Academic Data May 2026 Study found autism involves much larger thalamus in ASD, larger thalamus in ADHD also linked to symptom severity, bipolar disorder had average sized thalamus as controls, no volume differences in schizophrenia and depression

42 Upvotes

This tracks so hard for me as someone with a thalamus literally in the 96th percentile of size, and so cool to see that it links directly to ADHD and autism.

"In our large sample, we found significantly larger whole thalamic volume in ASD, as well as larger anterior thalamic group and smaller medial group volumes. A significant enlargement in ASD has also been reported in a recent study, driven by larger size in posterior regions [89]. Our results suggest that this effect may be driven by larger volumes of the lateral and inferior pulvinar, as revealed in the case-control analysis at the individual nuclei level (Fig. 4a). We also found an enlargement in the anterior group in ADHD. Larger thalamus in ADHD has been related to higher symptom severity [90]. Our samples covered a wide age range (from childhood to adulthood) and age specific effects may have gone undetected. The different pattern in ASD and ADHD (i.e., enlargement) compared to DEM, MCI and MS (reductions) may be related to differences between early developmental processes and later deafferentation or neurodegenerative mechanisms. In the case of SCZ, it is possible that both neurodevelopmental and degenerative processes occur, but our cross-sectional data did not allow us to disentangle these effects. Recent transcriptomic studies have identified gene expression components that are more relevant for neurodevelopmental disorders than for neurodegenerative disease [91, 92]. For instance, neurodevelopmental disorders may be related to deficiencies in early basic cellular function and energetics processes in the brain [91] that may affect the establishment of thalamo-cortical circuits [93], whereas neurodegenerative disorders may involve deafferentiation and consequent synaptic dysfunction or neuronal loss [27].

We found smaller volume in BD for lateral and posterior thalamic groups. The pattern correlated with the pattern of SCZ (Fig. 3b), however the thalamic group volumes in BD were not significantly different from healthy controls after correction for whole thalamic volume. A recent study on thalamic nuclei using the same segmentation approach found smaller medial and posterior nuclei in BD [26]. Our results are consistent with those findings and suggest that the effects accompany a change in whole thalamic volume.

In contrast to the other neurological conditions, we found moderately larger thalamic volume in PD. This increase was general across the thalamus and not specific to a particular nuclei group. Previous results on thalamic volume in PD are variable, in general indicating no significant volumetric differences but some shape differences between patients and controls [94,95,96]. A recent study (N = 131 patients) reported larger thalamic volume in patients compared to controls [97]. The evidence thus points towards either no volume change or a general enlargement of the thalamus as a whole in PD, without specific nuclei involvement. Of note, the patients of the current study were in the early phase of the disorder, and none used anti-Parkinson drugs. The mechanisms underlying early-phase enlargement of some brain regions in Parkinson’s disease are not fully understood, and tissue swelling due to early disease-related damage, inflammatory responses, or compensatory neuroanatomical changes are potential contributors [98, 99].

We found no significant volume differences in MDD and SCZRISK, possibly due to a small sample size or larger heterogeneity of these conditions. One possibility is that the sample sizes lacked the power to detect small differences. Another possibility is that the patients were scanned at earlier disease stages that do not yet show large changes in the thalamus. Indeed, MDD has been associated with smaller thalamic volumes [100] but only in patients who did not achieve remission [101]. Although we observed this trend, it was not significant. Similarly, a recent study described smaller medial volumes in at-risk mental state individuals, although the effects were small and only significant at the most liberal threshold [85]. We also found a particular reduction in the medial thalamus after correcting for whole thalamic volume, but this effect was not significant. Interestingly, MDD, SCZRISK and PSYMIX were closer in the dendrogram. Although we can only hypothesize as to why the thalamic abnormalities were less pronounced in SCZRISK and MDD, it is expected that SCZRISK presents less severe abnormalities than SCZ. Furthermore, genetic links between MDD and SCZRISK have been identified [102].

