The National Heart, Lung, and Blood Institute (NHLBI) of the National Institutes of Health (NIH) hosted a two-day virtual workshop titled “Neurodevelopmental Disorders and Sleep” on Thursday, May 15, and Friday, May 16, 2025. The goals of this workshop were (1) to survey what is known about sleep and neurodevelopmental disorders (NDDs) and to define actionable gaps in knowledge to prioritize areas for future research; (2) to facilitate translation of preclinical (animal model) studies to clinical applications; (3) to promote a better understanding of the development of sleep regulation during neurotypical development as a framework to understand how developmental trajectories differ in NDDs (in both human and animal model studies); (4) to uncover factors that can distinguish vulnerability versus resilience when it comes to sleep loss; and (5) to promote dialogue and collaboration among investigators who work in the fields of sleep and NDDs.

Speakers from academia, clinical practice, and patient advocacy groups discussed associations—and potential causal relationships—between sleep and NDDs such as autism, epilepsy, attention-deficit/hyperactivity disorder (ADHD), and Down syndrome (DS). Presentations suggested that the majority of NDDs are associated with sleep disturbances and that poor sleep frequently correlates with more severe NDD symptoms.

Agenda

View the workshop agenda.

NIH VideoCast

Day 1: https://videocast.nih.gov/watch=56860
Day 2: https://videocast.nih.gov/watch=56861

Background

High-quality sleep in sufficient quantities is necessary for good health. Poor sleep quality across the life course, particularly at critical developmental stages, correlates with the onset, presentation, and severity of many NDDs, including autism spectrum disorder (ASD), attention deficit hyperactivity disorder (ADHD), Down syndrome (DS) and epilepsy.

Almost all NDDs are associated with prominent sleep disturbances, including sleep onset insomnia, delayed sleep onset, shorter sleep duration, night awakenings, poorer sleep quality, greater overall arousal, sleep maintenance insomnia, obstructive sleep apnea (OSA) and other sleep-related breathing disorders, daytime sleepiness, and nocturnal seizures. In many cases, poor sleep correlates with more severe NDD symptoms—and vice versa—suggesting bidirectional relationships between sleep and NDD etiologies and symptom severity. Poor sleep can create additional burdens and reduced quality of life for individuals with NDDs, their families, and their caregivers.

In addition to clinical interventions directly addressing NDDs, medical treatments (including pharmaceutical interventions, medical devices, and some surgeries), behavioral interventions, and other practices can help to improve sleep in individuals with NDDs. Often, improving sleep alleviates NDD symptom severity, and vice versa. Ongoing research into sleep and NDDs—including research with model organisms, behavioral genetics research, cohort-based studies, and big-data approaches—strives to enrich the current mechanistic understanding of the interrelations between NDDs and sleep and to inform development of effective treatments.

Summary

Overview of Neurodevelopmental disorders and Sleep

Sleep is critical for memory, learning, and physical, neurological, and cognitive development. Better sleep efficiency in the first few years of life is associated with more advanced executive function, whereas frequent night wakings are associated with poorer cognitive function and poorer performance on working memory tasks. Sleep problems are common in individuals with NDDs, and sleep disturbances can negatively affect emotional regulation, core NDD symptoms, and daytime behavior. However, in some cases treating sleep problems with supplemental melatonin, medications, behavioral interventions, and other practices can improve core NDD symptoms, mood, and quality of life.

Multifactorial contributions to sleep problems in individuals with NDDs include genetics, arousal dysregulation, and any circadian disruption. In addition, many medicines that treat NDDs or prevent associated seizures are stimulants that can affect sleep. For some patients, simple behavioral and environmental interventions can improve sleep for individuals with NDDs. These practices can avoid the repetitive cycle of hyperarousal and sleeplessness experienced by many with NDDs, and can be particularly effective for individuals with autism and other NDDs who are able to adhere to regular routines. More research is required, and deepening the understanding of the neurobiological underpinnings of sleep might inform future treatment approaches to improve sleep in patients with a variety of NDDs.

Key Themes and Opportunities:

• Sleep problems are common in children and adults with NDDs, and addressing sleep problems in these individuals could improve core NDD symptoms, mood, and quality of life.
• Supplemental melatonin, other medications, behavioral therapies, and other practices may be effective for improving sleep in individuals with NDDs. More research is needed into the side effects and long-term effects of medications, as well as toward developing effective treatment regimens integrating medication, behavioral approaches, and individual- and family-centered outcomes.

Common Human Disorders

Evidence suggests that most common NDDs are polygenic in origin and subject to a variety of influences. For example, the underlying mechanisms of Autism and ADHD most likely include genes, the environment, and multiple aspects of brain function. NDD-related dysfunction in the brain and atypical connectivity can result in sleep disturbances. In autism research has shown that dysfunction in the thalamic reticular nucleus creates measurable EEG irregularities during non-REM (NREM) sleep and may contribute to insomnia and other sleep problems.

