#autismresearch — Public Fediverse posts
Live and recent posts from across the Fediverse tagged #autismresearch, aggregated by home.social.
-
I’m autistic. Here’s what happened to us this week.
Federal officials are closing the comment window on a 336-page autism research plan. It could steer priorities at NIH, CDC, and beyond for the next two years. Advocates had to push for more time just to read it.
Meanwhile, prescriptions for leucovorin rose 46% after White House autism claims. But the largest supporting trial was retracted earlier this year.
And in North Carolina, new Medicaid rules for autism therapy are already raising access questions for families and providers.
This isn’t abstract policy. It shapes what gets studied, prescribed, funded, restricted... and who gets heard.
What story in this week’s briefing hits closest to home for you?
#ActuallyAutistic #DisabilityRights #Neurodivergent #MentalHealth #AutismResearch
https://johnnyprofaneknapp.substack.com/p/divergent-times-august-1319-2026
-
DATE: August 13, 2026 at 06:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Single dose of rapamycin rapidly reduces autism-like traits in adult mice
URL: https://www.psypost.org/single-dose-of-rapamycin-rapidly-reduces-autism-like-traits-in-adult-mice/
A new study published in the journal Nature Communications suggests that exposing mice to mild inflammation during pregnancy triggers brain and behavioral changes in their offspring that resemble autism spectrum disorder. The research provides evidence that a single dose of the immunosuppressive drug rapamycin can rapidly but temporarily reverse these symptoms in adult mice by altering brain function rather than physical structure.
Autism spectrum disorder is a complex condition associated with diverse changes in brain development, behavior, and sensory processing. One known risk factor is maternal immune activation, which occurs when a pregnant mother experiences an infection or inflammation. This inflammatory response can alter the development of the fetal brain. In both human and animal studies, such early immune events are linked to later neurodevelopmental differences, including increased brain volume in early life, altered social behaviors, and heightened sensitivity to sensory input.
At the cellular level, many of these changes are associated with the overactivation of the mTOR pathway. The mTOR pathway is a biological signaling network that regulates cell growth, division, and survival. When this system is hyperactive, it tends to lead to abnormal synapse formation, an imbalance between excitatory and inhibitory brain signals, and an increased susceptibility to seizures.
“We have a longstanding interest in the mTOR system in brain development and autism spectrum disorder,” said study authors Harley Kornblum, director of the UCLA Intellectual and Developmental Disabilities Research Center and a professor of psychiatry, pediatrics, and pharmacology; Neil Harris, a professor of neurosurgery; and Janel Le Belle, an associate professor of neurosurgery. “Our earlier study also led by Dr. Le Belle showed that mild maternal inflammation in a strain of mouse activated the mTOR system and resulted in many behaviors reminiscent of autism and that are also found in genetic mouse models in which we know that the affected genes cause autism in people.”
Rapamycin is an established drug that inhibits the mTOR pathway. It is commonly used in medicine to prevent organ transplant rejection. In previous animal research, treating young mice with rapamycin over several weeks prevented the physical brain abnormalities associated with certain genetic mutations linked to autism.
“We were interested in trying treatment with the mTOR inhibitor rapamycin, which is used in children with disorders that activate the mTOR pathway,” the researchers added. However, chronic use of rapamycin can suppress the immune system and inhibit healthy growth. The authors designed this study to observe what happens when adult mice receive a short-acting, single dose of the drug, focusing on immediate functional changes in the brain rather than long-term structural remodeling.
The authors triggered a mild maternal inflammatory response in pregnant mice by injecting them with lipopolysaccharide, a bacterial compound that induces an immune reaction. This low dose was designed to provoke a response without making the pregnant mice noticeably ill. The offspring were then raised to early adulthood or older adulthood, creating experimental groups of male and female mice to compare against a control group that received a harmless saline solution.
The researchers first evaluated the physical and molecular characteristics of the offspring exposed to maternal inflammation. They tracked brain weights from birth to 200 days old for 16 mice per group. The exposed mice experienced mild brain overgrowth early in life compared to the control group, but by day 200, this growth had slowed, resulting in brain weights slightly below the control average.
