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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/stanford-study-shows-autism-like-behaviors-can-be-switched-off-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;">Stanford study shows autism-like behaviors can be switched off in mice</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 10th 2025, 10:00</div>
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<p><p>New research from Stanford University suggests that an overactive brain circuit deep in the thalamus may contribute to behaviors linked to autism. In a mouse model of the condition, suppressing activity in this region reduced symptoms such as social withdrawal, repetitive behavior, and heightened sensitivity to sensory input. The findings, published in <em><a href="https://doi.org/10.1126/sciadv.adw4682" target="_blank">Science Advances</a></em>, point to the thalamus as a potential target for future therapies.</p>
<p>Autism spectrum disorder, or ASD, is a developmental condition marked by challenges in social interaction, communication differences, and restricted or repetitive behaviors. Many individuals also experience co-occurring conditions such as epilepsy, anxiety, or hyperactivity. While most research into autism has focused on areas of the cerebral cortex involved in language and social cognition, less attention has been paid to the deeper structures that relay sensory signals to the brain’s outer layers.</p>
<p>The thalamus is one such structure. Often described as the brain’s relay center, it sits deep in the brain and transmits sensory and motor signals to the cortex. </p>
<p>“We are very interested in the function of a part of the brain that is important for sensing the environment (sights, sounds, touch, etc) but also engaged in producing sleep. The thalamus is located at the center of the brain, above the spinal cord, but below the cerebral cortex. It is a place that relays (sends along) signals from the outside world where it can be processed and understood in the cortex,” said study author John Huguenard, a professor of neurology at Stanford University School of Medicine.</p>
<p>“The thalamus is capable of behaving erratically, and does so in some forms of epilepsy, which we have studied extensively. Some of the treatments for this type of epilepsy work by turning down activity of the thalamus. Given that many autism patients experience epilepsy, we wondered whether the thalamus may play a role.”</p>
<p>Surrounding part of the thalamus is the reticular thalamic nucleus, or RT, a shell-like structure made up of inhibitory neurons. It acts as a filter, regulating what sensory information is passed on to the cortex. The RT also helps orchestrate brain rhythms that regulate sleep, attention, and arousal. Disruption in this region has been associated with several psychiatric and neurological disorders, including schizophrenia, depression, and epilepsy.</p>
<p>The researchers were drawn to the RT partly because of its role in epilepsy. Individuals with autism are significantly more likely to have seizures than the general population, and the RT has long been known to generate seizure-like brain activity when overactive. This connection led the researchers to ask whether the same kind of hyperactivity in the RT might also contribute to the broader set of behaviors observed in autism.</p>
<p>To explore this idea, the researchers used mice lacking the gene Cntnap2, which is strongly linked to autism in humans. These Cntnap2 knockout mice display a range of autism-relevant features, such as social avoidance, repetitive grooming, heightened responses to sensory stimuli, and a tendency toward seizures. Using a variety of experimental techniques, the scientists recorded the activity of RT neurons in these animals and compared it to normal mice.</p>
<p>They found that RT neurons in the autism-model mice were hyperactive. These cells showed increased burst firing, a pattern of rapid activity known to amplify inhibitory signals in the brain. This heightened activity was linked to elevated oscillations in thalamocortical circuits, the loops that connect the thalamus and cortex. These rhythmic bursts have been associated with both seizures and abnormal sensory processing.</p>
<p>Fiber photometry, a technique for tracking real-time activity in live animals, showed that RT neurons in the Cntnap2 knockout mice fired more often in response to light, sound, and social interaction. Even when no stimulus was present, RT neurons in the autism-model mice were more active than those in control animals. This pattern suggested that the RT was not only more sensitive to input, but also more likely to produce spontaneous activity that could disrupt brain function.</p>
<p>“Most previous studies have focused on circuits within the the cerebral cortex, where higher order functions are carried out,” Huguenard told PsyPost. “These results suggest that the brain circuitry that is affected in autism might be a larger network involving both cortex and thalamus.”</p>
<p>Having identified this hyperactivity, the researchers next asked whether reducing RT activity could improve the animals’ behavior. They tested two approaches.</p>
<p>In the first, they used a drug called Z944, originally developed to treat seizures. This drug blocks T-type calcium channels, which are responsible for the burst firing of RT neurons. When the researchers gave the drug to the Cntnap2 knockout mice, it significantly reduced RT activity. The treated mice showed fewer repetitive behaviors, moved around less excessively, and spent more time engaging with other mice — behaviors more similar to typical mice.</p>
<p>In the second approach, the researchers used chemogenetics, a method that allows scientists to switch specific neurons on or off using designer drugs. By targeting RT neurons for inhibition, they were able to quiet the overactive circuit and again observed improvements in social behavior and reductions in hyperactivity and repetitive grooming. In contrast, when they artificially increased RT activity in typical mice, those animals began to display behaviors similar to the autism model mice, including social withdrawal and increased repetitive actions.</p>