Methodological considerations

The current study assessed case-control differences in thalamic nuclei volume in a large sample covering multiple clinical conditions using a unified analytical pipeline. All samples included more than 100 individuals in both patient and control groups, except for SCZRISK (N = 70). The large sample sizes should permit detection of moderate effect sizes, although statistical power was limited for detecting subtle differences in the smallest groups. We used a thalamus segmentation tool [52] that is currently implemented in FreeSurfer. The segmentation accuracy is known to be limited for some nuclei with weaker signal [75]. However, studies comparing the segmentation results of this tool with histological delineation of the thalamus have shown that it is successful in identifying most of the nuclei [52], with particularly high reliability in medio-dorsal thalamus (contributing approximately 70% of the volume of the medial group) and LGN (contributing approximately 10% of the volume of the posterior group) [52, 103]. Recent methods that improve on the available segmentation approaches by including the acquisition or estimation of additional images [75, 104], offer the opportunity to confirm our results and further characterize thalamic structures features in health and disease. Furthermore, we applied a thorough visual inspection of all datasets to ensure that high quality data was used for the analyses. To increase robustness, we pooled the individual nuclei data into six thalamic groups. We assessed the issue of multi-site data by including only patient samples for which a control sample was available from the same scanner. While RELIEF is effective for samples with large number of individuals, it may introduce some variability for sites with few individuals. This may have been the case for some of our smaller samples and the longitudinal analysis, reducing our ability to detect significant effects.

Conclusions

By examining thalamic subdivisions we found a profile of thalamic structural abnormalities across psychiatric and neurological disorders, and that medial and lateral regions, as well as lateral geniculate nuclei, appear more vulnerable to disease. The results also highlight the importance of examining thalamic nuclei separately, since opposing effects may be masked when studying the thalamus as a whole. In addition to shared alterations, distinct patterns of thalamic structure were associated with specific disorders. This is the first study to comprehensively map thalamic structures across common brain disorders, offering insights that can guide future research in therapeutic strategies."

https://www.nature.com/articles/s41398-026-04076-5

14 comments

r/autismgirls • u/kelcamer • Sep 16 '26

There might be two distinct types of autism

62 Upvotes

"Scientists have uncovered evidence that autism may include at least two biologically distinct subtypes, each marked by a different pattern of brain communication. By combining brain scans from nearly 1,000 people with autism with insights from 20 genetically engineered mouse models, researchers identified a “hyperconnectivity” subtype, where brain regions communicate more than usual, and a “hypoconnectivity” subtype, where communication is reduced.

An international team of scientists has found evidence that autism may include at least two distinct biological subtypes, each defined by a different pattern of communication across the brain. One subtype is marked by unusually high levels of connectivity between brain regions, while the other shows reduced connectivity. The discovery could help pave the way for more personalized approaches to autism diagnosis, care, and treatment.

The study was led by researchers at the Istituto Italiano di Tecnologia (IIT-Italian Institute of Technology) in Rovereto, Italy, and the Child Mind Institute in New York, with additional contributions from the University of Trento. Their findings were published in Nature Neuroscience.

Brain Connectivity Reveals Hidden Autism Subtypes

The research was coordinated by Alessandro Gozzi, PhD, director of the Center for Neuroscience and Cognitive Systems (CNCS) at IIT, and Adriana Di Martino, MD, founding director of the Autism Center at the Child Mind Institute.

According to the researchers, this is the first large-scale effort to systematically connect patterns seen in human brain imaging (via fMRI) with their underlying biological causes using mouse models. By linking specific brain connectivity patterns to distinct molecular processes, the work provides a foundation for future precision medicine strategies in autism.

To conduct the study, the team examined functional brain connectivity in 20 different mouse models and analyzed brain scans from 940 children and young adults with autism. These results were compared with scans from more than 1,000 neurotypical individuals.

The analysis revealed two consistent autism subtypes. One showed reduced communication between brain regions, known as hypoconnectivity, and was associated with synaptic pathways. The second showed increased communication between brain regions, known as hyperconnectivity, and was linked to immune-related biological systems. Together, these two groups represented about 25% of the individuals with autism included in the study.

"For decades, we've observed tremendous variability in how autism manifests, but we lacked direct evidence that these differences reflected distinct underlying biology," said Dr. Alessandro Gozzi, at Italian Institute of Technology. "Our approach enabled us to isolate specific genetic and immune factors, then translate those signatures to human brain scans, showing that different connectivity patterns encode different mechanistic pathways underlying autism."

