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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/neuroscientists-link-a-common-inflammatory-molecule-to-the-dopaminergic-mechanisms-of-addiction/" 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 link a common inflammatory molecule to the dopaminergic mechanisms of addiction</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 11th 2026, 08:00</div>
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<p><p>A new study published in the journal <em><a href="https://doi.org/10.1126/scisignal.ady8676" target="_blank">Science Signaling</a></em> has found that an immune system protein plays a central role in the addictive mechanisms of methamphetamine. The findings suggest that tumor necrosis factor-alpha, or TNF-α, works in tandem with dopamine transporters to amplify the drug’s effects on neural activity in the brain’s reward centers. </p>
<p>Methamphetamine use disorder presents a persistent and severe public health challenge. Unlike opioid or alcohol addiction, there are currently no FDA-approved pharmaceutical treatments available to help individuals stop using methamphetamine. This lack of therapeutic options makes the search for biological targets a high priority for medical science.</p>
<p>Scientists have understood for some time that methamphetamine use leads to severe inflammation throughout the body. This is visibly manifested in conditions such as severe dental decay, often called “meth mouth,” and systemic wound-healing issues. However, the specific relationship between this inflammation and the drug’s addictive properties in the brain has remained unclear.</p>
<p>The authors of this study sought to determine if the immune system directly influences the release of dopamine, the chemical messenger associated with pleasure and euphoria. They hypothesized that the inflammation caused by the drug might not just be a side effect, but a driver of the addiction itself. </p>
<p>“Methamphetamine addiction remains a major public health crisis with limited treatment options,” said study author <a href="https://www.khoshboueilab.org/" target="_blank">Habibeh Khoshbouei</a>, a professor and vice chair in the Departments of Neuroscience at the University of Florida College of Medicine.</p>
<p>“While we knew that methamphetamine triggers neuroinflammation and increases inflammatory molecules like TNF-α in the brain, the specific role of TNF-α in addiction mechanisms was unclear. We wanted to understand whether TNF-α contributes to methamphetamine’s effects on dopamine signaling, as this could reveal new treatment targets for addiction.”</p>
<p>To investigate, the research team conducted a series of preclinical experiments using brain tissue from mice. They focused specifically on the ventral tegmental area, a region of the brain critical for processing reward and motivation. The researchers utilized sophisticated electrical recording techniques to monitor the activity of individual neurons.</p>
<p>Khoshbouei and her colleagues identified dopamine neurons based on specific physiological criteria. They looked for neurons that showed a decrease in firing frequency when exposed to dopamine and an increase when exposed to a dopamine blocker. They also looked for specific electrical signatures, such as a “sag” in voltage during electrical testing, which is characteristic of these cells.</p>
<p>When the researchers applied methamphetamine to these brain slices, they observed a distinct pattern in the dopamine neurons. The drug caused a rapid acceleration in the firing frequency of these cells. This initial spike in activity was followed by a progressive deceleration over a period of several minutes.</p>
<p>The researchers used phase-plane plots to visualize the shape of the electrical spikes produced by the neurons. They found that methamphetamine altered the waveform of the action potentials, which are the electrical impulses neurons use to communicate. The drug suppressed the upward phase of the spike and broadened its duration.</p>
<p>The researchers then examined whether TNF-α alone could mimic these effects without the presence of methamphetamine. When they applied TNF-α to the brain slices, the dopamine neurons exhibited a similar biphasic increase in firing activity. This suggested that the immune protein itself has the capacity to stimulate the reward circuitry in a manner resembling the drug.</p>
<p>To test the necessity of this immune signal, Khoshbouei and her colleagues used a compound called UCB-9260 to inhibit TNF-α signaling. When they pre-treated the slices with this inhibitor, the methamphetamine-induced changes in neuronal firing were significantly reduced. The inhibitor effectively prevented the drug from altering the electrical properties and firing rates of the neurons.</p>
<p>The researchers also explored the role of the dopamine transporter, a protein responsible for recycling dopamine back into the neuron. They found that blocking this transporter with a drug called nomifensine prevented TNF-α from increasing neuronal activity. This finding indicates a bidirectional connection where the immune system and the dopamine transport system regulate each other.</p>
<p>“The most surprising findings were the bidirectional crosstalk between TNF-α and dopamine transporters, and the effect of TNF-α on increasing dopamine,” Khoshbouei told PsyPost. “We didn’t expect TNF-α might modulate methamphetamine’s effects, and we didn’t anticipate that blocking dopamine transporters would also prevent TNF-α from affecting neurons, and vice versa. This reveals these seemingly separate systems are interconnected.”</p>
<p>To further understand the mechanism, the team investigated the role of calcium, which is essential for neuronal firing. They utilized a technique called calcium imaging with a sensor named GCaMP6f to track calcium levels in living cells. Both methamphetamine and TNF-α triggered a significant rise in intracellular calcium levels.</p>
<p>The data showed that these effects relied on specific channels known as L-type calcium channels. These channels allow calcium to flow into the cell, increasing its excitability. Blocking these channels dampened the effects of both the drug and the immune protein.</p>
<p>Consequently, the study identified a shared pathway involving calcium influx that drives the increased excitability of dopamine neurons. The team confirmed this cross-talk using chemogenetics, a method that allows researchers to stimulate specific neurons using designer drugs. They expressed a receptor called hM3Dq in the dopamine neurons to artificially activate them.</p>
<p>Activating these receptors increased the firing frequency of the neurons, as expected. However, the researchers found that they could block this artificially induced firing by inhibiting either TNF-α signaling or the dopamine transporter. This reinforced the conclusion that these two systems are functionally intertwined.</p>
<p>The researchers also measured the release of dopamine directly using a genetically encoded sensor called GRAB-DA. This sensor becomes fluorescent when it binds to dopamine outside the cell. Imaging of mouse brain tissue showed that applying TNF-α caused a rapid increase in fluorescence, indicating dopamine release.</p>
<p>Methamphetamine caused an even larger increase in dopamine release, as anticipated. However, the application of the TNF-α inhibitor significantly reduced the dopamine release triggered by methamphetamine. Similarly, blocking the dopamine transporter reduced the dopamine release triggered by TNF-α.</p>
<p>“We discovered that inflammation isn’t just a side effect of methamphetamine use, it amplifies the drug’s addictive properties,” Khoshbouei explained. “TNF-α, an inflammatory molecule, works alongside methamphetamine to increase dopamine release and enhance the activity of reward-related brain cells. This means FDA-approved anti-inflammatory drugs that block TNF-α (already used for conditions like rheumatoid arthritis) could potentially be repurposed to help treat methamphetamine addiction.”</p>