<p>“We were surprised with degree to which the animals improved with treatment,” Huguenard said. “This suggests that key aspects of autism-related behavior may depend strongly on the thalamus.”</p>
<p>These results indicate that the RT is not just associated with autism-related behaviors but may actively drive them. Suppressing its activity reversed core features of the condition in mice, while increasing its activity was enough to induce them.</p>
<p>“The thalamus is an important part of the brain circuitry that can contribute to autism related behaviors, demonstrated so far in mice,” Huguenard explained. “Secondly, because some antiepileptic drugs target the thalamus, for example some calcium channel blockers, these provide a way to test the proposed role of the thalamus in autism behaviors. Our results suggest that this targeted approach can improve in animals autism-related behaviors.”</p>
<p>While the findings are promising, the researchers note several limitations. Most importantly, this study was conducted in mice, and it remains to be seen whether the same mechanisms apply in humans. The Cntnap2 gene represents just one of many genetic pathways involved in autism, and the findings may not generalize to all forms of the condition. The RT is also a small but complex structure, and the study did not examine whether subgroups of RT neurons play distinct roles in different behaviors.</p>
<p>In addition, while the seizure medication Z944 showed positive effects in this mouse model, it has not been approved for use in people with autism. Whether it could be safe and effective in humans, or whether more targeted versions of it could be developed, is a question for future studies.</p>
<p>“Before we get too much farther towards treatments, there are a few central questions we want to address,” Huguenard noted. “The main one is whether our findings apply more broadly to a range of ailments in ASD, or might they be specific to what we found in one genetic form of ASD, that of loss of function of Cntnap2 gene/protein. If the therapeutic effects of targeting the thalamus (with Z944 or other compounds) show improvements in a variety of forms/models of mouse ASD, then that would begin to support the idea of preclinical trials.”</p>
<p>The study, “<a href="https://doi.org/10.1126/sciadv.adw4682" target="_blank">Reticular thalamic hyperexcitability drives autism spectrum disorder behaviors in the Cntnap2 model of autism</a>,” was authored by Sung-soo Jang, Fuga Takahashi, and John R. Huguenard.</p></p>
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<td><a href="https://www.psypost.org/three-minute-brainwave-test-shows-promise-for-early-alzheimers-detection/" 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;">Three-minute brainwave test shows promise for early Alzheimer’s detection</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 10th 2025, 08:00</div>
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<p><p>A new test could help to diagnose memory issues associated with Alzheimer’s disease in as little as three minutes. According to <a href="https://doi.org/10.1093/braincomms/fcaf279">recently published findings</a> the test, called the Fastball EEG test, may one day help doctors flag people who need further checks for Alzheimer’s disease without the need for unnecessary waits or time-consuming procedures.</p>
<p><a href="https://www.alz.org/alzheimers-dementia/what-is-alzheimers">Alzheimer’s disease</a> affects millions of people worldwide. It’s a progressive condition, in which brain cells are slowly damaged and die – leading to memory loss, confusion and difficulties with thinking and daily tasks.</p>
<p>The disease process begins long before symptoms manifest. Proteins called amyloid and tau gradually build up in the brain, forming plaques and tangles that interfere with communication between nerve cells. By the time memory problems are significant enough for diagnosis, much of the damage has already been done.</p>
<p>It’s important to note that the signs of Alzheimer’s disease and symptoms <a href="https://doi.org/10.1038/s41582-022-00642-9">don’t develop similarly</a> in all patients. This means the amount of amyloid plaques and tau tangles a person has in their brain <a href="https://doi.org/10.1038/s41582-022-00642-9">doesn’t always match</a> the severity of the disease.</p>
<p>In addition, the amount of plaques and tangles can only be estimated via imaging or blood tests. These factors make Alzheimer’s disease difficult to diagnose and predict how it will progress. This is why researchers are keen to develop tests that can spot signs of the disease earlier.</p>
<p>Traditionally, diagnosis has relied on <a href="https://doi.org/10.2147/NDT.S212328">cognitive screening tests</a>, where a doctor asks a patient to remember words, copy drawings or complete problem-solving tasks. These tools are effective, but take time and require trained staff. They may also be stressful for the patients and can be influenced by factors such as a person’s education level, their <a href="https://doi.org/10.1177/15333175221117006">language skills</a> or <a href="https://doi.org/10.3390/jintelligence7040022">test-related performance anxiety</a>.</p>
<p>More advanced diagnostic options, including brain scans and laboratory analysis of cerebrospinal fluid (a fluid which protects the brain and spinal cord), can indicate the presence of Alzheimer’s disease in the brain. But these tests are <a href="https://doi.org/10.1016/j.drudis.2024.103911">expensive and invasive</a>.</p>
<p>But the <a href="https://www.bath.ac.uk/projects/diagnosing-dementia-using-fastball-neurocognitive-assessment/">Fastball EEG test</a> uses a different approach.</p>
<p>Instead of asking patients to actively recall or solve problems, it measures how the brain responds to images flashed on a screen. Participants first see a set of eight pictures, which they’re asked to name but not memorise.</p>
<p>Then, during the test, hundreds of images are shown in quick succession – around three per second. Every fifth image is one of the eight previously shown. The EEG headset records the brain’s electrical activity, picking up tiny signals that reveal whether the brain recognises these familiar images.</p>