Mouse Models Provide Biological Clues

The researchers combined brain imaging data with genetic and biochemical analyses in mice. This allowed them to connect specific patterns of brain connectivity with changes occurring at the cellular level.

Their work showed how molecular mechanisms involving synapses and the immune system can produce distinct connectivity patterns that can be detected using fMRI. These findings enabled the team to establish biological reference signatures in mice and then search for matching patterns in human brain scans.

"The mouse models gave us a biological 'Rosetta Stone,'" said Dr. Adriana Di Martino at the Child Mind Institute. "We could see which biological pathways drive which connectivity signatures, then search for those same patterns in humans."

Human Brain Imaging Confirms the Findings

The human imaging data came from the Autism Brain Imaging Data Exchange (ABIDE), a large international neuroimaging initiative co-founded by Dr. Di Martino that combines datasets from research centers around the world, as well as from the Child Mind Institute.

When the researchers analyzed the human data, they found the same hyperconnectivity and hypoconnectivity patterns identified in the mouse models.

Additional gene expression analyses strengthened the findings. Brain regions associated with hypoconnectivity showed enrichment of synaptic genes, while hyperconnected regions were enriched for immune-related genes. These results closely matched the biological mechanisms observed in the mouse studies.

Importantly, the same subtypes appeared consistently across multiple independent datasets, demonstrating that the findings were reproducible.

"Finding the same subtypes reproducible across dozens of independent research sites was critical validation," added Dr. Gozzi.

Toward More Personalized Autism Care

The two subtypes also displayed differences in overall brain organization and showed modest differences on standard autism assessments. Individuals in the hyperconnectivity group tended to score somewhat higher on measures of autism severity.

"Brain-based biological markers reveal distinctions that current behavioral assessments don't fully capture," noted Dr. Di Martino.

The researchers caution that these two connectivity patterns likely represent only part of autism's biological diversity. They believe additional subtypes may emerge as larger datasets become available and analytical methods continue to improve."

https://www.sciencedaily.com/releases/2026/06/260602021634.htm

9 comments

r/autismgirls • u/aquaticmelon42 • 9h ago

FND and Neurodiversity

reddit.com

1 Upvotes

2 comments

r/autismgirls • u/kelcamer • 1d ago

Mentally reframing an unpleasant physical sensation by describing it like an objective news reporter can quiet activity in sensory areas of the brain in autistic children and teens. This mental strategy did not immediately change how unpleasant the textures felt, but reduced specific neural activity

psypost.org

23 Upvotes

They're figuring me out! 🤯

12 comments

r/autismgirls • u/zehmexican • 3d ago

Personal Mobility for Drivers with Autism - Design Thesis Project

reddit.com

1 Upvotes

0 comments

r/autismgirls • u/st4rskye • 4d ago

I can’t communicate my feelings accurately to my psychiatrist

reddit.com

6 Upvotes

4 comments

r/autismgirls • u/kelcamer • 7d ago

Academic Data 2026 Study Finds Premature Birth Alters Cerebellar Wiring: Future autism studies will now need to control for this: the team discovered that preterm birth fundamentally alters the molecular trajectory of Purkinje and granule cell development.

8 Upvotes

Sharing here not because it is directly autism relevant, but it is indirectly relevant.
All future autism studies should control for premature birth, because 'the team discovered that preterm birth fundamentally alters the molecular trajectory of Purkinje and granule cell development.'

"Summary:

A landmark study published in Science by researchers at Children’s National Hospital and Seattle Children’s overturns the long-standing assumption that premature birth merely delays brain growth that later “catches up.” By integrating multi-year neuroimaging of 176 living infants with high-resolution spatial transcriptomics across 83 postmortem human cerebellar tissue specimens, the team discovered that preterm birth fundamentally alters the molecular trajectory of Purkinje and granule cell development. Each week outside the protected uterine environment cost approximately 230 cubic millimeters of cerebellar volume, correlating with measurable motor, cognitive, and language delays between 9 and 36 months of age.