<p>“Our findings show robust, consistent effects across multiple experimental approaches, from individual neurons to whole brain tissue. The fact that blocking either TNF-α signaling or dopamine transporters reduced methamphetamine’s effects by similar magnitudes suggests this is a fundamental mechanism, not a minor pathway.” </p>
<p>“The availability of existing TNF-α blockers makes this relevant for potential clinical translation,” Khoshbouei continued. “We plan to submit a grant to NIH to seek funding for clinical trials investigating the efficacy of TNF-α blockers on reducing methamphetamine reward properties that can reduce relapse rate.”</p>
<p>While the study establishes a mechanistic link in animal models, it is important to note that these findings come from experiments conducted on mouse brain tissue and cell cultures, which do not perfectly replicate the complexity of human addiction. The dosage and timing of drug exposure in a controlled dish differ from chronic use patterns in humans.</p>
<p>“While our findings suggest TNF-α blockers could help reduce the rewarding properties of methamphetamine and this methamphetamine addiction, we want to emphasize this was basic neuroscience research,” Khoshbouei said. Clinical trials would be needed to determine the dosage and efficacy in humans with methamphetamine use disorder.”</p>
<p>Although these inhibitors are already approved for conditions like rheumatoid arthritis and Crohn’s disease, their use in addiction treatment is novel. Safety profiles would need to be re-evaluated in this specific context. “Completely blocking TNF-α has risks since it plays important roles in normal immune function,” Khoshbouei noted.</p>
<p>TNF-α plays a vital role in the body’s normal immune defense against infections and tumors. Long-term suppression of this protein could lead to unwanted side effects or vulnerabilities to illness.</p>
<p>Future research aims to investigate whether these inhibitors can reduce drug-seeking behavior in live animals. The current study focused on cellular mechanisms, but behavioral studies are needed to see if this translates to reduced cravings or relapse. </p>
<p>“We’re conducting behavioral studies to test whether TNF-α inhibitors can reduce methamphetamine-seeking behavior in animal models,” Khoshbouei told PsyPost. “We’re also investigating whether this neuroimmune mechanism applies to other stimulants like cocaine. Ultimately, we hope to collaborate with clinical researchers to test whether existing TNF-α blockers could help people struggling with methamphetamine addiction.”</p>
<p>“This work highlights how addiction involves much more than just the brain’s reward system; it could be a neuro-immune dysregulation. Understanding the Brain-Body connections and how immune system affect the reward pathway open new avenues for treating addiction, potentially allowing us to repurpose existing FDA approved medications. We also want to thank NIH supporting our research and giving us the opportunity to do this work.” </p>
<p>The study, “<a href="https://doi.org/10.1126/scisignal.ady8676" target="_blank">TNF-α signaling mediates the dopaminergic effects of methamphetamine by stimulating dopamine transporters and L-type Ca2+ channels</a>,” was authored by Landon M. Lin, Marcelo Febo, Adriaan W. Bruijnzeel, Leah Phan, Adithya Gopinath, Jordan Seibold, Emily Miller, and Habibeh Khoshbouei.</p></p>
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<td><a href="https://www.psypost.org/psychopathic-women-are-more-likely-to-use-physical-aggression/" 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;">Psychopathic women are more likely to use physical aggression</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 11th 2026, 06:00</div>
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<p><p>New research provides evidence that women with high levels of psychopathy are more likely to engage in physical, verbal, and indirect aggression against other women. The study indicates that while women generally favor covert competitive tactics, those with specific dark personality traits may bypass these social norms to target rivals directly. These findings were published in <em><a href="https://psycnet.apa.org/record/2026-92559-001" target="_blank">Evolutionary Behavioral Sciences</a>.</em></p>
<p>Evolutionary theory suggests that humans compete for access to romantic partners through a process known as intrasexual selection. This competition can manifest in various ways depending on the sex of the individual. For women, biological factors related to reproduction play a significant role in shaping these competitive strategies.</p>
<p>The theory of obligatory parental investment notes that women face higher biological costs in reproduction than men. Because women carry the fetus during gestation and often care for infants, they must protect their physical well-being to ensure the survival of their offspring. This biological reality implies that direct physical confrontation is a high-risk strategy for women.</p>
<p>Consequently, evolutionary psychologists have observed that women typically compete using low-risk, indirect strategies. These tactics often include spreading rumors, gossiping, or social exclusion. These methods allow women to damage a rival’s reputation and reduce their attractiveness to potential mates without facing the danger of physical injury.</p>
<p>Despite this general tendency toward indirect aggression, individual differences in personality can alter these behaviors. Previous science has identified a cluster of personality traits known as the Dark Tetrad. This cluster includes narcissism, Machiavellianism, psychopathy, and sadism.</p>
<p>Machiavellianism involves a tendency to be manipulative and deceptive to achieve one’s goals. Narcissism is characterized by a sense of entitlement and a desire for admiration. Psychopathy is linked to high impulsivity, low empathy, and a lack of emotional attachment. Sadism involves the enjoyment of inflicting suffering or pain on others.</p>
<p>“We were primarily interested in the role of dark personality traits and intrasexual competition in women, where the research shows a positive association between the two. There was a gap where most of this research did not include sadism, which comprises the dark tetrad personality traits,” said study author Ray Garza Jr., an assistant professor of psychology and director of <a href="https://www.instagram.com/evolutionary_visual_lab/" target="_blank">the Evolutionary Visual Lab</a> at Texas A&M International University.</p>
<p>“We know that women tend to use more covert methods to compete with other women, such as verbal and indirect strategies, which typically are not high-risk compared to physical aggression. We were able to fill in the gap by also collecting women’s responses on their use of verbal, indirect (i.e., rumor spreading), and physical aggression.”</p>
<p>For their study, the research team recruited 136 women to participate in the study. The participants were students at a university in South Texas. The sample was predominantly Hispanic, with most participants identifying as being of Mexican descent. The average age of the participants was approximately 23 years old.</p>
<p>The participants completed an online survey consisting of three standardized psychological scales. The first measure was the Intrasexual Competition Scale. This tool assesses an individual’s attitude toward competing with members of the same sex for romantic partners. It includes items that measure how threatened a woman feels by attractive rivals.</p>
<p>The second measure was the Short Dark Tetrad scale. This assessment evaluates the four dark personality traits. Participants rated their agreement with statements reflecting manipulative tendencies, callousness, self-importance, and enjoyment of others’ suffering. This allowed the researchers to create a profile of each participant’s personality regarding these specific traits.</p>
<p>The third measure was the Direct and Indirect Aggression Scale. This instrument asks participants to report their actual engagement in aggressive behaviors. It is divided into three categories. Physical aggression includes actions such as hitting or shoving. Verbal aggression involves name-calling or yelling. Indirect aggression consists of malicious gossip or social exclusion.</p>