<p>In healthy people, the recognition response is clear. But in people with <a href="https://www.alzheimers.org.uk/about-dementia/types-dementia/mild-cognitive-impairment-mci">mild cognitive impairment</a> (problems with thinking, memory or problem-solving which often precedes Alzheimer’s disease) and especially those with memory issues, the response is weaker.</p>
<p>To understand the test’s suitability, researchers recruited 106 participants to their study. This included 54 healthy adults and 52 people with mild cognitive impairment (MCI). Among the latter group, some had memory-specific problems (amnestic MCI), while others had difficulties unrelated to memory – such as problems with attention (non-amnestic MCI).</p>
<p>The researchers found that the Fastball test was sensitive enough to distinguish between these groups. Those with amnestic MCI showed significantly reduced brain responses to the familiar images compared to healthy adults and those with non-amnestic MCI. In other words, the test quickly identified the kind of memory impairment most closely linked to early Alzheimer’s.</p>
<p>They then repeated the test a year later. Some of the participants who’d only had mild cognitive impairment in the first test had progressed to either Alzheimer’s disease dementia or another type of dementia, called <a href="https://www.alzheimers.org.uk/about-dementia/types-dementia/vascular-dementia">vascular dementia</a>, which manifests in symptoms similar to Alzheimer’s.</p>
<p>The researchers also asked the participants who developed dementia to perform the standard cognitive tests currently used to diagnose Alzheimer’s. These participants showed no or little difference in this test, which means the test wasn’t sensitive enough to detect the transition from mild cognitive impairment to dementia. But with the Fastball test, the participants performed marginally worse than they had previously.</p>
<p>However, of the 42 participants with mild cognitive impairment who repeated the Fastball test a year later, only eight had transitioned to dementia. So, although the results are very promising in illustrating the test’s accuracy, they should be interpreted with caution as they’re based on a small number of people.</p>
<h2>The future of diagnosis</h2>
<p>Crucially, the test is fast – lasting only three minutes. It also doesn’t rely on the participant’s effort, mood or test-taking ability, which can influence cognitive test results. It can also be done at home or in a GP’s office, which might reduce anxiety for patients and make it easier to reach a larger group of people.</p>
<p>However, the study did not include other conditions where <a href="https://www.alzheimers.org.uk/about-dementia/worried-about-memory-problems/causes-of-memory-problems">memory impairment is also present</a> – such as depression or thyroid problems – so it cannot be used as a standalone diagnostic tool for Alzheimer’s disease. Future studies in more diverse populations which take these other conditions into account will be needed to better understand the test’s strengths, limitations and potential.</p>
<p>Other tests, which are currently in development, may be better for diagnosing Alzheimer’s disease specifically. For example, <a href="https://www.alz.org/alzheimers-dementia/diagnosis/medical_tests#:~:text=Blood%20tests,-Researchers%20are%20investigating&text=These%20markers%20may%20include%20tau,tests%20to%20diagnose%20the%20disease.">blood tests</a> could transform Alzheimer’s diagnosis once they’re more widely rolled out.</p>
<p>These measure proteins linked to Alzheimer’s and can give a snapshot of disease processes happening in the brain. Some tests currently being studied would only require a <a href="https://aaic.alz.org/releases_2023/finger-prick-blood-test-alzheimers-disease.asp">finger-prick of blood</a>. If they prove to be accurate, this could mean patients could do these tests at home and mail them in for analysis.</p>
<p>Tools such as the Fastball test and blood tests could help shift the focus of Alzheimer’s care from late diagnosis to early intervention. By identifying people at risk of the disease years earlier, doctors could recommend lifestyle changes, monitor patients more closely or provide them with appropriate therapies earlier, while they can still make the most difference.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/264519/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/alzheimers-disease-new-three-minute-test-can-spot-memory-issues-heres-how-it-works-and-what-it-can-tell-you-264519">original article</a>.</em></p></p>
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<td><a href="https://www.psypost.org/scientists-identify-a-mysterious-brain-signal-tied-to-stress-and-hormone-pulses/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Scientists identify a mysterious brain signal tied to stress and hormone pulses</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 10th 2025, 06:00</div>
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<p><p>A new study published in <a href="https://doi.org/10.1073/pnas.2510083122"><em>PNAS</em></a> offers evidence that certain brain cells involved in regulating stress do not simply respond to threats, but operate on a repeating internal rhythm—roughly once every hour—even in calm conditions. Researchers at the University of Otago found that these neurons, located in the hypothalamus, exhibit spontaneous cycles of activity that align with patterns of alertness and behavior. The study suggests these patterns may play a broader role in shaping sleep, arousal, and possibly mood.</p>
<p>Scientists have long known about the body’s circadian rhythm, the roughly 24-hour cycle that governs sleep and wakefulness. But there are other biological cycles that occur over shorter periods. These so-called ultradian rhythms regulate many aspects of physiology, including hormone levels and fluctuations in behavior.</p>
<p>One particularly important example is the stress hormone cortisol, which pulses throughout the day every 60 to 90 minutes. While the medical importance of these pulses is well recognized—they influence energy levels, metabolism, and immune responses—the mechanisms that generate them have remained uncertain.</p>
