dark Triad traits are linked to anhedonia and alexithymia in women, but not in men. Additionally, individuals with high levels of Dark Triad traits tended to report more severe depressive symptoms. The paper was published in <a href="https://doi.org/10.3390/bs15101369"><em>Behavioral Sciences</em></a>.</p>
<p>The Dark Triad traits are a group of three socially aversive personality characteristics: narcissism, Machiavellianism, and psychopathy. Narcissism involves an inflated sense of self-importance, a constant need for admiration, and sensitivity to criticism. Machiavellianism reflects a manipulative, strategic, and calculating interpersonal style focused on personal gain. Psychopathy is marked by low empathy, impulsivity, shallow emotions, and a willingness to engage in harmful or risky behavior.</p>
<p>People high in Dark Triad traits are prone to using others instrumentally and prioritizing their own goals above social norms or moral considerations. In everyday life, they may appear charming at first but later reveal exploitative or callous behavior. Research shows that these traits are linked to aggression, infidelity, unethical decision-making, and lower prosocial behavior. However, in certain competitive environments, some aspects of the Dark Triad may provide short-term advantages.</p>
<p>Study author Daniel French and his colleagues wanted to examine the association between the Dark Triad traits and emotional functioning in the general population. They were also interested in exploring whether there were any sex differences in these associations. The study authors hypothesized that Machiavellianism and psychopathy would be associated with higher levels of alexithymia and anhedonia, but that the strength of these associations would depend on participants’ sex.</p>
<p>Alexithymia is a difficulty in recognizing, describing, and understanding one’s own emotions. Anhedonia is an inability to feel pleasure from activities that are normally enjoyable.</p>
<p>Study participants were 492 adults recruited via the social network Facebook, chain emails sent among students and staff members of the Université Libre de Bruxelles, and word of mouth between July 2017 and August 2018. 323 participants were women. Participants’ median age was 29 years. 17% were students.</p>
<p>Participants completed an online questionnaire containing assessments of Dark Triad traits (the Short Dark Triad scale), alexithymia (the Toronto Alexithymia Scale), anhedonia (the Consumptive and Anticipatory Anhedonia Questionnaire), and depressive symptoms (the Beck Depression Inventory – II).</p>
<p>Results showed that men, on average, scored higher than women on all three Dark Triad traits. Individuals scoring higher on the Dark Triad traits tended to report more severe depressive symptoms. They also tended to report higher levels of alexithymia and anhedonia. However, further analyses found that associations between Dark Triad traits, anhedonia, and alexithymia are present in women, but not in men. More specifically, it was Machiavellianism and psychopathy that were associated with anhedonia and alexithymia in women.</p>
<p>“In line with the existing literature, the findings confirm that Machiavellianism and psychopathy—but not grandiose narcissism— are associated with depressive symptoms and specific emotional deficits, particularly difficulty identifying emotions (alexithymia) and a reduced capacity to experience pleasure (anhedonia), even after adjusting for depression. The present sample showed that these associations are not uniform across sex: they are clearly present in females but absent in males,” the study authors concluded.</p>
<p>The study sheds light on the links between emotional functioning and Dark Triad traits. However, it should be noted that all study data came from self-reports, leaving room for reporting bias to have affected the results.</p>
<p>The paper, “<a href="https://doi.org/10.3390/bs15101369">Dark Triad, Depression, Anhedonia and Alexithymia: The Role of Sex Differences</a>,” was authored by Daniel French, Gwenolé Loas, and Matthieu Hein.</p></p>
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<td><a href="https://www.psypost.org/alzheimers-drug-lecanemab-works-by-triggering-a-specific-cleaning-program-in-immune-cells/" 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;">Alzheimer’s drug Lecanemab works by triggering a specific cleaning program in immune cells</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Dec 4th 2025, 10:00</div>