The exposed mice also maintained chronically elevated levels of immune proteins, known as cytokines, in their blood. Their brain tissue showed persistent overactivation of the mTOR pathway. To see if immune cells were driving the ongoing issues, the researchers depleted microglia, a type of brain immune cell, in some mice. This reduction improved behaviors in young adult mice but failed to help older adult mice, suggesting that other functional mechanisms maintain the behavioral traits later in life.
To test behavior, the scientists observed groups of 26 mice in open field tests. The exposed mice spent roughly twice as much time engaging in repetitive behaviors, such as grooming and circling, compared to the control mice. When the researchers administered a single injection of rapamycin at a dose of 5 milligrams per kilogram, the repetitive behaviors in the exposed mice dropped to match the levels seen in the control mice within two hours.
“We were very surprised by the rapidity of the effects of rapamycin,” the researchers told PsyPost. “We expected that if the mTOR system was still activated in the adult, it would be influencing the structure of how brain cells connect with each other, which would mean that anticipated effects would take longer than just a few hours.”
This behavioral rescue was temporary, as the repetitive behaviors returned to their previous elevated levels 72 hours later. The authors also tested daily injections over five weeks in groups of 10 mice. They found that the mice developed a tolerance to the drug, leading to a gradual loss of its behavioral benefits.
The study also measured sensory over-responsivity, a common trait where individuals are highly sensitive to touch or sound. Using groups of eight mice, the researchers tested tactile avoidance by placing the animals in a box with both smooth and rough floor surfaces. The exposed mice actively avoided the rough-textured floor, spending less time there than the control mice. Following a single dose of rapamycin, the exposed mice increased their time spent on the rough floor, indicating a normalization of their sensory tolerance.
Sensory sensitivities can disrupt daily life and exacerbate other challenges. “Our results point to a significant role of the sensory system in our mouse model and its correction with rapamycin,” the authors noted. “Sensory symptoms are known to be highly disabling in autism and now there is some evidence that abnormalities in sensory responsiveness may contribute to many of the behaviors that we don’t normally view as being mediated by the sensory system.”
Because sensory and behavioral changes often relate to how brain cells fire, the researchers examined the electrical activity of individual brain cells. They analyzed brain slices from 24 mice per group, focusing on pyramidal neurons in the sensory cortex. The neurons from the exposed mice exhibited a higher frequency and amplitude of spontaneous electrical discharges compared to the control neurons, indicating hyper-excitability. Treating the mice or the brain slices with rapamycin quickly reduced this hyperactivity.
To test this hyper-excitability in living animals, the researchers administered a seizure-inducing chemical to groups of eight mice. All eight exposed mice experienced visible seizures at a high dose, compared to only two out of eight control mice. Rapamycin administration lowered the severity of the seizure scores in the exposed group.
To observe brain-wide communication, the authors used functional magnetic resonance imaging to scan 16 mice per group. This technique measures functional connectivity, which tracks how different brain regions synchronize their activity. The exposed mice displayed higher levels of connectivity than the control mice, particularly between sensory processing areas and subcortical regions like the thalamus. Following the two-hour rapamycin treatment, this hyper-connectivity decreased in the sensory cortex and reorganized across the brain, restoring the functional network to a state that closely resembled the control mice.
This neural reorganization provides evidence that specific circuits remain adaptable in adult mice. The average person should take away the idea “[t]hat some behaviors associated with autism can improve, even after the brain has matured,” the authors said. “Furthermore, we have identified the pathways (connections) in the brain that are influenced in this mouse model and that are altered with rapamycin.”
Finally, the researchers analyzed gene expression in the brain cells. They found that the exposed mice had altered activity in genes related to ion channels, which control the flow of electrical charges in and out of cells. After the acute rapamycin treatment, the expression of genes associated with brain cell excitability and autism risk quickly shifted back toward typical levels. This indicates that the drug works by rapidly adjusting the molecular balance of excitation and inhibition.
The findings from this study rely on a specific animal model of maternal inflammation, and physiological responses seen in mice do not directly translate to human neurodevelopment. Because rapamycin has strong immunosuppressive properties, it is not a practical daily treatment for behavioral or sensory symptoms in humans.
“We don’t believe that rapamycin or its close relatives that are currently used clinically will be the ‘cure’ for autism,” the authors cautioned. “First, our effects were temporary and wore off after several treatments. Second, as a class of medications, they can have significant side effects, especially immunosuppression.” They emphasized that they “would not recommend treatment with these medications outside of the conditions for which they are approved.”
