Pramila Srinivasan, Ph.D is President and Board Member of BRAIN Foundation. She is also an entrepreneur in the healthcare industry and supporter of medical research.

Jeremy Veenstra-VanderWeele MD is William and Joy Ruane Professor of Pediatric Psychopharmacology; Associate Vice Chair and Director of the Division of Child and Adolescent Psychiatry and Developmental Sciences Columbia University College of Physicians and Surgeons; New York State Psychiatric Institute, NewYork-Presbyterian Hospital Center for Autism and the Developing Brain

Dr. Veenstra-VanderWeele is a child and adolescent psychiatrist who uses molecular and translational neuroscience research tools in the pursuit of new treatments in neurodevelopmental disorders. His molecular neuroscience laboratory at Columbia University and the New York State Psychiatric Institute focuses on genetic mouse models with abnormal social or repetitive behavior. His clinical/translational research program at the NewYork-Presbyterian Hospital Center for Autism and the Developing Brain studies potential interventions in autism and related genetic syndromes.

Dr. Veenstra-VanderWeele co-leads the Columbia University Autism Center of Excellence and leads the New York site of the ARIA IMPACT Network. He chaired the Developmental Brain Disorders Study Section for the National Institutes of Health from 2021-2023. His work has garnered multiple awards, including the George Tarjan Award for Contributions in Developmental Disabilities from the American Academy of Child and Adolescent Psychiatry.

Abstract:
Autism spectrum disorder describes a shared behavioral outcome rather than a single biological condition, and this heterogeneity remains the central challenge for both research and clinical care. Integrating genetic, neurobiological, and behavioral perspectives requires humility, since the medical model and the neurodiversity perspective can pull in different directions. Progress depends on listening to autistic people and families alongside science. This talk will briefly survey key challenges and opportunities for the field, organized around four themes. First, on current treatment, the evidence base is more limited than often assumed: early intensive behavioral and developmental interventions (such as UCLA/Lovaas-based and Early Start Denver Model approaches) show moderate evidence for improving cognitive, language, and adaptive outcomes in some children, while pharmacologic options are well supported only for associated symptoms rather than core features. Second, placebo response in autism trials is substantial and instructive. The rise and fall of secretin, and more recently oxytocin, illustrate how uncontrolled enthusiasm can outpace controlled evidence, underscoring the need to distinguish change due to treatment from change during treatment. Third, a new generation of promising trials reflects growing methodological rigor that has already yielded an FDA approval in Rett syndrome, with other approvals likely in the next five years. Finally, genetic medicine is emerging rapidly for single-gene syndromes associated with profound autism, raising the prospect that sequencing-based newborn screening could someday enable intervention before developmental symptoms appear, potentially bypassing today’s diagnosis-first treatment pathway entirely.

Dr. Hoffman is a child, adolescent, and adult psychiatrist who primarily works with the Immune Behavioral Health (IBH) clinic at Stanford University. Kevin completed his Bachelor’s degree at Haverford College. He then moved to New York to complete combined MD and PhD degrees at the Icahn School of Medicine at Mount Sinai, where his dissertation research in the department of microbiology was focused on how the immune system responds to viral neuroinvasion. Kevin returned to Pennsylvania for his psychiatry residency at the University of Pennsylvania and child and adolescent psychiatry fellowship at the Children’s Hospital of Philadelphia. As a resident and fellow, Kevin developed clinical interests in the overlap between medical and psychiatric illness, particularly with regards to neurodevelopmental and psychotic disorders. He also maintained research interests in the same areas, publishing on the influence inflammatory disorders and physiologic stress have on children’s mental health. Kevin has continued to pursue these interests at Stanford, where he works with children with combined immunologic and psychiatric illness, with special focus and research interests in areas of autism and psychosis.