<p>The researchers analyzed the data to determine which personality traits predicted the different types of aggression. They also examined whether the general drive to compete explained the relationship between personality and aggression. The results provided a detailed look at how dark personality traits manifest in competitive contexts.</p>
<p>The analysis showed that women who scored higher on the Intrasexual Competition Scale also tended to score higher on Machiavellianism, psychopathy, and sadism. This indicates that women with these traits are more likely to view other women as rivals. Narcissism was the exception, as it did not correlate with intrasexual competition.</p>
<p>Psychopathy emerged as the most consistent predictor of aggressive behavior. Women with higher levels of psychopathy were significantly more likely to report using physical aggression. This finding is notable because it contradicts the general evolutionary trend of women avoiding physical risks. It appears that the lack of empathy and impulsivity associated with psychopathy may override the instinct for self-preservation in competitive scenarios.</p>
<p>“Most research has shown that women do not utilize physical aggression because of its high-risk nature,” Garza told PsyPost. “We did find that dark personality traits predict physical aggression as well. Women do act out physically in situations that threaten their reproductive relevant goals, such as when other women target their sexual history.”</p>
<p>Psychopathy also predicted the use of verbal and indirect aggression. This suggests that women high in this trait utilize a versatile arsenal of competitive tactics. They do not limit themselves to covert methods but are willing to employ whatever strategy is available. They appear less concerned with the social or physical repercussions of their actions.</p>
<p>Sadism showed a specific relationship with verbal aggression. Women who scored high on sadism were more likely to use verbal attacks against others. The researchers propose that verbal aggression offers immediate feedback. The perpetrator can instantly see the distress they cause the victim.</p>
<p>This immediate reaction aligns with the sadistic desire to derive pleasure from another’s suffering. In contrast, sadism did not predict indirect aggression. Indirect tactics like rumor-spreading take time to cause harm. The delayed nature of indirect aggression may be less satisfying to individuals with high levels of sadism.</p>
<p>The researchers also found a negative relationship between narcissism and verbal aggression. Women with higher narcissism scores were less likely to engage in verbal attacks. Narcissists often seek to maintain a superior self-image. Engaging in overt verbal altercations might be viewed as beneath them or damaging to their social standing.</p>
<p>“The research should convey that some women are more inclined to use verbal, indirect, and physical aggression, but these behaviors are mostly driven by psychopathy and sadism,” Garza explained. “It could be argued that women with higher levels of psychopathy and sadism are better at implementing competitive strategies, and potentially expecting retaliation.”</p>
<p>As with all research, there are some limitations to consider. The sample size was relatively small and consisted of university students. This specific demographic may not represent the behavior of women in different age groups or socioeconomic environments. </p>
<p>“One could argue that older women may not use these strategies, as they are more common in reproductive aged women,” Garza noted. “From a practical viewpoint, we know that people act out aggressively, whether at school or at the workplace, and these findings may shed light onto the underlying traits associated with such behaviors.”</p>
<p>The study also relied on self-reported measures. Participants may not always be truthful about their aggressive behaviors due to social desirability bias. Women high in dark traits might be more willing to admit to aggression, which could influence the results. Future research could benefit from using experimental designs that observe behavior in real-time.</p>
<p>“One common misconception is that these behaviors are inherently bad,” Garza said. “But we interpret these behaviors and dark personality traits as being adaptive to one’s environment and fitness related threats.”</p>
<p>The researchers suggest that future studies should investigate the cognitive mechanisms behind these behaviors. For instance, they propose examining how women with dark personality traits process visual cues. Understanding how these women perceive threatening facial expressions could offer deeper insight into their aggressive responses. The current study serves as a step toward understanding the complex interplay between personality and female competition.</p>
<p>The study, “<a href="https://psycnet.apa.org/doi/10.1037/ebs0000395" target="_blank">Psychopathy Predicts the Use of Physical, Verbal, and Indirect Aggression in Women</a>,” was authored by Ray Garza, Jenna D. Arsuaga, and Farid Pazhoohi.</p></p>
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<td><a href="https://www.psypost.org/blue-blocking-glasses-fail-to-alleviate-mania/" 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;">Blue-blocking glasses fail to alleviate mania</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 10th 2026, 18:00</div>
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<p><p>A new clinical trial conducted by researchers in Canada has found that wearing blue-blocking glasses did not significantly reduce symptoms of mania in hospitalized patients when compared to control glasses. While the intervention was found to be safe and feasible for patients to use, the study failed to replicate earlier findings that suggested blocking blue light could be a highly effective treatment for acute mania. </p>
<p>These findings were published in the <em><a href="https://doi.org/10.1016/j.jad.2025.120910" target="_blank">Journal of Affective Disorders</a></em>. A companion study appearing in the <em><a href="https://doi.org/10.1080/17482631.2025.2540795" target="_blank">International Journal of Qualitative Studies on Health and Well-being</a></em> highlighted that despite the lack of clinical efficacy, patients with mania were highly willing and able to participate in rigorous research.</p>
<p>Bipolar disorder is a mental health condition marked by extreme shifts in mood and energy levels. One of the defining characteristics of the disorder is the presence of manic episodes. During a manic episode, an individual may experience heightened energy, racing thoughts, impulsive behavior, and a significantly decreased need for sleep. These episodes can be severe and often require hospitalization to ensure the safety of the patient and stabilization of symptoms.</p>
<p>Standard treatments for mania typically involve pharmaceutical interventions. Doctors often prescribe mood stabilizers and antipsychotic medications to help manage symptoms. While these medications are effective for many people, they often come with a range of side effects that can be difficult for patients to tolerate. </p>
<p>These side effects can include weight gain, tremors, and metabolic changes, which sometimes lead to patients stopping their medication. As a result, there is a strong interest in finding non-drug treatments that can support recovery without adding to the burden of side effects.</p>
<p>Scientists have recognized a strong link between bipolar disorder and the body’s internal clock, known as the circadian rhythm. Disruptions in sleep and daily rhythms are common triggers for manic episodes. Light is the primary environmental cue that regulates the human biological clock. </p>
<p>Specifically, short-wavelength blue light is known to signal the brain that it is daytime. When the eye detects blue light, it sends a signal to the brain to suppress the production of melatonin, a hormone that facilitates sleep.</p>
<p>In modern hospital environments, patients are often exposed to artificial light late into the evening. This exposure can potentially disrupt their circadian rhythms further, prolonging or intensifying manic symptoms. Previous research, including a notable case study involving total darkness therapy and a smaller clinical trial, suggested that controlling light exposure could help stabilize mood. </p>