<p>The Otago researchers were especially interested in understanding whether the brain’s stress-control system might contain its own internal rhythm generator. A specific set of neurons known as corticotropin-releasing hormone (CRH) neurons, located in the paraventricular nucleus (PVN) of the hypothalamus, plays a central role in triggering the hormonal stress response.</p>
<p>These neurons activate the hypothalamic-pituitary-adrenal (HPA) axis, leading to the release of cortisol and other hormones. Previous studies had focused mostly on how these neurons respond to external stressors, but the new research aimed to find out what they were doing in the absence of any obvious stress.</p>
<p>“While most people appreciate that our stress response system turns on when we encounter danger, not many people realize that this system is also active over the normal day night cycle. For this reason, I became interested in understanding more about the normal daily rhythms in the stress axis and how they are controlled,” said study author <a href="https://www.otago.ac.nz/neuroendocrinology/research/karl-iremonger" target="_blank" rel="noopener">Karl Iremonger</a>, an associate professor and director of the Centre for Neuroendocrinology at the University of Otago.</p>
<p>The researchers used a technique called fiber photometry, which allows them to monitor the real-time activity of specific neurons deep within the brain of living, freely moving animals. By genetically modifying mice and rats to express a fluorescent protein that lights up when neurons are active, the team could measure changes in neural signals with a high degree of precision. They also used an advanced video-tracking system, powered by deep learning software, to monitor subtle changes in the animals’ movement patterns.</p>
<p>The researchers connected the animals to the photometry recording system and let them move freely in their home cages for over 24 hours. To reduce stress effects related to handling, the first four hours of recordings were excluded from analysis. Across the day and night, CRH neurons displayed repeated bursts of activity that lasted around 15 minutes and occurred roughly every hour. These events were dubbed “upstates.” Notably, the frequency of these upstates was higher during the animals’ active (dark) phase compared to their resting (light) phase.</p>
<p>These brain rhythms were closely tied to changes in the animals’ behavior. Every time a mouse initiated movement—such as waking up and beginning to explore its cage—there was a corresponding rise in CRH neuron activity. The researchers ran statistical tests to determine the direction of this relationship and found that changes in brain activity typically preceded movement. In other words, the neurons seemed to be setting the stage for behavioral arousal, rather than simply reacting to it.</p>
<p>“We were surprised at how closely associated the rhythms in stress brain circuit activity were with physical activity (arousal) rhythms,” Iremonger told PsyPost. “This had not been previously shown before.”</p>
<p>To test whether CRH neurons could actively drive behavioral arousal, the team used a technique known as chemogenetics. This approach allowed them to artificially stimulate these neurons using a designer drug, which activated genetically modified receptors only present in the CRH neurons. When these neurons were activated in mice that were otherwise at rest, the animals showed a significant and prolonged increase in movement. This provided direct evidence that CRH neuron activity can prompt behavioral changes even in the absence of external threats.</p>
<p>The researchers then turned to rats, which are often used in studies of hormonal rhythms because they allow for easier blood sampling. Using CRISPR gene-editing technology, the team developed a rat line that enabled them to record CRH neuron activity and measure hormone levels in tandem. Similar to the mice, the rats exhibited hourly bursts of CRH activity, and these were again correlated with movement patterns. They also took blood samples every few minutes from the rats to measure corticosterone, the rodent equivalent of cortisol.</p>
<p>The findings indicated that in many cases, CRH activity preceded a pulse of corticosterone by about 15 minutes. But the relationship was not perfectly synchronized. Sometimes a burst of CRH activity did not lead to a hormone pulse, and sometimes hormone pulses occurred without a clear spike in CRH activity. On average, however, the data showed a consistent pattern: the neural bursts tended to come first.</p>
<p>The results support the idea that CRH neurons operate on an internal rhythm that influences behavior and hormone secretion. These patterns seem to act like a built-in “wake-up” signal, preparing the body for increased alertness. The research provides evidence that ultradian rhythms in behavior and stress hormones are, at least in part, generated by predictable fluctuations in brain activity.</p>
<p>It also suggests that these rhythms are not random. They are shaped by time of day and appear to be tied to the animal’s natural sleep-wake cycle. This has potential implications for understanding how stress affects health. Disruptions in the normal rhythmic activity of these neurons could interfere with sleep and potentially contribute to mood disorders.</p>
<p>“This study shows that there are a population of brain cells that turn on and off with an hourly rhythm,” Iremonger explained. “This rhythm not only drives a rhythm in stress hormone release, but also mediates a rhythm in arousal.”</p>
<p>But the study, like all research, has some limitations. “It is currently impossible to study brain stress circuits in humans as this level of detail,” Iremonger noted. “For this reason, we study them in rats and mice. While stress circuits in the brain are conserved between rodents and humans, there is always a chance there are slight differences in how the function.”</p>