Thus, sleep disturbances and disorders are common among the symptomatology of many common NDDs and may include insomnias, sleep apnea and other sleep-related breathing disorders, restless leg syndrome, and others. Further, many NDDs—notably ADHD—impair the ability to adhere to a consistent sleep schedule and to experience high-quality sleep, which can worsen NDD symptoms, family stresses, and comorbidities such as depression. Sleep-related breathing disorders frequently co-occur with some NDDs. For example, the majority of individuals with DS experience OSA, and people with both DS and OSA frequently have more profound cognitive and behavioral disabilities with less favorable long-term outcomes.

Improving sleep quality and duration for individuals with NDDs remains a priority for clinicians, researchers, individuals with these disorders, and their families. For several disorders abnormal sleep patterns in neonates can predict developmental outcomes, and parents of these children identify sleep disturbances as a top priority for research. Simultaneously addressing both NDD-related sleep problems and core symptoms could serve as an effective yet challenging treatment strategy to improve sleep, behavior, NDD symptom severity, quality of life, and overall health. Non-pharmacological interventions such as cognitive behavioral therapy, good sleep hygiene practices, and treatments for sleep-related breathing disorders can improve sleep in individuals with NDDs.

Supplemental melatonin, herbal supplements, and medicines for improving sleep in individuals with NDDs (e.g., clonidine, trazodone, antihistamines such as hydroxyzine, and gabapentin) hold potential and warrant additional research. However, these supplements and medications raise some concerns, such as long-term effects, dependence, abuse, and parent and prescriber resistance.

Key Themes and Opportunities:

• Sleep problems are characteristic of almost all NDDs.
• Simultaneously treating sleep disturbances and NDDs can prove challenging. For example, medications for treating ADHD and epilepsy can function as stimulants that disrupt sleep, and compliance with continuous positive airway pressure (CPAP) treatment for sleep apnea is low among those with DS or NDDs that involve sensory sensitivities.
• Adapting traditional cognitive behavioral therapies and similar approaches for patients with NDDs and intellectual disabilities holds potential for improving sleep.
• Sleep studies, although potentially revealing, often prove to be challenging in individuals with NDDs, who may have difficulty sleeping in unfamiliar environments or while connected to equipment such as electroencephalogram (EEG) electrodes or actigraphs. Unobtrusive wearable devices and other new technologies can facilitate data collection and assessment.
• Studies involving polysomnography (PSG), EEG, actigraphy, and other objective measures of sleep demonstrate connections between atypical sleep patterns and NDDs, seizures, NDD etiology, and NDD symptom severity. These studies may identify signatures and other indicators of NDDs and sleep disturbances. They could also suggest novel therapeutic targets and other promising avenues for research.
• Future research might examine the efficacy of treating NDDs and sleep with novel treatments and other treatments, such as vagal or hypoglossal nerve stimulation, myofunctional therapy, anti-inflammatory medications, weight loss medications, dental approaches, atomoxetine and oxybutynin, and other pharmacological treatments for sleep-related breathing disorders.

Population, Environmental and Other Influences

Scientists study sleep using many tools (e.g., self-reporting, diaries, actigraphy, EEGs, peripheral signals, PSGs, and wearables), but analysis of sleep in individuals with NDDs can prove challenging and must account for many considerations and complications (e.g., the location of sleep measurement, developmental/maturational status of the subject, environmental factors, the social milieu, medical complexity, cognitive ability, sensory differences, co-occurring conditions, scalability, and the potential for analyses across data sets and different study types). Sleep problems may constitute an emerging feature of the onset of some NDDs, may contribute to the developmental cascade preceding the onset of NDDs, or may do both. Research could examine how these features differ across NDDs and across phenotypes of the same NDD.

Studies involving twins, other siblings, and other family members could deepen our understanding of the genetic underpinnings of NDDs such as autism, the heritability of these conditions, and the roles environmental and other factors play in the etiologies, presentations, and outcomes of these disorders. For instance, infants with elder siblings with autism are at higher risk for autism and other learning and developmental challenges. Thus, infant sibling study designs such as that of the Infant Brain Imaging Study (IBIS) may enable researchers to understand any alterations in brain development in individuals with autism. IBIS and similar studies involve magnetic resonance imaging (MRI) scans, developmental assessments, standardized questionnaires, and clinical assessments for autism and other NDDs. Although IBIS and some other studies did not initially include measures of sleep, follow-ups and other studies with these cohorts and other well defined and characterized populations are enriching data collection with information on sleep and sleep disturbances related to NDDs.