Abstract:
Autistic children can experience the same illnesses and discomforts as any other child, yet changes in behavior, sleep, appetite, communication, or participation may be their clearest way of showing that something is wrong. Because differences in sensory processing, communication, interoception, and baseline behavior can make symptoms harder to recognize, medical concerns are sometimes mistaken for “just autism” or a behavioral problem. This talk will help parents and caregivers consider when a sudden or meaningful change may warrant a medical evaluation. We will review why identifying pain and illness can be especially challenging, including limited access to internal sensations, atypical expressions of distress, diagnostic overshadowing, and the difficulty of separating longstanding traits from new symptoms. The presentation will summarize commonly co-occurring medical concerns reported in autistic children, such as gastrointestinal problems, sleep disorders, seizures, feeding difficulties, constipation, dental pain, headaches, allergies, and other conditions. Parents will learn practical clues that should prompt timely discussion with a clinician: abrupt regression or loss of skills; new self-injury, aggression, agitation, or withdrawal; persistent changes in sleep, eating, toileting, energy, movement, or mood; unexplained crying; episodes of staring or altered awareness; recurrent vomiting, constipation, diarrhea, pain behaviors, fever, weight change, or reduced activity. We will also discuss how to prepare useful observations for appointments, including a timeline, videos when appropriate, medication and diet changes, and patterns linked to meals, sleep, environments, or menstrual cycles.

Ahmed Z. Obeidat, MD, PhD, is an Associate Professor of Neurology, Vice Chair for Academic Affairs, and Chief of the Multiple Sclerosis and Neuroimmunology Program at the Medical College of Wisconsin, where he founded Wisconsin’s first neuroimmunology and MS fellowship and directs the INTERTWINE Laboratory. He is Secretary of the Consortium of Multiple Sclerosis Centers, President-Elect of the Wisconsin Neurological Society, and Editor-in-Chief of GENERATIONS. His research advances therapies for MS, NMOSD, MOGAD, and autoimmune encephalitis; he is principal investigator on more than 25 active clinical trials and has authored more than 80 publications. He lectures on neuroaesthetics and the role of the arts in neurological care.

Abstract:
When a child or young adult suddenly changes, showing new anxiety, unusual behaviors, loss of skills, confusion, or withdrawal from the world, families are often told it is “just psychiatric.” But sometimes the immune system is part of the story. Inflammation affecting the brain can mimic a psychiatric illness, and recognizing it early can change outcomes. In this talk, we will explore, in plain language, how doctors distinguish between a primary psychiatric condition and one driven by inflammation: the warning signs that prompt a deeper look, the tests we use (blood work, spinal fluid, brain imaging, EEG), and the treatments available when the immune system is involved. Drawing on published research and cases from my own practice, I will share what recovery can look like, why persistence matters, and how families, who know their loved ones best, play a central role in reaching the right diagnosis.

Dr. Samuel J. Pleasure is a neurologist who has expertise in caring for patients with epilepsy as well as years of experience in managing a variety of neurological conditions in both clinic and hospital settings. Pleasure is the Glenn W. Johnson, Jr. Memorial Endowed Chair in Neurology at UCSF.

Abstract:
Regression in children with autism can be devastating – leading to major loss of functional capacity, severe psychiatric morbidity and difficult to manage behavioral syndromes. We know that regression can occur in response to physiologic stress following infections or metabolic stress. Things that should absolutely lead to evaluation by a neurologist include changes in level of consciousness, new or changed patterns of seizures, focal neurologic symptoms (eg new balance problems, weakness, changes in vision). With regard to brain inflammation in autism it is also important to remember that autism is also frequently associated with changes in immune responsiveness and that this may lead to autoinflammatory conditions which may require specialized treatments. Our research is focused on identifying humoral (autoantibody) autoimmune phenomena associated with autism and with regression in autism in hopes that we may find treatable causes to help restore function in these children.

Craig J. Rouskey, MSc is co-founder and Chief Executive Officer of Flore Inc., a test-to-treat gut health company that builds a personalized intervention from each person’s own microbiome data. Trained in molecular microbiology and immunology, Craig has been engineering the microbiome since 2005, with earlier roles at Avant Immunotherapeutics and Pando Nutrition. In 2026 Flore Inc. acquired Sun Genomics, bringing with it nine years of paired microbiome and outcome data across more than 18,000 people, 23,000+ sequenced microbiome tests, and 40,000+ personalized formulations. Flore’s precision synbiotics have been evaluated in a peer-reviewed pilot open-label study in autism spectrum disorder, published in mSystems (ASM, 2024), with additional clinical trials now underway.