<p>Another open question is how these rhythms are generated in the first place. Unlike circadian rhythms, which are governed by a central master clock in the brain, ultradian rhythms appear to arise from local circuits. The study hints at the possibility that neighboring regions, such as the subparaventricular zone, could be involved. More research will be needed to explore how these circuits interact.</p>
<p>“The next step in our research is to understand the other parts of the brain that send signals to the stress brain cells to control their excitability patterns over the day night cycle,” Iremonger said.</p>
<p>The study, “<a href="https://doi.org/10.1073/pnas.2510083122">Ultradian rhythms of CRHPVN neuron activity, behaviour and stress hormone secretion</a>,” was authored by Shaojie Zheng, Caroline M. B. Focke, Calvin K. Young, Isaac Tripp, Dharshini Ganeshan, Emmet M. Power, Daryl O. Schwenke, Allan E. Herbison, Joon S. Kim, and Karl J. Iremonger.</p></p>
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<td><a href="https://www.psypost.org/many-autistic-adults-feel-torn-about-revealing-their-diagnosis-a-new-study-explores-why/" 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;">Many autistic adults feel torn about revealing their diagnosis — a new study explores why</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 9th 2025, 16:00</div>
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<p><p>A new study published in the journal <em><a href="https://doi.org/10.1177/13623613251337504" target="_blank">Autism</a></em> sheds light on how autistic adults navigate the complex and deeply personal decision to share their autism diagnosis with others. Researchers found that disclosure can serve meaningful purposes, such as accessing support, fostering self-acceptance, and engaging in activism, but also exposes people to disbelief, stereotyping, and emotional vulnerability. The findings suggest that many newly diagnosed adults in the United Kingdom lack adequate guidance on how to manage disclosure and would benefit from more structured post-diagnostic support.</p>
<p>Autism spectrum conditions affect how people experience the world, often influencing communication, social interaction, and behavior. While autism is frequently diagnosed in childhood, a growing number of people—especially women and those with less apparent support needs—are receiving diagnoses in adulthood. This shift reflects increasing awareness and improved diagnostic practices, but it also leaves many adults to navigate their diagnosis without the kind of developmental support available to younger individuals.</p>
<p>Receiving an autism diagnosis later in life can prompt a major re-evaluation of one’s identity and past experiences. But it also raises an important practical and emotional question: should one share this diagnosis with others, and if so, how? Disclosure can be necessary to access workplace accommodations, social services, or healthcare support. Yet many people fear being misunderstood or judged.</p>
<p>While previous studies have examined autism disclosure in specific contexts like employment, few have explored the broader, everyday experiences of adults who receive a diagnosis later in life. This study sought to fill that gap, focusing on adults in the United Kingdom who were diagnosed within the past ten years.</p>
<p>To investigate these questions, researchers from the University of Sheffield and Cardiff University used a qualitative method known as interpretative phenomenological analysis. This approach emphasizes understanding how individuals make sense of significant life events—in this case, the experience of disclosing an autism diagnosis.</p>
<p>The researchers conducted in-depth interviews with twelve autistic adults who had received their diagnosis in adulthood. Participants ranged in age, gender identity, and life experience. The team analyzed the interview transcripts to identify recurring themes and patterns in how participants thought about and approached diagnostic disclosure.</p>
<p>The study found that disclosure is rarely a simple or one-time decision. Rather, it is an ongoing process shaped by a person’s environment, relationships, and emotional readiness. From the interviews, the researchers identified four major themes: the functions of disclosure, how individuals approached the conversation, the effects of negative preconceptions, and the role of acceptance and community.</p>
<p>One key theme to emerge was that disclosure often served multiple functions. For some participants, sharing their diagnosis was a practical decision—it was the only way to access support at work, in healthcare, or in social services. Others saw disclosure as a step toward being more authentic in their relationships or workplace, allowing them to “be themselves” without masking their traits. For a few, disclosure also became a form of advocacy, as they sought to raise awareness or improve conditions for other autistic people.</p>
<p>At the same time, disclosing a diagnosis often felt fraught. Some participants described carefully managing who they told, how they explained it, and how they responded to other people’s reactions. Others said they began disclosing even before receiving a formal diagnosis, often discussing the possibility with close friends or family. In some cases, this made the eventual diagnosis easier to accept—for both the person diagnosed and those around them.</p>
<p>However, many also reported negative responses. Several participants described encountering disbelief, especially when they did not match other people’s stereotyped views of autism. Comments like “you don’t seem autistic” were common, leaving participants feeling invalidated or doubting themselves. This led some to experience what they described as “imposter syndrome,” questioning whether they really “deserved” the diagnosis.</p>
<p>These reactions were often shaped by widespread misconceptions about autism—such as the idea that autistic people must be male, socially isolated, or visibly struggling. Participants said these assumptions made it harder for them to be understood, even when they were seeking support.</p>
<p>The study found that people’s decisions to disclose—or not to—were often based on weighing potential risks and benefits. If participants believed disclosure would lead to meaningful support or understanding, they were more likely to share. If they anticipated judgment, discrimination, or indifference, they often withheld the information or disclosed only partially.</p>