Instead of acting as a direct treatment, the drug helps reveal underlying mechanisms for scientists to target. “We look at our findings as a fulcrum to further study autism-associated behaviors and symptoms and how they can be treated,” the authors explained.
Moving forward, the research team plans to explore other interventions. “In one set of studies we are trying to discover the downstream molecular pathways by which rapamycin acts so that we can potentially develop new therapies,” they said. “In the other approach, we are investigating the neural pathways that are misregulated in our model to see if these pathways can be functionally manipulated by therapeutic means, such as transcranial magnetic stimulation.”
The study, “Acute rapamycin treatment reveals distinct mechanisms of dysfunction in a maternal inflammation mouse model,” was authored by JE Le Belle, M. C. Condro, C. Cepeda, KD Oikonomou, K. Tessema, L. Dudley, J. Schoenfield, R. Kawaguchi, D. Geschwind, AJ Silva, Z. Zhang, K. Shokat, NG Harris, and HI Kornblum.
URL: https://www.psypost.org/single-dose-of-rapamycin-rapidly-reduces-autism-like-traits-in-adult-mice/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #Rapamycin #mTOR #MaternalInflammation #Neuroscience #BrainPlasticity #AutismTherapies #Neurodevelopment #SensoryProcessing #NeuralConnectivity
-
DATE: August 12, 2026 at 07:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Social anxiety, not masking, may drive mental health struggles in autistic adults
For autistic adults, hiding or suppressing traits to fit in with social expectations is often linked to higher rates of depression and distress. A recent study published in Autism Research reveals that these negative mental health outcomes may actually be driven by underlying social anxiety and social challenges, rather than the act of camouflaging itself. The findings suggest that current psychological questionnaires might be measuring overlapping concepts, pointing to a need for more precise tools to understand autistic well-being.
Autism is a neurodevelopmental condition characterized by differences in social communication, interaction, and sensory processing. Many autistic individuals use a coping strategy known as camouflaging to navigate social environments. This practice involves suppressing natural behaviors, such as avoiding eye contact or repetitive physical movements, while mimicking the speech patterns and gestures of people who are not autistic.
Psychologists divide camouflaging into three distinct categories. Compensation involves actively developing techniques to manage social interactions, such as practicing scripted conversations. Masking refers to deliberate efforts to hide autistic traits. Assimilation involves adapting behaviors to blend into a group, often by avoiding situations where differences might be noticed.
People camouflage for various reasons, including a desire to avoid discrimination, reduce stigma, and foster a sense of belonging in social groups. This effort often comes at a high personal cost. Previous research has consistently linked camouflaging to physical exhaustion, identity confusion, and elevated rates of depression and anxiety.
These established associations prompted researchers to ask a more specific question. Bruna B. Roisenberg, a researcher at the University of Sydney, along with senior author Adam J. Guastella and their colleagues, wanted to know if camouflaging independently predicts poor mental health. They suspected that the negative outcomes often attributed to camouflaging might actually stem from overlapping issues, such as social anxiety or broader difficulties with social responsiveness.
Social anxiety involves an intense fear of being judged or evaluated negatively in social situations. Social responsiveness refers to how an individual perceives, interprets, and reacts to social cues. The researchers theorized that because camouflaging involves intense self-monitoring and a fear of negative evaluation, it shares many fundamental features with social anxiety.
To investigate this relationship, the research team analyzed data from 113 autistic adults. The participants ranged in age from 17 to 75. All of them were experiencing social anxiety and had expressed interest in receiving therapeutic interventions for their anxiety symptoms.
The participants completed a series of standardized questionnaires. These surveys measured their levels of camouflaging, social anxiety, and social responsiveness. The participants also completed assessments evaluating their current levels of depression, psychological distress, and daily disability.
In addition to these mental health metrics, the researchers assessed the participants’ overall quality of life. This evaluation covered four distinct areas. The surveys measured physical health, psychological well-being, the quality of social relationships, and environmental factors like access to resources and daily safety.
The researchers used a statistical method called hierarchical regression to evaluate the data. This technique allowed them to test the variables in a step-by-step manner. By controlling for basic demographic factors like age and sex assigned at birth, they could observe the isolated effects of social responsiveness, social anxiety, and finally, camouflaging.