<p>“Mania can be very disruptive to patients lives, often requiring hospitalization. Existing treatment for mania is medication focused and the medications available carry risk for various side-effects,” said study author Jess G. Fiedorowicz, head of the Department of Mental Health at The Ottawa Hospital.</p>
<p>“A treatment with lower risk of side-effects that could speed up response to treatment is highly desirable. I was inspired by a study of blue-blocking glasses for mania presented by Tone Henriksen at the International Society of Bipolar Disorders Conference in Washington, D.C. in 2017.”</p>
<p>However, that study had design limitations, such as the fact that the raters assessing the patients knew who was wearing the active glasses. Fiedorowicz and his colleagues sought to test the efficacy of blue-blocking glasses using a more rigorous scientific design.</p>
<p>The clinical trial took place at The Ottawa Hospital in Ontario, Canada. The research team recruited 42 adult participants who had been admitted to the hospital with a diagnosis of mania. To be eligible, participants had to be between the ages of 18 and 70 and willing to comply with the study procedures. The researchers utilized a randomized controlled design, which is considered the gold standard in clinical research.</p>
<p>Participants were randomly assigned to one of two groups. The experimental group received amber-tinted glasses designed to block approximately 99 percent of blue light. The control group received smoke-tinted glasses that blocked ultraviolet light but allowed most blue light to pass through. </p>
<p>To maintain a fair comparison, the researchers used a form of mild deception during the consent process. They informed participants that the study was testing two different types of light-filtering lenses, without specifying that one was a placebo. This helped ensure that the participants’ expectations did not influence the results.</p>
<p>The protocol required participants to wear their assigned glasses from 6:00 p.m. until 8:00 a.m. the following morning. They were instructed to wear the glasses anytime they were awake during this window. If they woke up in the middle of the night, they were asked to put the glasses on before turning on any lights. </p>
<p>The intervention lasted for two weeks or until the patient was discharged from the hospital. Throughout the study, all patients continued to receive their standard medical care, including any medications prescribed by their treating psychiatrists.</p>
<p>The primary measure of success was the change in scores on the Young Mania Rating Scale. This is a standardized tool used by clinicians to assess the severity of manic symptoms. </p>
<p>Crucially, the physicians who performed these assessments were blinded to the treatment assignment. They did not know which pair of glasses the patient had been wearing. This blinding prevented the raters from unintentionally biasing the scores based on their knowledge of the intervention.</p>
<p>The results of the quantitative study showed that participants in both groups experienced improvements in their symptoms over time. However, the researchers found no statistically significant difference between the group wearing the blue-blocking glasses and the group wearing the control glasses. </p>
<p>Both groups recovered at a similar rate. At the end of the two-week period, the reduction in mania scores was comparable for both the experimental and control arms of the study.</p>
<p>Secondary outcomes also failed to show a benefit for the blue-blocking lenses. The researchers tracked the amount of medication patients required during their hospital stay. There was no significant difference in the dosages of antipsychotics or sedatives used by the two groups. </p>
<p>Self-reported measures of sleep quality and mood also showed no distinct advantage for the blue-blocking intervention. The study did confirm that the blinding was successful, as neither the raters nor the participants were able to guess which group they were in better than chance.</p>
<p>“Circadian rhythms are very relevant to the pathophysiology of bipolar disorder and can be disrupted,” Fiedorowicz told PsyPost. “Circadian therapies therefore hold great promise but are not commonly utilized and require more study. </p>
<p>“Our study did not find a benefit to blue blocking glasses in patients with mania who were severely ill and being intensively treated with medications. We need more studies to understand circadian disruptions in bipolar disorder to develop better treatments. Our study was negative, but we hope that informs design of future studies of circadian treatments for bipolar disorder.”</p>
<p>Despite the lack of clinical benefit, the study demonstrated that the intervention was safe. The frequency of adverse events, such as headaches, was similar in both groups. </p>
<p>Adherence to the protocol was notably high. Most participants were able to wear the glasses for the required time, with 80 percent of the sample classified as mostly adherent. This finding challenges the common assumption that patients with acute mania are too disorganized or agitated to follow complex research protocols.</p>
<p>To gain a deeper understanding of the participants’ experiences, the research team conducted a separate qualitative study. This involved in-depth interviews with 24 of the patients and 10 clinical staff members. The researchers used a method called grounded theory to analyze the interview data. This approach allows themes to emerge directly from the participants’ words rather than testing a preconceived hypothesis.</p>
<p>The qualitative analysis revealed that patients were highly motivated to participate in the research. Three main drivers for participation emerged from the interviews. First, many participants expressed an altruistic desire to help others who might suffer from bipolar disorder in the future. Second, some viewed the study as a way to help themselves, hoping the glasses might aid their recovery. Third, the financial compensation provided for participation was a practical motivator for some.</p>
<p>A major theme identified in the interviews was the value of the patient-centered approach used by the research team. Participants described the study visits as a positive addition to their hospital stay. They reported that the regular check-ins with research staff made them feel heard and validated. </p>
<p>The process of answering questions about their mood and sleep provided them with greater insight into their own condition. Some participants noted that the research interactions felt less clinical and more personal than their standard medical interactions, creating a sense of safety and community.</p>
<p>The qualitative study also explored the feasibility of the intervention from the patients’ perspective. Most participants found the glasses acceptable and easy to use. They appreciated having a choice of frame styles. Challenges were minor and included physical discomfort from wearing glasses over prescription lenses or difficulties remembering to put them on immediately upon waking at night. However, patients generally felt capable of adhering to the rules, even while experiencing symptoms of mania.</p>
<p>Clinicians interviewed for the study also expressed support for the research. Psychiatrists and nurses viewed the blue-blocking glasses as a low-risk intervention that complemented their clinical care. They did not find that the study disrupted the workflow on the inpatient units. </p>
<p>Clinicians noted that the study provided patients with additional structure and resources, which was seen as a benefit regardless of the intervention’s efficacy. The staff also reported that introducing the research opportunity helped build rapport with their patients.</p>
<p>The study has some limitations. The sample size, while larger than previous trials, was still relatively small. This limits the statistical power to detect small differences between groups. </p>