<p>Many adopted what the researchers called “partial disclosure” strategies. For example, someone might tell an employer that they had specific sensory sensitivities or social challenges without naming autism directly. This allowed them to seek accommodations without risking stigma.</p>
<p>Others described limiting their disclosures to people they trusted or to environments where neurodiversity was understood and respected. Workplaces or communities that emphasized inclusivity were often seen as safer spaces for disclosure. On the other hand, experiences of dismissal or discrimination in education, healthcare, or employment led some participants to withdraw or avoid further interactions.</p>
<p>The emotional toll of disclosure was another recurring theme. Some participants spoke of feeling exhausted by having to educate others repeatedly. Others described the tension between wanting to be honest and not wanting to disrupt relationships or be perceived differently. In some cases, loved ones reacted with guilt or denial, especially if the diagnosis prompted them to reflect on their own traits or parenting.</p>
<p>Despite these challenges, many participants also described disclosure as a source of connection and support. When others responded with openness, curiosity, or a willingness to learn, it often led to stronger relationships. Some participants said that sharing their diagnosis had helped them find supportive communities, both online and in-person, where they felt seen and accepted.</p>
<p>Disclosure could also spark broader conversations about neurodiversity, both in families and workplaces. Several participants described how their openness had encouraged others to seek their own diagnoses or rethink assumptions about autism. For some, this brought a sense of purpose and belonging.</p>
<p>These positive experiences were most likely when others were already familiar with autism, had lived experience themselves, or were part of communities that valued inclusion. Participants emphasized that these interactions helped counteract feelings of isolation and reinforced a sense of identity.</p>
<p>The study’s authors argue that there is a significant need for structured post-diagnostic support for adults. At present, many people are left to navigate disclosure alone, without guidance on how to communicate their diagnosis or respond to others’ reactions.</p>
<p>The findings suggest that clinicians should incorporate conversations about disclosure into routine post-diagnostic care. This could include discussing who to tell, how to disclose, and how to handle potential challenges. Peer support groups, one-on-one counseling, and access to community resources were all highlighted as helpful by participants.</p>
<p>But the researchers caution against placing the burden of education solely on autistic individuals. While some participants found activism empowering, others felt overwhelmed by the expectation that they must constantly explain themselves. Services and employers need to improve their own understanding of autism rather than relying on individuals to do that work for them.</p>
<p>The study’s limitations include several factors related both to its design and to the inherent constraints of qualitative research. With a small sample of twelve participants, the findings may not be generalizable to the broader population of autistic adults. Additionally, while interpretative phenomenological analysis allows for deep exploration of lived experiences, it is shaped by the researcher’s interpretations and cannot provide objective or quantifiable conclusions. </p>
<p>The study, “<a href="https://doi.org/10.1177/13623613251337504" target="_blank">‘Am I gonna regret this?’: The experiences of diagnostic disclosure in autistic adults</a>,” was authored by Sheena K Au-Yeung, Megan Freeth, and Andrew R Thompson.</p></p>
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<td><a href="https://www.psypost.org/common-adhd-medication-linked-to-increased-frontal-brain-volume-in-children/" style="font-family:Helvetica, sans-serif; letter-spacing:-1px;margin:0;padding:0 0 2px;font-weight: bold;font-size: 19px;line-height: 20px;color:#222;">Common ADHD medication linked to increased frontal brain volume in children</a>
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<p><p>A longitudinal neuroimaging study of youth with attention-deficit/hyperactivity disorder (ADHD) in Taiwan found that higher cumulative doses of methylphenidate were associated with increased gray matter volume in several frontal regions of the brain. However, this association was observed only in participants who began treatment before the age of 12 and was absent in those who started later. The findings were published in <a href="https://doi.org/10.1016/j.pnpbp.2025.111429"><em>Progress in Neuropsychopharmacology & Biological Psychiatry</em></a>.</p>
<p>Methylphenidate is a stimulant medication commonly prescribed for ADHD. It works primarily by increasing dopamine and norepinephrine activity in the brain, which can enhance attention, concentration, and impulse control. The drug is also used to treat narcolepsy, a sleep disorder characterized by excessive daytime sleepiness.</p>
<p>Typically taken orally—via tablets, capsules, or liquid solution—methylphenidate is classified as a controlled substance in many countries due to its potential for misuse. It is sometimes misused by individuals without prescriptions in an attempt to boost academic or cognitive performance, a practice that carries health risks and ethical concerns.</p>
<p>Study author Jung-Chi Chang and colleagues sought to investigate whether cumulative exposure to methylphenidate was associated with structural changes in the brain’s frontal lobes, and whether these changes were related to ADHD symptom improvement—especially in relation to the age at which treatment began. The researchers hypothesized that starting methylphenidate treatment during childhood (before age 12) would be more likely to affect brain development than starting during adolescence or adulthood.</p>