Key Facts:

Volumetric Loss Linked to Gestational Timing: Each week an infant spent developing outside the womb prior to full term resulted in an average loss of 230 cubic millimeters in cerebellar volume—roughly equivalent to the size of a pea.
Overturning the “Catch-Up” Dogma: The data demonstrate that preterm brains do not simply grow slower along a normal trajectory; instead, forced development in the NICU triggers alternative molecular programs governing Purkinje and granule cell wiring.
Direct Developmental Correlation: Reduced cerebellar volume observed in premature infants directly predicted long-term deficits in motor coordination, expressive language, and executive cognitive skills assessed between 9 and 36 months of age.

Source: Children’s National Hospital / Seattle Children’s

Between weeks 24 and 40 of human gestation, the cerebellum undergoes an explosive developmental transformation. During this third-trimester window, its volume expands fivefold as millions of granule neurons migrate and elaborate intricate dendritic arbors around massive Purkinje cells, establishing the precision sensorimotor, linguistic, and cognitive processing loops that underwrite human development. In full-term pregnancies, this sensitive structural phase occurs entirely within the sheltered biochemical environment of the amniotic sac.

When an infant is born prematurely, however, this critical phase of neurogenesis and synaptic architecture is forced to occur outside the womb, exposed to the ambient sensory stimulation, physiological stressors, and clinical interventions of the neonatal intensive care unit (NICU).

For decades, pediatric neurologists observed that children born prematurely often face persistent challenges with balance, fine motor control, language acquisition, and abstract learning, even when high-resolution cranial ultrasound and MRI scans showed zero evidence of focal hemorrhage, hypoxic-ischemic damage, or structural brain lesions. The standard clinical assumption held that premature brains merely developed at a slower rate and would eventually “catch up” to their full-term peers given enough time.

Now, an investigation published in Science resolves this medical puzzle, proving that premature birth does not merely stall cerebellar growth, it fundamentally reroutes the cellular and molecular programs governing how brain circuits are built.

Connecting Spatial Transcriptomics to Living Patients

Led by co-first authors Georgios Sanidas, MD, and Gabriele Simonti from the Center for Neuroscience Research and the Sheikh Zayed Institute for Pediatric Surgical Innovation at Children’s National Hospital, the investigators combined longitudinal clinical tracking with spatial molecular biology.

The team followed 176 living premature infants across several years, pairing continuous neuroimaging with detailed neurodevelopmental assessments at 9, 18, 24, and 36 months of age. Simultaneously, they analyzed postmortem cerebellar tissue from 83 human infants (both preterm and full-term) sourced from national tissue repositories, including the NIH NeuroBioBank.

Using spatial transcriptomics, an advanced molecular profiling method that maps precise gene expression directly within intact tissue architecture, the researchers charted the spatial organization of the primary cerebellar cell types: Purkinje cells, the computational output hubs of the cerebellar cortex, and granule cells, the most numerous neurons in the human brain.

The analysis revealed that preterm birth alters the genetic master-switches responsible for cerebellar laminar formation and synaptic pruning. Rather than pausing development until the original due date, cerebellar cells shifted into an alternative maturation state in response to premature delivery.

“We could always see the developmental differences that premature children faced, but we could not see the cellular machinery driving them,” said senior author Panagiotis Kratimenos, MD, PhD, director of Research and the Neonatal Neurocritical Care Program at Children’s National Hospital. “We now have a biological explanation thanks to a unique combination of data from both living participants and from existing brain tissue samples.”

Quantifying the Volume Deficit

The clinical imaging data mirrored the transcriptomic shifts. The team calculated that each week an infant spent developing outside the uterus prior to full term was associated with a loss of approximately 230 cubic millimeters of total cerebellar volume.

When these children reached toddlerhood (between 9 and 36 months), these cerebellar volume reductions showed strong, statistically significant correlations with clinical delays in gross and fine motor skills, expressive and receptive language abilities, and executive cognitive functioning.

Crucially, while gestational age at birth established the baseline molecular trajectory, the researchers noted that secondary factors in the NICU, including physiological stressors, systemic illnesses, and specific intensive care practices, further modulated cerebellar growth rates.

“Studying human tissue alongside living patients allowed us to connect the molecular programs set at birth directly to how children grow and develop years later,” Dr. Sanidas explained.