Abstract:
Autism is diagnosed by behavior, but the chemistry underneath it is not one thing. Two children with the same label can carry gut communities that look nothing alike — and where the mechanism differs, one intervention cannot serve both. This talk presents what we found when we stopped sorting children by diagnosis and started sorting by what their gut can metabolically do. Reanalyzing 768 autistic and neurotypical metagenomes, we found an eight-species Firmicutes consortium enriched more than twentyfold that carries none of the relevant enzymes. It enriches substrate and cofactors instead, setting conditions for rarer organisms to act. What follows is a layered system rather than a list of markers. Tryptophanase is the gate — elevated in 96.5% of autistic samples against 51.7% of controls, but carried so diffusely that no single organism can be removed. Lysine decarboxylase is the amplifier, and E. coli carries most of it, which is what makes it targetable. Together the two produce a dose-response: above the 95th centile on both, no neurotypical sample remains. That asymmetry shapes the study now recruiting. One hundred participants aged 7 to 35, stool and urine at entry and at six months. Stage 1 uses a precision synbiotic aimed at the amplifier. Stage 2, in adults only, asks whether a bacteriophage against the same organism goes further, read out as urinary indoxyl sulfate. The work is hypothesis-generating and ethics review is pending. I will be candid about both.

Dr. Niesen is president of AMS Therapeutics and runs a busy child neurology practice in Pasadena, CA. He is a former Associate Professor of Neurology and Pediatrics at the Geffen UCLA School of Medicine and Cedars-Sinai Medical Center in Los Angeles, CA. He received his medical degree from the Sackler School of Medicine, Tel Aviv University in Tel Aviv, Israel and his undergraduate degree from Cornell University. His research interests include language development in autism, seizure resolution in genetic epilepsies and role of ketone bodies in seizure management. He has received funding from NIH, University of Southern California Faculty Fund, Children’s Hospital
Los Angeles Board of Trustees and the Brain Foundation. He is married with 2 children.

Abstract:
Quantitative EEG (qEEG) analysis has been used to characterize brain functional connectivity (FC) in autism spectrum disorder (ASD), though consistent changes have been difficult to verify. In this study, we use qEEG techniques to compare EEG patterns in children with ASD before and after treatment with ethosuximide (ETS), a medicine we have shown to improve language and social behavior in ASD children. Subjects between the ages of 6-12 years old are randomized to receive either ETS or placebo with routine EEG testing before and after treatment. Three different qEEG metrics-coherence analysis, aperiodic slope analysis, and directed asymmetry index (DAI), were used to study brain FC and excitatory balance. We have compared these metrics in 20 children with autism and 14 typically developing children and evaluated the effects of ETS in 6 ASD children. We found more hypoconnectivity in frontal, central and temporal regions in children with ASD compared to TD children, while posterior networks showed hyperconnectivity. We identified a novel subgroups in ASD with distinct speech and oromotor features. Because of unclear speech and difficulty repeating words, they were determined to have speech apraxia. Functional connectivity in these children showed hyperconnectivity in fronto-central areas and asymmetric connectivity in left-right temporal lobes. Treatment with ETS showed selective action in improving FC in left frontal-central networks and reducing posterior hyper-connectivity. These findings identify potential qEEG biomarkers that can lead to a more reliable diagnosis, classification and treatment of autism.

Dr. Richard Jin is a board-certified adult psychiatrist and a psychiatrist-scientist at the University of California, San Francisco (UCSF), where he specializes in caring for patients with concurrent neuropsychiatric symptoms and neuroinflammatory or autoimmune disorders. He manages an outpatient consultation clinic for adults and children with these overlapping conditions. His primary research interest is in understanding how immune responses in the brain impact behavior. Dr. Jin received his M.D. and Ph.D. in Microbiology and Immunology from the Jacobs School of Medicine and Biomedical Sciences, where his graduate work focused on the regulation of tissue-specific immunity in chronic infection and sterile injuries. He completed the UCSF Psychiatry Research Resident Training Program with an Area of Distinction in Clinical Neurosciences and served as Chief Resident for Research. Following residency, he treated complex and refractory psychiatric conditions as a provider on the UCSF ECT service. He is now pursuing specialty training in Child and Adolescent Psychiatry at UCSF while studying the effects of early-life viral infection on brain development and behavior in the laboratory of Dr. Anna Molofsky. His research is supported by the A.P. Giannini Foundation and a UCSF Weill Clinician-Scientist Award.