<p>Additionally, the study was conducted in a hospital setting where patients have limited exposure to natural outdoor light. This environment might dampen the potential contrast between blocking and receiving blue light. The researchers also acknowledged that while they attempted to measure sleep using actigraphy watches, this data was only available for a subset of participants.</p>
<p>Future research directions were suggested by the findings. While blue-blocking glasses may not be sufficient as a standalone or additive treatment for acute mania in patients already on heavy medication, they might still have a role in other contexts. </p>
<p>The researchers suggest exploring the use of these glasses for the prevention of manic episodes in people showing early warning signs. Investigating their use in outpatient settings, where light exposure is more variable, could also yield different results.</p>
<p>The qualitative findings provide evidence that people with acute mania are capable partners in scientific research. The authors argue that illness severity should not automatically exclude patients from participating in clinical trials. The study showed that with appropriate support and accommodations, such as repeated explanations and patience during the consent process, vulnerable patients can provide informed consent and adhere to study protocols.</p>
<p>“There was a lot of interest in blue blocking glasses in participants,” Fiedorowicz said. “There is great interest in non-medication treatments for bipolar disorder for sure and circadian therapies in particular are appealing to individuals.”</p>
<p>“On rare occasion, I’ve encountered naysayers who suggest that people when manic can’t do studies like this. Our qualitative and quantitative data strongly rebuts this misguided assertion. Studying people with mania is, of course, not without its challenges, but it can be done with the right supports and team in place and providing participants accomodations and flexibility.”</p>
<p>The study, “<a href="https://doi.org/10.1016/j.jad.2025.120910" target="_blank">The Ottawa sunglasses at night study: A randomized controlled trial of blue-blocking glasses for mania</a>,” was authored by Jess G. Fiedorowicz, Eric Mikhail, Marco Solmi, Joseph K. Burns, Jessica Yu, Sara Siddiqi, Thanh Nguyen, Andrew L. Smith, and Rébecca Robillard.</p>
<p>The study, “<a href="https://doi.org/10.1080/17482631.2025.2540795" target="_blank">The feasibility of conducting non-pharmacological research studies in participants with mania: a grounded theory qualitative analysis of the Ottawa Sunglasses at Night study</a>,” was authored by Jessica Yu, Joseph K. Burns, Eric Mikhail, Marco Solmi, Simon Hatcher, Andrew L. Smith, Rébecca Robillard, Thanh Nguyen, Nicole Edgar, Tetyana Kendzerska, Mark Kaluzienski, Andrea Bardell, and Jess G. Fiedorowicz.</p></p>
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<td><a href="https://www.psypost.org/intranasal-5-meo-dmt-effects-peak-within-15-minutes-and-lack-strong-visuals-study-finds/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Intranasal 5-MeO-DMT effects peak within 15 minutes and lack strong visuals, study finds</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 10th 2026, 16:00</div>
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<p><p>A study examining subjective experiences after intranasal application of 5-MeO-DMT found that its effects peak 8-15 minutes after application. Consciousness-altering effects typically ended after 45-60 minutes. The research was published in <a href="https://doi.org/10.1038/s41598-025-22620-z"><em>Scientific Reports</em></a>.</p>
<p>5-methoxy-N,N-dimethyltryptamine or 5-MeO-DMT is a naturally occurring psychedelic compound belonging to the tryptamine class. It is found in certain plants and in the venom of the Incilius alvarius (Sonoran Desert toad), as well as produced synthetically.</p>
<p>The substance is known for producing extremely intense and short-lasting altered states of consciousness. Its effects typically include profound changes in perception, a strong sense of ego dissolution, and altered awareness of time and self.</p>
<p>Compared to DMT, the effects of 5-MeO-DMT are less visual but more immersive and abstract. Users report the experience as emotionally powerful and sometimes overwhelming. Research interest in 5-MeO-DMT has increased due to its potential relevance for understanding consciousness and mental health. However, scientific evidence on its therapeutic effects and risks is still limited.</p>
<p>Study author Anna O. Ermakova and her colleagues wanted to understand the experiences of individuals participating in a study that involved taking 5-MeO-DMT intranasally to examine its pharmacological effects. The study focused on the psychoactive effects of 5-MeO-DMT.</p>
<p>While the broader clinical trial enrolled 50 healthy volunteers, this specific study analyzed interviews from 40 participants aged between 25 and 55 years. They had no prior experience of using psychedelics in their lifetime.</p>
<p>Thirty-two participants received doses of 5-MeO-DMT ranging from 1 mg to 12 mg (each participant was assigned a single dose). Eight participants received a placebo (i.e., had intranasal application of a substance that did not contain 5-MeO-DMT and produced no effects).</p>
<p>5-MeO-DMT used in the study was in the form of dry powder for intranasal application. In the dosing session, a participant would take his/her assigned dose and for up to 90 minutes after that provided ratings of overall subjective drug intensity.</p>
<p>As soon as possible after the dosing session, the participants took part in a guided interview discussing their psychedelic experiences. Study authors used natural language processing software and machine learning techniques to interpret transcripts of participants’ interview responses.</p>
<p>Results showed that psychedelic effects of 5-MeO-DMT started between 0 and 2 minutes after application. The effects peaked 8-15 minutes after intranasal application and gradually dissipated from 15 to 40 minutes. Some effects lingered up to 90 minutes in some participants. The peak was slightly longer with higher doses and dissipation also lasted longer. Consciousness-altering effects typically ended 45-60 minutes after application.</p>
<p>While the effects lasted, participants reported alterations in sensory and emotional experiences, cognition, metacognition, arousal, and perceived relationship between self, other, and the environment.</p>
<p>“5-MeO-DMT has a distinctive profile of subjective effects relative to published reports of other psychedelics, with a short duration of action, relative lack of visual effects, strong emotional or bodily experiences and the potential to elicit therapeutically relevant content, such as emotional breakthroughs and personal insights,” study authors concluded.</p>
<p>The study sheds light on the psychoactive effects of 5-MeO-DMT. However, it should be noted that the number of participants in the study was too small to draw definitive conclusions on the differences between 5-MeO-DMT doses.</p>
<p>The paper, “<a href="https://doi.org/10.1038/s41598-025-22620-z">Mapping the phenomenology of intranasal 5-MeO-DMT in psychedelic-naïve healthy adults,</a>” was authored by Anna O. Ermakova, Fiona Dunbar, Mathieu Seynaeve, and Raphaël Millière.</p></p>
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<td><a href="https://www.psypost.org/does-asmr-really-help-with-anxiety-a-psychology-expert-explains-the-evidence/" 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;">Does ASMR really help with anxiety? A psychology expert explains the evidence</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 10th 2026, 14:00</div>
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<p><p>Most of us have experienced tingling or “goosebumps” at some point, especially when we feel a strong positive emotion such as awe or excitement.</p>
<p>But some people have this response when they listen to certain sounds. <a href="https://www.vox.com/2015/7/15/8965393/asmr-video-youtube-autonomous-sensory-meridian-response">Online videos</a> which feature sounds of people whispering, crackling packets, and brushing or combing a microphone are all geared towards making you feel this positive tingle – the autonomous sensory meridian response, or ASMR.</p>