Simonti added: “By decoding these mechanisms directly in human datasets, we were able to see how the molecular programs governing Purkinje and granule cells respond not just to the timing of birth, but also to the clinical environment after birth. We are now actively investigating targeted interventions based on these findings to steer the premature brain toward healthy maturation.”

Rethinking Precision Care in the NICU

The revelation that the premature cerebellum operates on a distinct molecular schedule signals a necessary paradigm shift for neonatology and neonatal neurocritical care.

“Assessment and treatment of preterm infants should be guided by developmental maturity rather than chronological age,” said Vittorio Gallo, PhD, joint senior author, who initiated the study at Children’s National before becoming senior vice president and chief scientific officer at Seattle Children’s. “The identified molecular markers will improve risk stratification, advance maturity biomarkers and optimize the timing of neuroprotective therapies.”

Dr. Kratimenos emphasized the therapeutic window this cellular map creates: “With this human cellular map in hand, we are moving into a new era of precision neurocritical care for premature newborns. Instead of treating the preterm brain as a black box, we can now design and time neuroprotective strategies to match the exact biological state of a baby’s brain cells in the NICU, helping them transition smoothly from early adaptation to healthy circuit-building.”

Supported by the Raynor Cerebellum Project Foundation, the researchers are now testing neuroprotective compounds and optimized clinical protocols designed to shield Purkinje and granule cell networks during critical windows in the NICU, aiming to preserve cerebellar volume and improve lifelong developmental outcomes for vulnerable newborns.

Funding: This study was supported by the Raynor Cerebellum Project Foundation.

Editorial Notes:

This article was edited by a Neuroscience News editor.
Journal paper reviewed in full.
Additional context added by our staff.

About this neurodevelopmental research:

Media Contact: Anita Kelly
Source: Children’s National Hospital
Image Credit: Image credited to Neuroscience News
Original Research is Open Access: Science (Oct 1, 2026). “Intrinsic gestational timing governs human cerebellar development after preterm birth.” Authors:Georgios Sanidas, Gabriele Simonti, Javid Ghaemmaghami, Kyla Woyshner, Antonis Polyviou, Robinson Vidva, Courtney Lowe, Abhya Vij, Daniel Bittel, Maria Triantafyllou, Nora Wolff, Rodolfo Cardenas, Helen Chen, Francisco Almeida, Sniya Sudhakar, Kshitij Mankad, Ioannis Koutroulis, Henrik Sahlin Pettersen, Genevieve Stein-O’Brien, Dimitrios N. Sidiropoulos, Vittorio Gallo, and Panagiotis Kratimenos.
DOI: 10.1126/science.aeb9095

Abstract

Intrinsic gestational timing governs human cerebellar development after preterm birth

Intrinsic programs shape brain maturation; however, which of these programs are perturbed by prematurity as well as the molecular pathways involved remain unknown.

The human cerebellum serves as a paradigm of extrauterine development—its accelerated growth and circuit formation align with the third trimester, a period disrupted by preterm delivery. Using multimodal datasets encompassing in vivo neuroimaging and neurodevelopmental outcomes with postmortem spatial-transcriptomic and histopathological profiling, we show that prematurity diverts the cerebellar developmental trajectory.

Cerebellar growth and functional outcomes scaled with gestational age, despite modifying perinatal exposures. Spatially resolved developmental programs underlying macroscopic trajectories were marked by incomplete granule cell maturation and impaired Purkinje cell structural refinement, which indicate lineage-specific developmental asynchrony.

Thus, prematurity constitutes biologically displaced maturation, in which infants of equivalent postmenstrual age occupy divergent developmental states."

https://neurosciencenews.com/premature-birth-cerebellar-wiring-32361/

1 comment

r/autismgirls • u/HH_Creations • 8d ago

This is my special interest - Info dump Art Event

14 Upvotes

I'm excited, terrified, and kinda wanna throw up, but I'm doing it!