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<p><p>New research provides evidence that the Alzheimer’s disease drug Lecanemab functions by activating a specific cleaning mechanism within the brain’s immune cells. The study indicates that the therapeutic antibody requires a precise interaction with microglia to physically remove amyloid plaques, which are toxic protein aggregates associated with neurodegeneration.</p>
<p>The findings offer a detailed biological explanation for the clinical success of the drug, which has been shown to slow cognitive decline in patients. The study was published in <em><a href="https://doi.org/10.1038/s41593-025-02125-8" target="_blank" rel="noopener">Nature Neuroscience</a></em>.</p>
<p>Alzheimer’s disease is characterized by the accumulation of amyloid-beta proteins in the brain, forming clumps known as plaques. Lecanemab, an antibody therapy recently approved for medical use, targets these proteins.</p>
<p>Clinical trials have demonstrated that the drug can slow the rate of cognitive decline by approximately 27 percent. Despite this success, the exact cellular processes that allow Lecanemab to clear these plaques more effectively than previous antibody treatments remained a subject of scientific debate.</p>
<p>A prevailing theory suggested that the drug might trigger microglia to engulf and digest the plaques. Microglia are the primary immune cells of the central nervous system. In the brains of Alzheimer’s patients, these cells often surround amyloid plaques but fail to remove them effectively. This failure creates a biological conundrum that researchers have sought to resolve.</p>
<p>A team of scientists, led by Giulia Albertini, Magdalena Zielonka, and Bart De Strooper from the VIB-KU Leuven Center for Brain & Disease Research in Belgium, conducted this study to determine if and how Lecanemab reprograms these cells to resume their protective duties.</p>
<p>To investigate this mechanism, the researchers utilized a specialized mouse model designed to mimic the human brain’s immune environment. These mice, known as AppNL-G-F Csf1rΔFIRE/ΔFIRE mice, were genetically engineered to lack their own endogenous microglia.</p>
<p>The research team then transplanted human microglial cells into the brains of these animals. This xenotransplantation model allowed the investigators to observe the interaction between the human antibody and human immune cells within a living organism, providing a more relevant setting than standard mouse models.</p>
<p>The study employed an experimental design comparing the standard Lecanemab antibody with a modified variant. Antibodies typically possess a region known as the fragment crystallizable, or Fc, region. This section of the molecule acts as a signaling beacon that connects to receptors on immune cells. The researchers engineered a version of Lecanemab, termed Lecanemab LALA-PG, in which the Fc region was mutated to prevent it from binding to immune receptors.</p>
<p>The researchers administered weekly intraperitoneal injections of either the standard Lecanemab, the modified LALA-PG variant, or a control substance to the mice over an eight-week period. The experimental groups consisted of approximately 10 to 12 mice per condition. Following the treatment regimen, the team extracted the brains and performed detailed histological analyses to quantify the amount of amyloid pathology remaining.</p>
<p>The results provided evidence that the functional Fc region is essential for the drug’s efficacy. Mice treated with standard Lecanemab showed a significant reduction in the area covered by amyloid plaques.</p>
<p>In contrast, the mice treated with the LALA-PG variant exhibited no significant reduction in plaque load. This occurred even though the modified antibody successfully bound to the amyloid plaques, accumulating on them in large amounts. This finding indicates that simply binding to the toxic protein is insufficient for clearance. The antibody must also engage the microglia to initiate removal.</p>
<p>To examine the cellular changes driving this process, the authors utilized a spatial transcriptomics technique called Nova-ST. This advanced method allows scientists to map gene expression across tissue sections while simultaneously visualizing the location of amyloid plaques.</p>
<p>The analysis revealed that microglia located in close proximity to the plaques in Lecanemab-treated mice underwent a distinct transcriptional shift. These cells upregulated genes associated with lysosomes and phagosomes, which are the cellular organelles responsible for ingesting and breaking down waste.</p>