<p>Not everyone responds to ASMR content. But many who do say it makes them less anxious and helps them sleep. What does the science say?</p>
<h2>What is ASMR?</h2>
<p>ASMR is an involuntary emotional and physical response, typically to a sound, which causes <a href="https://doi.org/10.1371/journal.pone.0196645">a reflexive tingling sensation</a> on the scalp and back of the neck.</p>
<p>This multi-sensory experience <a href="https://doi.org/10.1016/j.concog.2023.103477">can make us feel</a> euphoria and “psychological stability”, meaning we experience less inner turmoil and feel more calm.</p>
<p>However, we still don’t have much evidence about what happens in the brain and the body when this occurs.</p>
<p><a href="https://doi.org/10.1007/s00221-022-06377-9">Some argue</a> that ASMR is simply an example of <em>frisson</em> (French for “shiver”). This is when an intense emotional stimulus – such as a tender moment in a movie – triggers tingling or gives us “the chills”.</p>
<p><a href="https://doi.org/10.3389/fpsyg.2014.00790">Research suggests</a> these so-called “skin orgasms” are due to a sudden rush of the chemical dopamine in the brain’s reward centres.</p>
<p>However, the sense of awe or inspiration felt during a frisson experience is brief, (typically 4–5 seconds). In contrast, ASMR is <a href="https://doi.org/10.1177/0305735610362950">usually described</a> as inducing an enduring state of calm.</p>
<h2>What triggers ASMR?</h2>
<p>Almost everyone <a href="https://doi.org/10.1098/rstb.2011.0219">will jump out of their skins</a> if they experience a sudden and loud sound. This is because we’ve evolved to fear what is unpleasant or unexpected, to keep us safe from danger.</p>
<p>When it comes to sounds that can make us feel good, it’s not as easy to confirm whether there are universal triggers – that is, sounds that would make most people have the same positive reaction.</p>
<p>Research in ASMR has identified some common triggers, <a href="https://doi.org/10.7717/peerj.851">including</a> whispering, tapping and crackling sounds. But we can’t say if these sounds would have the same effect on everyone.</p>
<p>ASMR videos often <a href="https://www.youtube.com/shorts/3WG714Qu2g0">combine</a> these sounds with video and role play known as “personal attention”. This means treating the camera like it is the viewer, speaking and interacting directly with it, and even simulating activities such as brushing hair or applying makeup to the viewer.</p>
<h2>Why doesn’t it affect everyone?</h2>
<p>Not everyone responds to ASMR triggers, with <a href="https://doi.org/10.7717/peerj.3846">some estimates</a> suggesting only one in five people can experience ASMR.</p>
<p>Whether or not you do is <a href="https://doi.org/10.1016/j.concog.2023.103477">likely due</a> to personality type and your predisposition to susceptibility, meaning how easily others can influence you.</p>
<p>Studies <a href="https://doi.org/10.1016/j.concog.2023.103477">have found</a> those who respond are typically younger, experience more negative emotions, and are more introverted and critical. But they also tend to be more open to trying new things.</p>
<p>Some <a href="https://doi.org/10.1016/j.concog.2023.103477">research</a> has suggested “expectancy effects” could play a role. This is like a placebo – people who are invested in ASMR’s potential as a therapeutic tool may be more likely to feel its effects.</p>
<p>However, we still don’t know precisely how ASMR works to induce positive emotions.</p>
<p>More than a dozen studies have <a href="https://doi.org/10.7717/peerj.7122">reported</a> on how <a href="https://doi.org/10.1016/j.concog.2020.103053">the brain</a> behaves <a href="https://doi.org/10.1016/j.ibneur.2024.12.001">during ASMR</a>. But the findings across them are inconsistent and many have a very small number of participants or no comparison group, so we can’t draw conclusions.</p>
<p>Studies looking at the body’s response during ASMR experiences have had similarly mixed results. Some <a href="https://doi.org/10.1037/cns0000368">have found</a> people may experience both increased sweating (linked to the stress response) and decreased heart rate (linked to relaxation).</p>
<p>To describe this apparently contradictory state, some <a href="https://doi.org/10.1016/j.concog.2023.103477">researchers</a> have coined the term “arousing relaxation”.</p>
<p>Another <a href="https://doi.org/10.1016/j.concog.2023.103477">theory</a> is that the social or erotic aspects of ASMR videos are a more important trigger than sounds or other stimuli – basically, that it is a kind of sexual arousal. But we would need more evidence on this.</p>
<h2>The bottom line</h2>
<p>Without being able to identify universal triggers, it’s also difficult to apply ASMR as an evidence-based tool in therapy. To date, there are no clinical trials that link ASMR with short- or long-term therapeutic effects.</p>
<p>Nevertheless, many people in the “whisper community” – those who produce and consume ASMR content online – claim ASMR helps them to relax, sleep better and reduce stress.</p>
<p>So, there’s no harm in ASMR if it helps you relax. But we would need more research to establish whether it’s effective as a clinical intervention for anxiety, insomnia or other conditions.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/252181/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
<p> </p>
<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/does-asmr-really-help-with-anxiety-a-psychology-expert-explains-the-evidence-252181">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/random-signals-in-support-cells-help-cement-long-term-memories/" 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;">Random signals in support cells help cement long-term memories</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 10th 2026, 12:00</div>
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<p><p>A new study challenges the traditional view that neurons are the sole architects of memory in the brain. Researchers have discovered that astrocytes, a type of star-shaped support cell, generate random electrical signals that are essential for cementing long-term memories. This research, published in the <em><a href="https://doi.org/10.1073/pnas.2500511122" target="_blank">Proceedings of the National Academy of Sciences</a></em>, suggests that the brain incorporates an element of unpredictability to stabilize neural circuits.</p>
<p>For decades, neuroscientists viewed astrocytes primarily as the “glue” of the nervous system. These glial cells were thought to provide structural support and nutrients to neurons. Over time, this perspective shifted as evidence emerged that astrocytes actively participate in brain signaling. They respond to chemical messengers released by neurons with their own internal calcium flares.</p>
<p>However, astrocytes also exhibit spontaneous activity that does not seem to be triggered by any specific neural input. These calcium fluctuations occur in tiny, localized regions of the cell called microdomains. Because these events appear random, or stochastic, their function has remained a mystery.</p>
<p>A team of researchers led by Gabriele Losi and Beatrice Vignoli, alongside senior authors Giorgio Carmignoto and Marco Canossa, sought to understand if this background noise serves a purpose. They focused on the perirhinal cortex. This region of the brain is responsible for recognition memory, such as identifying familiar objects.</p>
<p>The investigators hypothesized that these random signals might influence how the brain consolidates memories over time. Memory consolidation is the process by which a temporary memory trace is stabilized into a long-lasting one. This often depends on a phenomenon called long-term potentiation.</p>
<p>Long-term potentiation refers to the persistent strengthening of synapses, the connections between neurons. When neurons fire together repeatedly, their connection becomes stronger. This synaptic strengthening is the cellular foundation of learning.</p>