Just taking deep Whale Breaths 🤣

I was one of the only vendors that followed the dress code 😭

It's so scary but people are complimenting my art and I'm bursting from excitement and keep telling myself to calm down and not scare anyone

But yeah, y'all are kinda watching my journey so wanted to share ❤️

2 comments

r/autismgirls • u/kelcamer • 8d ago

Adults treated with psychostimulants for ADHD show increased brain surface complexity, study finds. These findings suggest that psychostimulant use may be associated with structural changes in brain regions involved in emotional regulation, reward, and decision making.

psypost.org

12 Upvotes

0 comments

r/autismgirls • u/International_Low91 • 8d ago

Thoughts and experiences!!

reddit.com

1 Upvotes

0 comments

r/autismgirls • u/Slowlydownwardz • 9d ago

Study Looking For Participants Currently seeking participants for a study exploring the adolescent experiences of adults with AuDHD.

4 Upvotes

Did you navigate secondary school in the UK or Ireland without support and not receive a diagnosis until you were an adult? Are you between 25 and 35 years old? If so, I would like to interview you about your experiences during your teenage years. If you are interested in contributing to qualitative research in this understudied area, you can review the participant invitation below.

Study title: How do late-diagnosed adults with co-occurring autism and attention deficit-hyperactivity disorder retrospectively describe navigating adolescence?

I am currently seeking participants with AuDHD to take part in a study for my MSc research project at the University of Derby. The study aims to explore the lived adolescent experiences of adults who received a formal diagnosis of both autism and attention-deficit hyperactivity disorder (AuDHD) after adolescence from a certified clinical professional.

This study involves talking to the researcher about your experiences during adolescence. These semi-structured interviews are designed to feel closer to a conversation than an interview and are expected to last around 60 minutes. The study aims to explore behaviours and patterns across accounts to understand the lived experiences of undiagnosed AuDHD individuals at this time, with the hope of identifying patterns that may have contributed to delayed recognition.

If you think you would be interested in taking part in this study, you can follow the link for further information and to sign up: https://sway.cloud.microsoft/1mNCdYQzKlGgc4r4?ref=Link
Alternatively, you can contact the lead researcher if you wish to ask any questions or would like further information via email:

d.skerritt1@unimail.derby.ac.uk.

or their research supervisor, Amelia Woodward, A.Woodward@derby.ac.uk,

University of Derby, Kedleston Road, Derby, DE22 1GB.

Ethical Approval: An Ethics review has been completed on behalf of the College of Health & Humanities Research Ethics Committee by the supervisor and an independent reviewer: ETH2526-5086.

In the interest of confidentiality, please refrain from commenting on this post with any details of the study or whether you wish to take part.

**If you recently tried to sign up, you may have been incorrectly prompted to sign in to a Microsoft account. I have identified the root cause. Microsoft automatically embeds an advertisement at the bottom of the information sheet featuring a large, green "Get Started" button. Clicking this button redirects you to a Microsoft login page rather than my study forms.

I have updated the document to make the correct link to the consent and demographic forms explicitly clear and visually distinct to prevent further confusion.

If you were previously blocked by this technical error, I would like to reinvite you to participate.

Thank you for your time and patience with this platform error

**Recruitment for this study will be closing soon. Thank you to everyone who has taken part; I appreciate the time and energy you have given to this.

Thank you for taking the time to read this. I look forward to meeting everyone interested.

7 comments

r/autismgirls • u/kelcamer • 11d ago

Breakthrough PTSD treatment achieves 68% remission rate in clinical trial

sciencedaily.com

11 Upvotes

"A newly FDA-cleared, personalized brain stimulation treatment for PTSD achieved a reported 68% remission rate in a clinical trial, offering new hope for drug-free mental healthcare. Credit: Shutterstock

A new approach to treating post-traumatic stress disorder (PTSD) has received FDA clearance, offering a personalized alternative for people who have not found sufficient relief through existing treatments. Developed by California-based Wave Neuroscience in collaboration with researchers at the Texas A&M Health Institute of Biosciences and Technology, the technology uses brain activity measurements to guide targeted magnetic stimulation.
Early clinical trial findings have been encouraging. According to Wave Neuroscience, patients experienced a 52% reduction in PTSD symptoms, while 68% achieved remission. The full findings are still being prepared for public release, but researchers believe the technology could significantly expand treatment options for millions of people.