Dr. Hoffman is a child, adolescent, and adult psychiatrist who primarily works with the Immune Behavioral Health (IBH) clinic at Stanford University. Kevin completed his Bachelor’s degree at Haverford College. He then moved to New York to complete combined MD and PhD degrees at the Icahn School of Medicine at Mount Sinai, where his dissertation research in the department of microbiology was focused on how the immune system responds to viral neuroinvasion. Kevin returned to Pennsylvania for his psychiatry residency at the University of Pennsylvania and child and adolescent psychiatry fellowship at the Children’s Hospital of Philadelphia. As a resident and fellow, Kevin developed clinical interests in the overlap between medical and psychiatric illness, particularly with regards to neurodevelopmental and psychotic disorders. He also maintained research interests in the same areas, publishing on the influence inflammatory disorders and physiologic stress have on children’s mental health. Kevin has continued to pursue these interests at Stanford, where he works with children with combined immunologic and psychiatric illness, with special focus and research interests in areas of autism and psychosis.

Abstract:
Catatonia is a complex neuropsychiatric syndrome characterized by a severe disruption in motor function and behavior, ranging from complete immobility (stupor) to frantic, purposeless movement (excitement). While catatonia is a rare neuropsychiatric condition in the general population, it is highly prevalent in autism spectrum disorder (ASD), affecting ~10% individuals with ASD. Differentiating catatonia from baseline autism is exceptionally challenging due to overlapping traits, often leading to diagnostic overshadowing and delays in care. This presentation focuses on equipping both families and providers with the core knowledge needed to suspect this treatable syndrome and access effective care. First, we describe the clinical range of catatonia symptoms and etiologies, with special considerations in autism. Second, we address the diagnostic challenges of identifying catatonia in ASD. Attendees will learn how to start to distinguish stable, developmental baseline traits from a new catatonic syndrome. Finally, we outline gold-standard and emerging treatment options. We will review the evidence-based treatment hierarchy, starting with first-line cornerstones. By bridging clinical evidence with the lived experience of caregivers, this talk empowers families and clinicians to collaborate as active partners in identifying catatonia and seeking treatment.

Dr. Shebani Sethi is a Clinical Associate Professor at Stanford Medicine and the founding director of the university’s Metabolic Psychiatry Program, the first academic clinic to formally unite nutrition, metabolism, and mental health care. Dr. Sethi is board-certified in both psychiatry and obesity medicine and leads NIH and foundation-funded clinical trials on nutritional and metabolic interventions. She is an entrepreneur and the founder of Metabolic Psychiatry Labs, a clinical platform translating research into accessible, real-world care through a tech-enabled model designed to expand access to metabolic psychiatry. Dr. Sethi coined the term Metabolic Psychiatry in 2015 to describe this emerging field, whichaddresses metabolic dysfunction, including insulin resistance, inflammation, and mitochondrial impairment, as a root cause of mental health conditions such as depression, anxiety, bipolar disorder, and schizophrenia. Her work has been featured in The New York Times, NPR, Forbes, Good Morning America, and recognized as one of Stanford’s Top 10 Scientific Advancements of 2024.

Abstract:
Autism spectrum disorder (ASD) and serious mental illness (SMI) are associated with substantial clinical and socioeconomic burdens, while metabolic dysfunction, including obesity, insulin resistance, dyslipidemia, hypertension, and inflammation, is increasingly recognized across these conditions. This presentation examines the emerging field of Metabolic Psychiatry, which considers metabolic dysfunction in the body and brain as a potential contributor to neuropsychiatric symptoms and a therapeutic target. Shared metabolic mechanisms across ASD and SMI include altered brain energy metabolism, mitochondrial dysfunction, oxidative stress, disrupted amino acid and neurotransmitter metabolism, and inflammatory signaling. Conventional treatments for SMI, while often effective and life-saving, may also contribute to metabolic adverse effects and complicate long-term health outcomes. Metabolic Psychiatry therefore offers a complementary framework that integrates metabolic assessment with psychiatric care and explores interventions targeting metabolic dysfunction. The presentation reviews ketogenic metabolic therapy (KMT) and metabolic pharmacotherapy, with emphasis on emerging clinical evidence. Small clinical studies in ASD, including the University of Hawaii pilot study, have reported improvements in core autism features alongside associations between metabolic biomarkers and clinical outcomes. Evidence from the Stanford pilot study and a completed UCSF randomized controlled trial in SMI demonstrates improvements in metabolic health, psychiatric symptoms, cognition, and sustained ketosis. The presentation concludes with clinical implications for clinicians and families and identifies research priorities, particularly larger randomized controlled trials involving individuals with ASD and co-occurring SMI. Integrating metabolic assessment and evidence-based metabolism-focused interventions may represent an important emerging direction for improving brain and metabolic health.