<p>This activation of the digestive machinery was absent in the mice treated with the antibody lacking a functional Fc region. The data suggests that the engagement of the Fc receptor on the microglia by the antibody acts as a switch, turning on a dormant plaque-clearing program.</p>
<p>The researchers further investigated the specific molecular pathways involved using single-cell RNA sequencing. This analysis identified a specific gene network induced by the treatment. One of the most highly upregulated genes was SPP1, which encodes a protein called osteopontin. The expression of this gene was strongly associated with the microglia involved in phagocytosis.</p>
<p>To validate the role of osteopontin, the team performed in vitro experiments using human microglial cultures. They exposed these cells to amyloid plaques on brain tissue sections and added increasing concentrations of the osteopontin protein.</p>
<p>The results showed that higher levels of osteopontin significantly enhanced the ability of the microglia to clear the amyloid deposits. This suggests that the production of osteopontin is a key component of the mechanism by which Lecanemab promotes plaque removal.</p>
<p>A critical concern in Alzheimer’s immunotherapy is the potential for damage to healthy brain tissue, particularly the synapses where neurons communicate. The researchers assessed the density of synaptic markers surrounding the plaques to determine if the increased microglial activity caused collateral damage.</p>
<p>The analysis indicated that Lecanemab treatment did not lead to a reduction in synaptic density. This implies that the induced phagocytosis is specific to the amyloid plaques and preserves the integrity of neuronal connections.</p>
<p>The team also sought to confirm that these findings were not an artifact of the specific mouse model used. They repeated the experiments in mice with intact, fully functional mouse immune systems using a mouse-specific version of the antibody. These groups included eight to nine animals each.</p>
<p>The results mirrored the findings in the humanized model, confirming that the Fc-dependent mechanism is robust and functions in the presence of a complete adaptive immune system.</p>
<p>The study does have certain limitations. The primary mouse model used for the human cell experiments lacked an adaptive immune system, which includes T cells and B cells. While the parallel experiment in immunocompetent mice supports the general conclusions, the complex interactions between microglia and the broader human immune system may influence the therapy’s effects in patients.</p>
<p>Additionally, the animal models used in this research do not typically develop significant vascular pathologies. In human clinical trials, a subset of patients treated with amyloid-clearing antibodies experiences side effects known as amyloid-related imaging abnormalities, which can involve brain swelling or bleeding. The current study could not fully assess how the observed microglial activation might contribute to or interact with these vascular issues.</p>
<p>Future research directions may focus on investigating the diversity of Fc receptors on microglia to understand which specific receptors mediate the beneficial effects versus potential inflammatory side effects.</p>
<p>The identification of the osteopontin pathway also opens new avenues for therapeutic development. It suggests that triggering this specific clearing program, perhaps through small molecules rather than antibodies, could offer an alternative strategy for reducing amyloid burden.</p>
<p>The authors provided a disclosure regarding potential conflicts of interest. Bart De Strooper, the senior author, has served as a consultant for several major pharmaceutical entities, including Eli Lilly, Biogen, Janssen Pharmaceutica, Eisai, and AbbVie. He is also a scientific founder of Augustine Therapeutics and Muna Therapeutics, holding stock in the latter. The remaining authors declared no competing interests.</p>
<p>The study, “<a href="https://doi.org/10.1038/s41593-025-02125-8" target="_blank" rel="noopener">The Alzheimer’s therapeutic Lecanemab attenuates Aβ pathology by inducing an amyloid-clearing program in microglia</a>,” was authored by Giulia Albertini, Magdalena Zielonka, Marie-Lynn Cuypers, An Snellinx, Ciana Xu, Suresh Poovathingal, Marta Wojno, Kristofer Davie, Veerle van Lieshout, Katleen Craessaerts, Leen Wolfs, Emanuela Pasciuto, Tom Jaspers, Katrien Horré, Lurgarde Serneels, Mark Fiers, Maarten Dewilde and Bart De Strooper.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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