<p>The study included 89 individuals diagnosed with ADHD and 91 typically developing controls, matched on age, sex, and intelligence quotient. ADHD is a neurodevelopmental disorder characterized by persistent inattention, hyperactivity, and impulsivity that interferes with daily functioning and development.</p>
<p>Participants with ADHD were recruited from the child psychiatric outpatient clinic at National Taiwan University Hospital, while control participants were recruited from nearby communities. Magnetic resonance imaging (MRI) scans were conducted at baseline and again approximately five years later (ranging from 2.2 to 9.1 years). Parents completed the SNAP-IV questionnaire to assess ADHD-related symptoms at both time points.</p>
<p>The researchers reconstructed each participant’s methylphenidate treatment history using parent reports and electronic medical records. All ADHD participants had used methylphenidate, and none were treated with other stimulant medications such as dexamphetamine, which is not approved for use in Taiwan. The researchers calculated cumulative dosage by multiplying the dose by the number of days taken between assessments.</p>
<p>Among participants who were younger than 12 years old at baseline, those with ADHD showed distinct developmental trajectories in frontal brain regions compared to typically developing controls. In this early-exposure group, higher cumulative methylphenidate doses were significantly associated with increased gray matter volume in multiple frontal regions, including the right paracentral, caudal middle frontal, superior frontal, lateral orbitofrontal, rostral middle frontal, and precentral cortices, as well as the left pars opercularis, paracentral, and superior frontal cortices.</p>
<p>Increases in volume in some of these same areas—such as the right rostral middle frontal, right paracentral, right superior frontal, and left paracentral cortices—were also associated with greater reductions in oppositional symptoms, suggesting a possible link between frontal brain development and behavioral improvement. However, these brain–behavior correlations did not remain statistically significant after correction for multiple comparisons.</p>
<p>In contrast, participants who were 12 or older at baseline did not show significant structural changes in relation to cumulative methylphenidate exposure. However, in this older group, higher cumulative dosage was still associated with greater improvements in inattention and overall ADHD symptoms, indicating that methylphenidate can be clinically effective even when started later, though without the same measurable brain structure associations.</p>
<p>“Our findings indicate that early methylphenidate exposure may affect frontal brain morphology and its association with symptom improvement in ADHD. These age-dependent patterns of psychostimulants on brain structure provide further insight into treatment response and disorder progression monitoring,” the study authors concluded.</p>
<p>The study sheds light on potential effects of methylphenidate on young brain development. However, study authors report that there were many more male than female participants in the study and it remains unclear whether the observed effects are gender dependent. Additionally, drug holidays (periods when participants were not taking drugs) were not systematically documented, and thus not included in cumulative drug dosage calculations.</p>
<p>The paper, “<a href="https://doi.org/10.1016/j.pnpbp.2025.111429">Age-dependent effects of cumulative methylphenidate exposure on brain structure and symptom amelioration in youth with ADHD: A longitudinal MRI study,</a>” was authored by Jung-Chi Chang, Hsiang-Yuan Lin, and Susan Shur-Fen Gau.</p></p>
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<td><a href="https://www.psypost.org/science-shows-why-dogs-sense-when-youre-sad-stressed-or-smiling/" 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;">Science shows why dogs sense when you’re sad, stressed, or smiling</a>
<div style="font-family:Helvetica, sans-serif; text-align:left;color:#999;font-size:11px;font-weight:bold;line-height:15px;">Sep 9th 2025, 12:00</div>
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<p><p>Your dog tilts its head when you cry, paces when you’re stressed, and somehow appears at your side during your worst moments. Coincidence? Not even close.</p>
<p>Thousands of years of co-evolution have given dogs special ways to tune in to our voices, faces and even brain chemistry. From brain regions devoted to <a href="https://pubmed.ncbi.nlm.nih.gov/24560578/#:~:text=evolutionary%20distance,evolutionary%20origin%20than%20previously%20known">processing our speech</a> to the “love hormone” or <a href="https://journals.lww.com/obgynsurvey/abstract/2015/07000/oxytocin_gaze_positive_loop_and_the_coevolution_of.14.aspx#:~:text=Gazing%20behavior%20increased%20urinary%20oxytocin,intranasal%20oxytocin%20in%20dog%20owners">oxytocin</a> that surges when we lock eyes, your dog’s mind is hardwired to pick up on what you’re feeling.</p>
<p>The evidence for this extraordinary emotional intelligence begins in the brain itself. Dogs’ brains have dedicated areas that are sensitive to voice, similar to those in humans. In a <a href="https://pubmed.ncbi.nlm.nih.gov/24560578/#:~:text=evolutionary%20distance,evolutionary%20origin%20than%20previously%20known">brain imaging study</a>, researchers found that dogs possess voice-processing regions in their temporal cortex that light up in response to vocal sounds.</p>
<p>Dogs respond not just to any sound, but to the emotional tone of your voice. Brain scans reveal that emotionally charged sounds – a laugh, a cry, an angry shout – activate dogs’ auditory cortex and the amygdala – a part of the brain involved in processing <a href="https://www.mdpi.com/2076-3417/14/24/12028#:~:text=faces,processing%20regions%20when%20viewing%20their">emotions</a>.</p>