The goal was to see if camouflaging added any unique explanatory power to the mental health outcomes. If camouflaging was an independent driver of poor mental health, it would predict higher levels of depression or distress even after the other variables were taken into account.
The results told a different story. In the initial analyses, camouflaging was indeed associated with greater psychological distress, more severe depression, and increased disability. Those who reported higher levels of masking their traits also reported worse overall mental health.
This relationship vanished in the step-by-step statistical models. The researchers found that social responsiveness and social anxiety strongly predicted depression, psychological distress, and disability. Once the models accounted for these two factors, camouflaging did not explain any additional differences in the participants’ mental health.
The same pattern emerged when looking at quality of life. Higher levels of social anxiety and social challenges were associated with a lower quality of life. Camouflaging provided no independent predictive value for a person’s physical health, psychological well-being, social relationships, or environmental satisfaction.
The findings held true even when the researchers broke down camouflaging into its specific components. None of the individual strategies, compensation, masking, or assimilation, independently predicted negative mental health outcomes beyond the effects of social anxiety and social impairments.
The results imply that the questionnaires currently used to measure camouflaging might be capturing the same psychological processes as tools used to measure social anxiety. Because both concepts involve a heightened focus on how one is perceived by others, they are difficult to untangle with standard surveys. The emotional and functional costs attributed to camouflaging may largely reflect a broader fear of negative evaluation.
The study provides an updated perspective on how autistic adults experience mental health challenges, but it relies on cross-sectional data. This means the researchers measured all variables at a single point in time. Because of this design, the study cannot determine whether social anxiety leads to increased camouflaging, or if the effort of camouflaging exacerbates social anxiety.
The researchers also noted that the study relied entirely on self-reported questionnaires. This type of data can be influenced by a participant’s level of self-awareness or their interpretation of the questions. Relying solely on self-reporting increases the likelihood that overlapping concepts will blend together in the final data.
The study participants were all actively seeking treatment for social anxiety, which means the group may not represent the broader autistic population. Autistic individuals who do not experience high levels of social anxiety, or who are not actively seeking mental health support, might exhibit different patterns of well-being.
Future research will need to track autistic individuals over extended periods to see how camouflaging and mental health interact as people age. Expanding the ways in which researchers measure camouflaging, perhaps through observational methods or interviews, could help isolate its specific effects on an individual’s quality of life.
The study, “Does Camouflaging Predict Functioning, Distress, and Quality of Life for Autistic Adults?” was authored by Bruna B. Roisenberg, Kelsie A. Boulton, Emma E. Thomas, and Adam J. Guastella.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismMentalHealth #CamouflagingMyth #SocialAnxiety #AutisticAdults #MentalHealthAwareness #SocialResponsiveness #DepressionInAutism #QualityOfLife # neurodiversity #AutismResearch
-
DATE: August 7, 2026 at 08:38AM
SOURCE: SCIENCE DAILY PSYCHIATIRY FEEDTITLE: New autism therapy shows surprising benefits even in adult mice
URL: https://www.sciencedaily.com/releases/2026/08/260805082508.htm
Blocking the glycine transporter SLC6A20 restored important brain signaling and improved social, communication, and repetitive behaviors in autism-related mouse models. The treatment also worked in human brain organoids and showed lasting effects in adult mice, suggesting the brain may remain more treatable later in life than previously thought.
URL: https://www.sciencedaily.com/releases/2026/08/260805082508.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismTherapy #GlycineTransporterSLC6A20 #BrainSignaling #AutismResearch #MouseModel #SocialBehavior #CommunicationSkills #RepetitiveBehaviors #AdultMice #NeurodevelopmentalTherapy
-
DATE: August 7, 2026 at 08:38AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: New autism therapy shows surprising benefits even in adult mice
URL: https://www.sciencedaily.com/releases/2026/08/260805082508.htm
Blocking the glycine transporter SLC6A20 restored important brain signaling and improved social, communication, and repetitive behaviors in autism-related mouse models. The treatment also worked in human brain organoids and showed lasting effects in adult mice, suggesting the brain may remain more treatable later in life than previously thought.