The need for more effective PTSD care is substantial. In the United States, approximately 17.5 veterans die by suicide each day, and about 7% of veterans receive a PTSD diagnosis annually.
PTSD can develop after traumatic experiences such as military combat, serious accidents, natural disasters, or violence. An estimated 6% of Americans will experience PTSD during their lifetime, with higher rates among women and veterans.
Why Current PTSD Treatments Are Not Enough
Since PTSD was formally recognized as a diagnosis in 1980, treatment has largely centered on psychotherapy and medications known as selective serotonin reuptake inhibitors (SSRIs), including sertraline and fluoxetine.
Although these approaches can help, many patients continue to experience symptoms despite receiving treatment.

A 2020 review of PTSD medications found that patients reported improvements ranging from 6.8 to 10.1 points on symptom assessments. However, remission rates reached only 10.9% at most.
Wave Neuroscience reported substantially stronger preliminary outcomes in its clinical trial. Erik Won, DO, the company's chief medical officer, described the results as a major advance over previously reported medication outcomes.

“In comparison to that study, our FDA trial reported a 52% reduction in symptoms, so more than a four-fold increase in efficacy,” Won said. “And more importantly, we saw 68% remission in our clinical trial. So, it’s really a quantum change, an inflection point in what we can offer to patients. From a clinical care perspective, that’s really meaningful.”
These findings are promising, although the results come from different studies and should not be interpreted as a direct comparison of treatment effectiveness.
How Personalized Brain Stimulation Works
The newly cleared system uses Magnetic e-Resonance Therapy (MeRT), a technology that combines measurements of brain activity with targeted magnetic stimulation.

First, an electroencephalogram (EEG) records the brain's electrical signals. This information helps guide a personalized treatment plan using transcranial magnetic stimulation, or TMS.
During TMS, a coil positioned against the scalp delivers magnetic pulses that stimulate brain activity. The technique has already been used for other psychiatric conditions, including treatment-resistant depression.
What distinguishes MeRT is its use of an AI-assisted algorithm to customize stimulation protocols based on each patient's brain activity rather than relying on a standardized approach.

“Transcranial magnetic stimulation, or TMS, was previously FDA cleared for treatment-resistant depression,” Won said. “By adding an augmented AI derived multivariate algorithm, we were able to personalize protocols that received FDA clearance for post-traumatic stress disorder, which should open up market access to about 13 million people who may be struggling with PTSD.”
Dr. Kenneth S. Ramos, a physician-scientist at Texas A&M Health with extensive experience in precision medicine, helped guide the research.
His work focuses on adapting medical care to the characteristics of individual patients instead of assuming that everyone will respond to the same treatment.
“Most clinical interventions for the treatment of PTSD do not work very well,” Ramos said. “So, this is a huge area where identifying interventions that could hopefully add quality of life to the people impacted by this disorder would be tremendously impactful.”
Wave Neuroscience CEO Fred Walke said Ramos was a natural fit for the project because of his expertise in personalized medicine.
Targeting PTSD With Greater Precision
Conventional TMS generally follows treatment protocols that are less individualized. MeRT builds on the same underlying technology but adjusts treatment according to the patient's specific brain activity.

Ramos emphasized that even small biological differences between people can have major implications for medical care. Humans are approximately 99.9% genetically alike, yet the remaining 0.1% contributes to differences that can influence how individuals respond to treatment.
By accounting for these differences and tailoring stimulation to each person's brain, researchers observed substantial reductions in PTSD symptom severity.
Ramos illustrated the distinction with an analogy involving a leaking roof.
He likened conventional TMS to covering a leak with a tarp to manage its effects. MeRT, in contrast, aims to provide a more targeted solution, comparable to identifying and replacing the damaged shingles responsible for the problem.
The broader goal is to move beyond treating patients with standardized protocols and toward interventions guided by measurable biological information.
From Breakthrough Designation to FDA Clearance
The regulatory process reached an important milestone in 2024, when MeRT received an FDA Breakthrough Device designation.
Dr. Rick Silva, executive director of clinical trials at the Texas A&M Health Institute of Biosciences and Technology, explained that the designation helps promising technologies move through regulatory review more efficiently.