<p>Dogs are also skilled face readers. <a href="https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0149431#:~:text=and%20unrestrained%20inside%20an%20MRI,study%20introduces%20the%20temporal%20cortex">When shown images</a> of human faces, dogs exhibit increased brain activity. <a href="https://www.mdpi.com/2076-3417/14/24/12028#:~:text=,processing%20regions%20when%20viewing%20their">One study</a> found that seeing a familiar human face activates a dog’s reward centres and emotional centres – meaning your dog’s brain is processing your expressions, perhaps not in words but in feelings.</p>
<p>Dogs don’t just observe your emotions; they can “catch” them too. Researchers call this <a href="https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2019.01678/full">emotional contagion</a>, a basic form of empathy where one individual mirrors another’s emotional state. <a href="https://www.frontiersin.org/journals/psychology/articles/10.3389/fpsyg.2019.01678/full">A 2019 study</a> found that some dog-human pairs had synchronised cardiac patterns during stressful times, with their heartbeats mirroring each other.</p>
<p>This emotional contagion doesn’t require complex reasoning – it’s more of an automatic empathy arising from close bonding. Your dog’s empathetic yawns or whines are probably due to learned association and <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10886274/#:~:text=process%20that%20does%20not%20necessarily,167">emotional attunement</a> rather than literal mind-mirroring.</p>
<h2>The oxytocin effect</h2>
<p>The most remarkable discovery in canine-human bonding may be the chemical connection we share. When dogs and humans make gentle eye contact, both partners experience a surge of oxytocin, often dubbed the “love hormone”.</p>
<p>In <a href="https://journals.lww.com/obgynsurvey/abstract/2015/07000/oxytocin_gaze_positive_loop_and_the_coevolution_of.14.aspx#:~:text=Gazing%20behavior%20increased%20urinary%20oxytocin,intranasal%20oxytocin%20in%20dog%20owners">one study</a>, owners who held long mutual gazes with their dogs had significantly higher oxytocin levels afterwards, and so did their dogs.</p>
<p>This oxytocin feedback loop reinforces bonding, much like the gaze between a parent and infant. Astonishingly, this effect is unique to domesticated dogs: hand-raised wolves did not respond the same way to human eye contact. As dogs became domesticated, they evolved this interspecies oxytocin loop as a way to glue them emotionally to their humans. Those soulful eyes your pup gives you are chemically binding you two together.</p>
<p>Beyond eye contact, dogs are surprisingly skilled at reading human body language and facial expressions. <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8382916/#:~:text=%28perspective%20taking%3B%20Catala%20et%20al,43%20Somppi%20et%20al">Experiments</a> demonstrate that pet dogs can distinguish a smiling face from an angry face, even in photos.</p>
<p>Dogs show a subtle right-hemisphere bias when processing emotional cues, tending to gaze toward the left side of a human’s face when assessing expressions – a pattern also seen in humans and primates.</p>
<p>Dogs rely on multiple senses to discern how you’re feeling. A cheerful, high-pitched “Good boy!” with a relaxed posture sends a very different message than a stern shout with rigid body language. Remarkably, they can even sniff out emotions. <a href="https://pubmed.ncbi.nlm.nih.gov/28988316/#:~:text=the%20predicted%20behaviors%20in%20the,communication%20is%20facilitated%20by%20chemosignals">In a 2018 study</a>, dogs exposed to sweat from scared people exhibited more stress than dogs that smelled “happy” sweat. In essence, your anxiety smells unpleasant to your dog, whereas your relaxed happiness can put them at ease.</p>
<h2>Bred for friendship</h2>
<p>How did dogs become so remarkably attuned to human emotions? The answer lies in their evolutionary journey alongside us. Dogs have smaller brains than their wild wolf ancestors, but in the process of domestication, their brains may have rewired to enhance social and emotional intelligence.</p>
<p>Clues come from a <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC8276742/#:~:text=from%20selection%20for%20tameness%20versus,In%20one">Russian fox domestication experiment</a>. Foxes bred for tameness showed increased grey matter in regions related to emotion and reward. These results challenge the assumption that domestication makes animals less intelligent. Instead, breeding animals to be friendly and social can enhance the brain pathways that help them form bonds.</p>
<p>In dogs, thousands of years living as our companions have fine-tuned brain pathways for <a href="https://pmc.ncbi.nlm.nih.gov/articles/PMC10886274/#:~:text=process%20that%20does%20not%20necessarily,167">reading human social signals</a>. While your dog’s brain may be smaller than a wolf’s, it may be uniquely optimised to love and understand humans.</p>
<p>Dogs probably aren’t pondering why you’re upset or realising that you have distinct thoughts and intentions. Instead, they excel at picking up on what you’re projecting and respond accordingly.</p>
<p>So dogs may not be able to read our minds, but by reading our behaviour and feelings, they meet us emotionally in a way few other animals can. In our hectic modern world, that cross-species empathy is not just endearing; it’s evolutionary and socially meaningful, reminding us that the language of friendship sometimes transcends words entirely.<!-- Below is The Conversation's page counter tag. Please DO NOT REMOVE. --><img decoding="async" src="https://counter.theconversation.com/content/261720/count.gif?distributor=republish-lightbox-basic" alt="The Conversation" width="1" height="1"><!-- End of code. If you don't see any code above, please get new code from the Advanced tab after you click the republish button. The page counter does not collect any personal data. More info: https://theconversation.com/republishing-guidelines --></p>
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<p><em>This article is republished from <a href="https://theconversation.com">The Conversation</a> under a Creative Commons license. Read the <a href="https://theconversation.com/your-dog-can-read-your-mind-sort-of-261720">original article</a>.</em></p></p>
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<p><strong>Forwarded by:<br />
Michael Reeder LCPC<br />
Baltimore, MD</strong></p>
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