Dr. Pace is a physician-scientist specializing in neuroimmunogastroenterology, with expertise in diagnosing and treating complex multisystem disorders involving the neuroimmune axis. She serves as Director of the Neuroimmune Axis Disorders Program at Meliora Bio, where she leads initiatives in precision diagnostics and personalized medicine. As Chief Medical Officer at Meliora Genomics, she leverages whole genome sequencing to further advance the diagnosis of neuroimmune axis Disorders. Dr. Pace is board certified in Internal Medicine and Gastroenterology through the American Board of Internal Medicine, and Autonomic Disorders through the United
Council for Neurologic Subspecialties. Additionally, she has formalized clinical training in Neurogastroenterology and Medical Genetics, and a PhD in Neuroscience. She has been part of the NIH Undiagnosed Diseases Network (2017-2024) and is a former NIH Building Interdisciplinary Careers in Women’s Health (BIRCWH) Scholar. To date she
has published over 150 peer reviewed scientific articles.

Abstract:
The gastrointestinal tract is the largest interface between the nervous, immune, and endocrine systems. The neuroimmune axis mediates multidirectional communication between these systems, maintaining mucosal integrity, regulating barrier permeability, motility, and secretion, and coordinating local and systemic immune responses. Dysregulation of this axis contributes to a range of gastrointestinal, neurological, immune, and connective tissue disorders that frequently present as overlapping, chronic multisystem conditions. Viewing neurogastrointestinal disorders through the lens of the neuroimmune axis clarifies their underlying biological drivers and supports selection of true disease-modifying therapies rather than symptom-directed treatment. Achieving precision medicine in this space requires advanced diagnostics, including whole genome sequencing, deep immune profiling, and confocal laser endomicroscopy (CLE), paired with targeted immune- and nervous-system-modifying therapies. Together, these tools enable more accurate diagnosis and more effective treatment of these complex, life-altering conditions.

Dr. Bauer is board-certified in both General Pediatrics and Pediatric Hospital Medicine. She first came to Stanford for her pediatric residency, and for the past 15 years she has worked at Stanford Children’s Hospital, as a community physician. She cares for a wide range of patients, both healthy and sick newborns, as well as hospitalized children and young adults, and works closely with the Stanford Immune Behavioral Health Clinic team. As an Adjunct Clinical Associate Professor at the Stanford School of Medicine, she teaches medical students and residents. Dr. Bauer is transitioning into private practice this fall at the Maison Medical Group, where she will continue to care for children, with a focus on personalized care. She previously served on the San Francisco Firefighters’ Cancer Prevention Foundation board, which was instrumental in changing consumer laws that allowed the removal of toxic chemicals from children’s products, including mattresses and car seats.

Abstract
When behavior suddenly changes in an autistic child, there are a variety of possible causes and determining the actual cause can sometimes be challenging. This session focuses on two key areas that may lead to sudden changes — (1) pain/discomfort and (2) infection. Together we will review what physicians think through as they evaluate your child for behavior changes, discuss red flags that should prompt more urgent evaluation, and discuss common infections that may lead to these sudden changes. Most importantly, parents should leave knowing they are a key part of the care team, and their role is often critical in finding the root cause.

Dr. Jennifer Frankovich is a Clinical Professor in the Department of Pediatrics, Division of Allergy, Immunology Rheumatology (AIR) at Stanford Children’s Hospital. Her clinical expertise is in systemic inflammatory and autoimmune diseases that co-occur with psychiatric symptoms. She completed her training in general pediatrics, pediatric rheumatology, and clinical epidemiology at Stanford School of Medicine/Stanford Children’s Hospital. For the past 12 years she has directed a multidisciplinary clinic and research program to study PANS and related psychiatric deteriorations. To facilitate basic science discoveries, she created a longitudinal biorepository of patient and control biospecimens along with clinical data. She is collaborating with ~10 basic science labs to understand the immune basis of psychiatric deteriorations.