URL: https://www.sciencedaily.com/releases/2026/08/260805082508.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #AutismTherapy #SLC6A20 #GlycineTransporter #Neurology #BrainHealth #MiceModel #Organoids #AdultBrains #SocialBehaviorTherapy
-
DATE: August 5, 2026 at 09:00AM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Miniature brain models reveal varied electrical activity in different types of autism
Researchers have grown miniature, three-dimensional brain models from the cells of autistic and nonautistic individuals to study how their neural networks communicate. The models demonstrated that different types of autism spectrum disorder produce vastly different patterns of electrical activity, highlighting the wide biological variety underlying the condition. The small study was published in the journal Translational Psychiatry.
Autism spectrum disorder is a neurodevelopmental condition involving differences in social communication and repetitive behaviors. The biological roots of the condition remain difficult to map out. While many cases have no known genetic cause, a portion of autistic individuals have what is known as syndromic autism. This form of the condition is linked to specific single-gene mutations that alter how brain cells develop and communicate.
Because traditional animal models often fail to accurately reflect the specific features of human brain development, researchers have increasingly turned to brain organoids. These are tiny, self-organizing bundles of tissue grown from human stem cells. Brain organoids replicate the early stages of human brain development while retaining the exact genetic code of the person who provided the original cells.
Lead researchers Nisim Perets and Liya Kerem, along with a team of colleagues at Itay and Beyond and the Hebrew University of Jerusalem, wanted to see if organoids could reveal the functional differences between various forms of autism. They focused on comparing the baseline electrical activity and network connections among several distinct genetic subtypes of the disorder. Extrapolating how a single mutated gene alters whole-brain activity is challenging in living humans, making these laboratory-grown models highly useful for observing live neural networks in action.
The researchers collected urine samples from fifteen human participants. Four participants were neurotypical, serving as a control group. Ten participants had syndromic autism stemming from five different genetic mutations, including the genes SHANK3, SCN2A, STXBP1, PPP2R5D, and GRIN2B. One participant had idiopathic autism, meaning their condition had no identified genetic origin.
Using epithelial cells extracted from the urine, the team reprogrammed the cells back into a basic stem cell state. They then placed these induced pluripotent stem cells into special nutrient baths, guiding them to grow into more than four hundred brain organoids. To ensure the models were developing correctly, the researchers analyzed the cells using genetic sequencing and fluorescent imaging. This confirmed that the organoids contained the right mix of brain cells, including neural progenitors, developing neurons, and mature cortical cells.
After growing the organoids for about two months, the researchers placed them onto special plates equipped with microscopic electrodes. These multi-electrode arrays allowed the team to record the spontaneous electrical signals passing between the neurons. The researchers tracked metrics like the firing rate, the size of the electrical spikes, and the frequency of synchronized bursts across the neural network.
The resting electrical activity in the autism models differed substantially from the neurotypical control models. The organoids derived from the participant with idiopathic autism exhibited a generally hypoactive profile. They showed lower firing rates, weaker signal strengths, and fewer bursts of activity compared to the control group.
Conversely, organoids derived from most of the syndromic autism subtypes showed higher firing rates than the control group. Organoids from participants with SCN2A mutations had varying firing rates but consistently produced weaker electrical signal strengths. This initial observation confirmed that genetic differences lead to physical differences in how brain cells spontaneously fire.
Next, the research team tested how the neural networks responded to new stimuli, a process known as short-term synaptic plasticity. In a living brain, neural networks adapt to incoming information by temporarily adjusting their sensitivity. They might dampen their activity, known as short-term depression, or temporarily boost it, known as short-term potentiation. The researchers delivered brief electrical pulses to the organoids and recorded the changes in activity over the following five minutes.
The high-frequency stimulation mostly caused the networks to dampen their activity. However, organoids from patients with STXBP1, SHANK3, and SCN2A mutations displayed abnormally high levels of short-term depression and reduced potentiation compared to the control group. Organoids with GRIN2B mutations showed the opposite trend, with slightly elevated potentiation and reduced depression. These varied responses suggest that different genetic mutations disrupt the brain’s ability to adapt to incoming signals in entirely different ways.
The researchers also mapped the functional connectivity of the networks before and after the stimulation. In response to the electrical pulses, the neurotypical organoids displayed a stable, predictable decrease in network connectivity. Organoids from the autism groups displayed highly erratic responses.