<p>To test their hypothesis, the team used advanced imaging techniques to observe astrocyte activity in mouse brain tissue. They utilized a calcium indicator that glows when calcium levels rise inside the cell. This allowed them to track the flickering activity of the microdomains in real time.</p>
<p>The researchers confirmed that these calcium flashes occurred spontaneously. They persisted even when the researchers used toxins to silence the electrical firing of nearby neurons. This proved that the astrocytes were generating these signals independently.</p>
<p>Next, the team investigated whether this spontaneous activity influenced synaptic strengthening. They stimulated the neurons to induce long-term potentiation. Under normal conditions, the synaptic connection remained strong for hours.</p>
<p>The researchers then introduced a genetic tool to dampen the calcium signaling within the astrocytes. When the spontaneous calcium flashes were suppressed, the synaptic strengthening collapsed. The connection initially grew stronger but faded back to baseline levels within roughly an hour.</p>
<p>This result implied that while neurons can initiate a memory trace, they cannot maintain it without the help of astrocytes. The researchers pinpointed the molecular mechanism behind this failure. They looked at a protein called brain-derived neurotrophic factor, or BDNF.</p>
<p>BDNF acts like a fertilizer for brain cells, promoting growth and survival. The study revealed that the spontaneous calcium flashes trigger the astrocytes to release BDNF. This protein then binds to specific receptors on the neurons called TrkB receptors.</p>
<p>Sustained activation of these receptors is required to lock in the changes at the synapse. The random, recurring nature of the astrocyte signals ensures that BDNF is released over a prolonged period. This extends the window of time for the neurons to solidify their connection.</p>
<p>To prove that BDNF was the missing link, the scientists applied the protein directly to the brain tissue where astrocyte activity was blocked. The external supply of BDNF rescued the synaptic strengthening. The memory trace persisted just as it would in a healthy brain.</p>
<p>The team then moved from tissue samples to live animal behavior. They used a standard memory assessment known as the object recognition test. In this task, mice spend time exploring two identical objects.</p>
<p>Later, one of the objects is replaced with a new one. Mice with normal memory will spend more time exploring the novel object. This indicates they remember the familiar one.</p>
<p>The researchers engineered the astrocytes in the mice to allow for temporal control. They could switch off the spontaneous calcium signals using a specific chemical drug. This allowed them to disrupt astrocyte activity at precise moments during the memory process.</p>
<p>When the researchers inhibited the astrocytes immediately after the mice learned the objects, the animals failed the test 24 hours later. They explored both objects equally, indicating they had forgotten which one was familiar. The initial learning had occurred, but the long-term memory had not formed.</p>
<p>However, if the researchers waited to inhibit the astrocytes until hours after the learning event, the memory remained intact. This demonstrated that the spontaneous activity is required only during a critical window following the experience. The astrocytes provide the necessary chemical support to stabilize the circuit while the memory is fresh.</p>
<p>The study highlights the stochastic nature of this process. The calcium events in the microdomains do not follow a set pattern. They are inherently unpredictable.</p>
<p>The authors propose that this randomness is not a flaw but a feature. It may introduce a probabilistic element to memory storage. By randomly engaging different parts of the astrocyte, the brain might select which synaptic connections are worth preserving.</p>
<p>This mechanism ensures that not every fleeting neural activation becomes a permanent memory. Only those connections that receive the sustained chemical support from astrocytes will endure. The random activity acts as a filter for information retention.</p>
<p>The findings also clarify the relationship between the evoked responses and spontaneous ones. When neurons fire rapidly, they can trigger a large calcium response in the astrocyte soma, or main body. But this main response is not enough for consolidation.</p>
<p>The localized, random microdomain flashes are distinct from the global cell response. They operate autonomously. This adds a layer of complexity to how non-neuronal cells process information.</p>
<p>There are caveats to consider in this research. The study was conducted in mice, and human brain physiology differs in complexity. Whether this specific mechanism operates identically in humans remains to be verified.</p>
<p>Additionally, the exact source of the randomness requires further exploration. While the signals appear stochastic, underlying intracellular processes likely govern their frequency and distribution. Understanding these drivers is a necessary next step.</p>
<p>Future research will likely focus on how this mechanism applies to other types of memory. The perirhinal cortex handles object recognition, but other areas like the hippocampus manage spatial and episodic memory. Astrocytes in those regions may behave differently.</p>
<p>The researchers also aim to investigate the implications for brain disorders. Issues with memory consolidation are hallmarks of conditions such as Alzheimer’s disease. Dysfunctional astrocyte signaling could be a contributing factor.</p>
<p>If the spontaneous activity of astrocytes is dampened in neurodegenerative diseases, it could explain why new memories fail to stick. Restoring this signaling could theoretically offer a therapeutic pathway. This is a speculative but promising avenue for future medical research.</p>
<p>Ultimately, this work elevates the status of the astrocyte. It suggests that our ability to remember the past depends on the random flickering of cells once thought to be passive bystanders. The brain’s stability appears to rely on a fundamental element of chaos.</p>
<p>The study, “<a href="https://doi.org/10.1073/pnas.2500511122" target="_blank">Spontaneous activity of astrocytes is a stochastic functional signal for memory consolidation</a>,” was authored by Gabriele Losi, Beatrice Vignoli, Rocco Granata, Annamaria Lia, Micaela Zonta, Gabriele Sansevero, Francesca Pischedda, Angela Chiavegato, Spartaco Santi, Lorena Zentilin, Nicoletta Berardi, Gian Michele Ratto, Giorgio Carmignoto, and Marco Canossa.</p></p>
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<td><a href="https://www.psypost.org/sex-differences-in-alzheimers-linked-to-protein-that-blocks-brain-cell-growth/" 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;">Sex differences in Alzheimer’s linked to protein that blocks brain cell growth</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Jan 10th 2026, 10:00</div>
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<p><p>Recent research has identified a specific biological mechanism that may explain why females experience more severe impairments in brain cell regeneration associated with Alzheimer’s disease. The findings, published in the journal <em><a href="https://link.springer.com/article/10.1186/s13293-025-00799-0" target="_blank">Biology of Sex Differences</a></em>, suggest that a family of signaling proteins becomes overactive in the female brain and suppresses the growth of new neurons. This study indicates that blocking these proteins could offer a potential strategy for restoring brain function in patients.</p>
<p>Alzheimer’s disease affects a substantial portion of the aging population. In the United States alone, the prevalence of the condition has exceeded 7 million individuals. A distinct disparity exists within these numbers. Women account for nearly two-thirds of the affected population. This difference persists even when accounting for the fact that women generally live longer than men. </p>
<p>The biological drivers behind this susceptibility have remained largely elusive. Researchers are working to understand how sex-specific biological processes interact with the pathology of the disease.</p>