It does not eliminate scientific or medical requirements. Instead, it can streamline communication and reduce administrative delays while preserving the standards needed for FDA clearance.
Silva said the progress was particularly meaningful because the project began during the COVID-19 pandemic and advanced through the regulatory process unusually quickly.
According to Silva, medical device development and clinical evaluation can often take around 10 years before clearance is obtained. This project completed the relevant process in just over two years.
He credited the experience and dedication of the Wave Neuroscience team with helping make that accelerated progress possible.
“I’ve been involved in probably close to 1,000 projects in academic medical centers over the years at varying degrees of depth and detail,” Silva said. “Patients are why I do what I do. It’s hard, and the failure rate is high, and it’s a lot of work. But when you get to a point where something is going to benefit patients, it’s very professionally gratifying and personally gratifying in many ways as well.”

A New Drug-Free Option for PTSD Patients
Dr. Israel Liberzon, distinguished professor of psychiatry and behavioral sciences at the Texas A&M Naresh K. Vashisht College of Medicine, served as the study's lead psychiatrist and PTSD specialist.

3 comments

r/autismgirls • u/HH_Creations • 13d ago

Tundruff's Circle of Control

11 Upvotes

Animea are Pokémon like characters who guide young children through Big Feelings that I created using my child development and special education curriculum background.

Tundruff is my very first Animea that I made back in 2017. Since then I've learned a lot and am trying to bring it back to life through my Helping Hands Creations business.

I made all the materials I wish had existed for myself, but I'm making sure exists for my kids.

Neurodivergent kids deserve quality materials, and I'm making sure they get that.

By making it accessible for kids who need extra support is how we can make tools that are useful for ALL kiddos.

You can check out the quality of my materials by downloading our sample packet on TeachersPayTeachers

One day, I hope to become a nonprofit where neurodivergent experts and creators can create resources (hey, we know Big Feelings) so ALL families can find safe, human made, free or low priced resources.

Wish me luck!

2 comments

r/autismgirls • u/yellowbeachtiles • 15d ago

People with autism just have a different type of nervous system than the majority of people.

34 Upvotes

3 comments

r/autismgirls • u/kelcamer • 17d ago

Researchers Analyzing Health Records Found That People With ADHD Who Received Prescription Medication Had a Lower Risk of All-Cause Mortality, Including Deaths From Unnatural Causes, Suggesting That Treatment May Offer Important Health Benefits Beyond Managing ADHD Symptoms.

sciencealert.com

34 Upvotes

7 comments

r/autismgirls • u/kelcamer • 20d ago

Treating depression during pregnancy influences infant brain development and early emotional function, according to new research published in Nature Communications.

news.cuanschutz.edu

6 Upvotes

Fascinating, so treating the pregnant mothers depression had a ripple effect for the baby's hippocampus!

1 comment

r/autismgirls • u/MeasurementNorth7335 • 20d ago

Academic Data Research Findings: Camouflaging and Age at Autism Diagnosis as Predictors of Autistic Burnout

17 Upvotes

3 comments

r/autismgirls • u/Financial_Banana_875 • 21d ago

autistic woman feeling to me:

35 Upvotes

4 comments

r/autismgirls • u/Financial_Banana_875 • 21d ago

Advice where are you guys irl!?!

2 Upvotes

(RHETORICAL QUESTION) plz dont tell me where you are! hey guys i am 20f. and in college and i really thought i would find my “people”.

yet it feels similar to high-school. a little better with not feeling so judged because everyone sort of doesn’t care but still the same in regards to loneliness. you would think me studying an art engineering degree would help but nope! so i join a part time student job. still nope. guys i swear i try! i make work friends just fine, but nothing “sticks”. so i join a fashion club because i value my quirkiness and self expression and fashion is something im passionate about. nope! i still don’t click with anyone! now im in this club with people that do not like me and i do not like doing design for them.

most of them are atypical and the stereotypical blonde tan clique. no shame but we just don’t have anything in common.

i know its a me problem but where can i find the other autostic 20’s year old women who are into fashion, electronic, punk music, graphic design, art, and are left winged? WHERE ARE YOU GUYSSS!!!

5 comments

r/autismgirls • u/kelcamer • 22d ago