The neural networks in organoids with a STXBP1 gene mutation collapsed almost immediately after stimulation, failing to recover normally. Models with a PPP2R5D mutation experienced a sharp, sudden drop in connectivity. Models with GRIN2B mutations showed an inconsistent, fluctuating response across the entire observation period. The organoids representing idiopathic autism barely changed at all, showing a rigidity not seen in the control group.
To visualize these vast differences, the researchers mapped eighteen separate electrical characteristics onto a three-dimensional graph using a mathematical technique called principal component analysis. Organoids grown from the same person behaved similarly, and the entire neurotypical control group clustered tightly together. The organoids from the autistic participants scattered widely across the graph.
Even organoids grown from patients sharing the exact same genetic mutation sometimes displayed different patterns of electrical activity. One participant with a GRIN2B mutation had a clinical history of seizures, and their corresponding organoids exhibited abnormal rhythmic bursting. Another participant with the same GRIN2B mutation did not have a history of seizures, and their organoids did not display that specific bursting pattern.
While these three-dimensional models provide a window into early brain development, they do not replicate the full structural architecture of a mature human brain. The study also relied on a small sample size of fifteen patients, with only a single individual representing the idiopathic autism category. The association between specific electrical patterns in the organoids and clinical symptoms like seizures will require testing in larger patient cohorts to verify that the results were not statistically anomalous.
The researchers noted that tracking functional electrical differences in brain organoids could help classify different subtypes of autism based on brain circuitry rather than just behavioral observations. Because autism encompasses such a wide array of biological mechanisms, grouping patients by how their neural networks actually function might eventually guide the development of tailored therapeutic interventions.
The study, “Patient-derived brain organoids reveal divergent neuronal activity across subpopulations of autism spectrum disorder,” was authored by Nisim Perets, Liya Kerem, Nir Waiskopf, Noa Horesh, Itay Goldman, Jasmine Avichzer, Doron Bril, William Tobelaim, Milcah Barashi, Liat David, and Ariel Tenenbaum.
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #BrainOrganoids #NeuralActivity #AutismSubtypes #GeneticAutism #Neuroscience #SynapticPlasticity #BrainConnectivity #TranslationalPsychiatry #NeuralNetworks
-
DATE: July 27, 2026 at 12:00PM
SOURCE: PSYPOST.ORG** Research quality varies widely from fantastic to small exploratory studies. Please check research methods when conclusions are very important to you. **
-------------------------------------------------TITLE: Brain structure differences in autism map onto serotonin receptor locations
URL: https://www.psypost.org/brain-structure-differences-in-autism-map-onto-serotonin-receptor-locations/
A neuroimaging study found that autistic individuals whose cortical thickness deviated most from that of neurotypical peers tended to experience greater social and communication difficulties. In autistic individuals, the cortical regions showing the greatest differences in thickness relative to neurotypical individuals also tended to have a higher density of serotonin receptors. The research provides evidence linking brain structure, neurochemistry, and behavioral traits in autism. The paper was published in Autism Research.
Autism is a neurodevelopmental condition that affects how a person communicates, interacts with others, processes sensory information, and experiences the world. It is called a spectrum because its characteristics and level of support needs vary widely between individuals.
Some autistic people have difficulty interpreting social cues, maintaining conversations, or understanding unwritten social rules. Others are able to communicate fluently but still find social interaction tiring, confusing, or overwhelming. Repetitive movements, strong preferences for routines, intense interests, and unusual responses to sounds, lights, textures, or smells are also common.
Autism begins early in development, although it may not be recognized until later in childhood or adulthood. It is a lifelong form of neurological difference that may bring both difficulties and strengths. Many autistic people show beneficial qualities such as strong attention to detail, deep knowledge in areas of interest, logical thinking, creativity, or exceptional memory.
Study author Livio Tarchi and his colleagues note that previous research indicates consistent structural differences between the brains of individuals with autism and their neurotypical peers. The authors suggest these differences might be connected to the brain’s neurotransmitter systems. Neurotransmitters are chemical messengers that carry signals between brain cells. The researchers specifically focused on systems using serotonin, dopamine, and glutamate.