<p>A primary area of interest is the hippocampus. This region of the brain is essential for learning and memory. It is also one of the few areas where the adult brain can generate new neurons. This process is known as neurogenesis. In patients with Alzheimer’s disease, this regenerative ability is severely compromised. The failure to replace or repair neural connections contributes to cognitive decline.</p>
<p>Previous investigations have pointed to a group of signaling molecules called bone morphogenetic proteins, or BMPs. These proteins are vital during early development for establishing the body’s architecture. </p>
<p>However, in the aging brain or in diseased states, their presence can be detrimental. Elevated levels of certain BMPs have been observed in the brains of patients with Alzheimer’s disease. These elevated levels appear to correlate with a halt in the production of new brain cells.</p>
<p>A research team from Waseda University and the RIKEN Center for Brain Science in Japan sought to determine if these proteins play a role in the sex differences observed in the disease. The study was led by Xingyu Su, a doctoral student at Waseda University, under the supervision of Dr. Toshio Ohshima. </p>
<p>The team hypothesized that BMP signaling might function differently in males and females. They also sought to determine if these differences directly impacted the brain’s ability to regenerate.</p>
<p>To investigate this, the researchers utilized a specific mouse model of Alzheimer’s disease known as APPNL-G-F. Many traditional mouse models rely on the artificial overexpression of amyloid precursor protein. This can sometimes lead to physiological artifacts that act as confounding variables. </p>
<p>The APPNL-G-F model is a “knock-in” model. This means the mice express humanized amyloid-beta sequences at physiological levels. This approach provides a more accurate reflection of how the pathology develops in a natural biological context.</p>
<p>The researchers analyzed the hippocampi of these mice at six months of age. They measured the levels of various BMP molecules. They compared these levels against those found in healthy, wild-type mice of the same age. The analysis focused on gene expression to see which BMPs were being produced more aggressively.</p>
<p>The results showed a clear distinction between the sexes. The female Alzheimer’s model mice exhibited higher expression levels of BMP family members, specifically BMP4, BMP6, and BMP7. While the male mice also showed some elevation compared to healthy controls, the increase was much more pronounced in the females.</p>
<p>Simultaneously, the team examined the rate of neurogenesis. They looked for specific markers that indicate cells are dividing and growing. One such marker is a protein called PCNA, which appears in cell nuclei during replication. </p>
<p>Another is doublecortin, or DCX, which helps identify immature neurons. The female mice showed a marked reduction in these markers compared to the males. This indicated that the process of generating new neurons was more severely inhibited in the female brain.</p>
<p>The correlation was strong. The mice with the highest levels of BMPs had the lowest levels of new neuron growth. This suggested a direct link between the two phenomena. The researchers posited that the overactive BMP signaling was acting as a brake on the neural stem cells. This prevented them from proliferating and differentiating into functioning neurons.</p>
<p>To confirm this causal relationship, the team performed a rescue experiment. They treated the female Alzheimer’s model mice with a drug named LDN193189. This compound is known to inhibit the signaling pathway used by BMPs. The mice received daily injections of the inhibitor for three weeks. Following the treatment, the researchers examined the brain tissue again.</p>
<p>The inhibition of BMP signaling produced a positive outcome. The number of dividing stem cells in the hippocampus increased. The levels of neurogenesis in the treated female mice were restored to levels comparable to those seen in healthy, wild-type mice. This demonstrated that the suppression of neurogenesis was reversible. It also confirmed that BMP signaling was the primary driver of this impairment in the female mice.</p>
<p>The researchers also explored why these differences might exist. They turned their attention to estrogen. Estrogen is the primary female sex hormone. To study its effects, they utilized a mouse nerve cell line called Neuro2a. These cells are useful for laboratory experiments because they possess estrogen receptors.</p>
<p>The team exposed these cells to estradiol. This is a potent form of estrogen. They then measured the resulting changes in gene expression. The stimulation caused a distinct rise in the levels of BMP6. It also increased the levels of a transcription factor called TFAP2B, which regulates BMP expression.</p>
<p>This finding presents a complex biological picture. Estrogen is typically considered neuroprotective. In many contexts, it supports the health and survival of neurons. However, this study indicates that in the specific context of Alzheimer’s pathology, estrogen signaling might drive the upregulation of BMPs. This upregulation subsequently inhibits the generation of new neurons.</p>
<p>The team also conducted a separate experiment to see if acute injury caused the same sex-dependent results. They injected amyloid-beta peptides directly into the brains of normal mice. This caused immediate damage and increased BMP levels. </p>
<p>However, in this acute model, there was no difference between males and females. Both sexes suffered equal impairment. This suggests that the sex differences observed in the genetic model are likely due to long-term, chronic physiological processes involving hormones.</p>
<p>There are caveats to these findings. The study was conducted in mice. While the genetic model is advanced, it does not perfectly replicate human biology. The interaction between estrogen and BMPs is likely nuanced. In humans, Alzheimer’s disease is most common in post-menopausal women who have lower estrogen levels. The researchers suggest that dysregulation of estrogen signaling pathways, rather than simple levels of the hormone, may be at play.</p>
<p>Additionally, the researchers measured cell proliferation using specific markers. While this indicates that cells are dividing, it does not fully track the long-term survival of these new neurons. </p>
<p>Future research will need to determine if these new cells mature and integrate into the brain’s circuitry to improve memory function. The team also noted that while neurogenesis improved, they did not measure the effect on amyloid plaques or other disease markers in this specific study.</p>
<p>The study opens new avenues for therapeutic development. Current treatments for Alzheimer’s disease often focus on removing amyloid plaques. This research highlights the potential of targeting the brain’s regenerative capacity. </p>
<p>Drugs that modulate BMP signaling could potentially serve as a complementary therapy. Such an approach would aim to maintain the brain’s ability to repair itself even as the disease progresses.</p>
<p>This work underscores the importance of considering sex as a biological variable in medical research. Mechanisms of disease can differ fundamentally between males and females. Understanding these differences is essential for developing effective treatments for all patients.</p>
<p>“Our study provides new insights into the role of BMP signaling activation in impaired neurogenesis in AD, which will guide future translational research,” says Su. “Ultimately, this knowledge can lead to the development of novel intervention strategies, reducing the clinical and caregiving burdens associated with AD.”</p>
<p>The study, “<a href="https://link.springer.com/article/10.1186/s13293-025-00799-0" target="_blank">Sex-related upregulation of bone morphogenetic protein signaling inhibits adult neurogenesis in APPNL−G−F alzheimer’s disease model mice</a>,” was authored by Xingyu Su, Rina Takayanagi, Hiroki Maeda, Takaomi C. Saido, and Toshio Ohshima.</p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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