The scientists investigated how structural differences in the brain might map onto the spatial distribution of these chemical messengers. They analyzed data from the Autism Brain Imaging Data Exchange. This public dataset contains physical measurements, behavioral assessments, and brain scans collected across twenty different sites.
The data used in this analysis came from 1,035 participants. The sample included 505 autistic individuals and 530 neurotypical individuals. The average age of participants was about 17 years old. Both groups were predominantly male, reflecting historical diagnosis patterns.
The study authors used structural magnetic resonance imaging (MRI) data to calculate deviations from expected cortical thickness. Cortical thickness refers to the depth of the brain’s outer layer of gray matter, which is responsible for complex thought and sensory processing. They measured this thickness across thousands of individual points, called vertices, on the surface of the brain. These measurements were adjusted for both the sex and age of each participant.
Next, the researchers compared these structural measurements against reference maps of neurotransmitter receptor density. Receptors are protein structures on cells that receive chemical messages. These reference maps were derived from separate, previously published imaging studies. This allowed the authors to see if areas with unusual thickness in autistic individuals aligned with regions known to have high concentrations of specific neurotransmitters.
The results showed widespread deviations in cortical thickness in the brains of autistic participants compared to neurotypical participants. The structural differences tended to be larger in areas of the brain with a higher density of serotonin receptors. The researchers did not find a similar spatial link for dopamine or glutamate receptors. At the individual level, greater deviations in cortical thickness were associated with greater difficulties in social and communication domains.
These findings provide evidence for a neurobiological link between autism, brain structure, and serotonin. However, the participants in this study were mostly male. Because brain development and cortical thickness can vary by sex, studies involving more female participants might yield different results. Future research could help clarify these connections and guide tailored support strategies for autistic individuals.
The paper, “Autism and Cortical Thickness Deviation From Neurotypical Controls: Evidence for a Spatial Association With Serotonin Receptors,” was authored by Livio Tarchi, Arne Doose, Julius Hennig, Fabio Bernardoni, Joseph A. King, Tiziana Pisano, Giovanni Castellini, Valdo Ricca, Inge Kamp-Becker, and Stefan Ehrlich.
URL: https://www.psypost.org/brain-structure-differences-in-autism-map-onto-serotonin-receptor-locations/
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismBrain #CorticalThickness #SerotoninReceptors #Neuroimaging #AutismResearch #Neurodevelopment #BrainStructure #SocialCommunication #NeurotypicalVsAutistic #SerotoninMapping
-
Rapamycin Treatment Reveals Mechanisms of Dysfunction in Maternal Inflammation Model
📰 Original title: A single dose reversed autism-like symptoms in adult mice within hours
🤖 IA: It's clickbait ⚠️
👥 Users: It's clickbait ⚠️ -
DATE: July 25, 2026 at 11:09AM
SOURCE: SCIENCE DAILY MIND-BRAIN FEEDTITLE: A single dose reversed autism-like symptoms in adult mice within hours
URL: https://www.sciencedaily.com/releases/2026/07/260724061436.htm
Even mild inflammation during pregnancy led mouse offspring to develop persistent brain overactivity, sensory sensitivity, repetitive behaviors, and increased seizure risk. Remarkably, one dose of rapamycin improved nearly all of these problems within about two hours. The benefits were temporary, but they suggest that adult brain circuits may remain far more adaptable than previously believed.
URL: https://www.sciencedaily.com/releases/2026/07/260724061436.htm
-------------------------------------------------
Private, vetted email list for mental health professionals: https://www.clinicians-exchange.org
Unofficial Psychology Today Xitter to toot feed at Psych Today Unofficial Bot @PTUnofficialBot
-------------------------------------------------
#psychology #counseling #socialwork #psychotherapy @psychotherapist @psychotherapists @psychology @socialpsych @socialwork @psychiatry #mentalhealth #psychiatry #healthcare #depression #psychotherapist #AutismResearch #Rapamycin #MiceStudy #Neuroplasticity #BrainHealth #Inflammation #SensorySensitivity #SeizureRisk #Neuroscience #OneDoseTherapy
-
"Autistic people aren’t afraid of genetic research – they are afraid of what scientists might do with it"
Thank you @rmblaber1956 for sharing this excellent article.
-
🗞️ JUST PUBLISHED: IHI's June newsletter!
👉 https://lnkd.in/eJE7Ej6X
⚡ The topic texts of call 13 are approved!
📺 #IHICallDays - 3 to go!
📆 IHI Forum: 20-21 Oct save the date
🧬ARDAT is tackling regulatory science for #ATMPs
🧩 @aims2trials.bsky.social release data ethically for #AutismResearch
#HorizonEU -
In research, education, & policy making, autistic people are expected to accept a situation where non-autistic "experts" speak with authority about them.
An autistic person's lived experience is seen as less valid than external observations of our behaviour.
-
Tylenol in pregnancy not linked with autism, Danish study finds.
Read Full Article
#PregnancyHealth #AutismResearch #TylenolSafety https://www.reuters.com/business/healthcare-pharmaceuticals/tylenol-pregnancy-not-linked-with-autism-danish-study-finds-2026-04-13/
Reenviado desde Science News
(https://t.me/experienciainterdimensional/10673) -
I also talked about monotropism; the distinctive depth and narrowness of autistic attention.
The tendency to go very deep, to struggle with switching, to get overwhelmed by competing demands - and to experience the world with such a particular intensity.
Again: not just ‘life is hard’, but a very specific way of processing and experiencing.
-
"Why we need to reframe autism"
⬇️
I've just been guest on the podcast that hosted the autism researcher Uta Frith. I did a thread about it: https://mas.to/@KatyElphinstone/116206483353899881
Here's my episode:
On substack (but I think anyone can listen to it):
https://neurosense.substack.com/p/why-we-need-to-reframe-autism-with
On Apple podcasts:
https://podcasts.apple.com/gb/podcast/lets-talk-neurosense-the-psychology-of-neurodiversity/id1883007944
On Spotify:
https://open.spotify.com/episode/19fSshl0XkXqiKPCp3uyzO?si=gDBCV9koQHKqvEMHqrZJnw&t=2249Pass it on if you like it!
Comments can be made on the Substack version, & very welcome ☺️
-
"The new Independent Autism Coordinating Committee will bring together accomplished scientific experts and stakeholders with research expertise, with the goal of accelerating scientific discovery, improving care, and positively impacting the lives of people with autism. ...The I-ACC will... serve as a credible source for anyone trying to understand the science of autism. "
Read here: https://autismsciencefoundation.org/press_releases/i-acc-announcement/
-
Then, as we’re not listened to, society's understanding of autism develops without us.🤷🏽♀️
That flawed understanding is then used to overrule us, again.
Strange little loop. ➰
6/11
-
GABA/glutamate imbalance is a core feature of Autism. A new review describes how reduced GABA signaling may lead to excessive excitation in key brain circuits. 🧠✨🔍
Read Full Article
#GABA #Glutamate #AutismResearch #Neuroscience #MentalHealth https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2025.1587432/full
Reenviado desde Science News
(https://t.me/experienciainterdimensional/9489) -
FDA Takes Action to Make a Treatment Available for Autism Symptoms
#HackerNews #FDA #Autism #Treatment #Action #AutismResearch #HealthNews #MedicalBreakthroughs
-
🚨 President Trump to announce findings linking Tylenol use during pregnancy to autism. The administration claims breakthroughs on root causes of autism, stirring debate with health experts. Stay informed on this developing story. 🧠👶 #AutismResearch #Tylenol #HealthNews https://www.independent.co.uk/news/world/americas/us-politics/trump-autism-pregancy-tylenol-kennedy-b2831108.html
-
Can anyone recommend any book(s) on #AuDHD? Looking for something that's not just a basic 'what's AuDHD?' but rather more about how #autism and #ADHD / #ADD interact, as well as how to cope. Bonus points if it also takes into account gender differences in presentation of both / either issues.
Articles / research projects also of interest, of course, if you're aware of any. -
When #ideology overwrites the #Evidence and politicians try to enforce new research that produces the results that they like instead of searching for the #truth. #Autism #autismresearch
https://www.propublica.org/article/rfk-jr-autism-environment-research-funding
-
If you, like me, are #autistic, then you might be immune to the effects of false or otherwise insidious advertising techniques
According to the article, #neurotypical people are more likely to get distracted by marketing techniques, while us autistics focus on the practical side of a product, rendering those techniques pointless.
#AutismResearch #Autism #News #Psychology #Neurospicy #Neurodiverse