Cohort-based studies such as the INCLUDE (INvestigation of Co-occurring conditions across the Lifespan to Understand Down syndromE) Project and ECHO (Environmental influences on Child Health Outcomes) are observational, analytic studies that provide a framework to assess causal factors, such as those pertaining to the etiologies of DS and autism. Studies such as EARLI (Early Autism Risk Longitudinal Investigation) combine features of cohort studies and sibling studies to examine early development of children with a high risk of autism, to collect exposure data and biosamples, and to assess clinical outcomes. Population-based cohorts such as the Nurses’ Health Studies II and III have informed sleep studies in individuals with autism. Cohort studies of sleep in NDDs could illuminate the nature of sleep problems, their timing and persistence, contributory factors, their health impact, and effective interventions. These studies could analyze longitudinal and big data sets to yield insight into NDD mechanisms, which could in turn inform more targeted assessments and treatments over the life course.

Longitudinal analyses of the interrelationships among sleep, behavior, and brain development may be particularly relevant to developing treatments for NDDs and associated sleep problems. Individuals with NDDs tend to have atypical and often immature sleep trajectories over the life course, and individualized medicine approaches might help improve sleep in these populations.

Key Themes and Opportunities:

• Population-based studies, behavioral genetics studies, and cohort studies provide a wealth of information on NDDs, other learning and developmental disorders, sleep, environmental factors, genes, and longitudinal data to examine disease etiology, natural history, outcomes, and treatment.
• Many of these studies have shown that sleep problems often precede the onset of NDD symptoms and diagnoses. Research has also shown that several characteristics of sleep disturbances can predict future health outcomes. Early sleep interventions may prevent or mitigate future NDD symptoms, as well as the worsening of sleep problems.
• In DS and other NDDs, residual symptoms of sleep problems tend to persist even after treatment, often for anatomical reasons, and the consequent effects of treatment on health and function require additional evaluation.
• Future directions for research may include evaluating longitudinal relationships among populations with NDDs. These could include analyses of the associations between sleep problems in the first years of life and school-age sleep and behavior patterns. Analyses of associations between sleep problems and altered brain development trajectories in school-age children with ASD would also be highly informative.

Perspectives from Parents, Caregivers and Patient Advocates

This session featured two speakers: an ADHD specialist who herself has ADHD and a patient advocate who is the founder of CureSHANK and the mother of a 26-year-old man with Phelan McDermid syndrome (PMS). These presenters shared their insights on both personal experiences of living with ADHD and the challenges of parenting an individual who has a severe NDD.

Research has shown that the brains of those with ADHD have smaller pineal glands, produce less melatonin, and tend toward time-blindness and disruption of circadian regulation. Good sleep hygiene is necessary to address ADHD symptoms but is seldom sufficient. Those with ADHD and sleep problems often have problems with obesity, poor academic performance, poor work performance, other dysfunctions resulting from nonrestorative and irregular sleep, shorter lifespans, household and scheduling disruptions, restless leg syndrome and other movement disorders, stress-related insomnia, daytime sleepiness, OSA, and other issues. Melatonin supplements and a variety of non-pharmacologic approaches can improve sleep in those with ADHD.

PMS results from the mutation or loss of the SHANK3 gene, which is expressed in the brain at postsynaptic densities. Alteration of this gene has profound consequences, which can include speech problems, ADHD, ASD, impulsiveness and other behavioral problems, intellectual disabilities, seizures, gastrointestinal symptoms, and a variety of sleep problems including apnea and insomnia. Parents of children and adults with PMS report high caregiver burdens, stress, household disruptions, and sleeplessness. Identification of the genetic cause of PMS may permit identification of precision medicine approaches to treatment.

Key Themes and Opportunities:

• Treatments must consider how co-occurring conditions may also contribute to sleep disturbances. Clinicians could prioritize practices, treatments, and medications that address both sleep and co-occurring conditions.
• A bidirectional relationship appears to exist between sleep and NDD symptoms.
• More precise ways to measure sleep quality and quantity and to collect behavioral data in real time are needed. These methods must accommodate the needs of individuals with NDDs, who may not tolerate the equipment (e.g., EEG electrodes and actigraphs) traditionally used in sleep studies.
• Future research might also consider genotype-to-sleep-phenotype studies, sleep studies leveraging electronic health records, genotype-based intervention trials, and in-home studies involving novel non-contact devices such as nearables.

Rare Diseases and Genetic Syndromes

Rare NDDs include PMS, Angelman syndrome (AS), Rett syndrome (RS), 22q11.2 deletion syndrome (also known as DiGeorge syndrome [DGS] and velocardiofacial syndrome), fragile X syndrome (FXS), Smith–Magenis syndrome, Prader–Willi syndrome, and others. These less common NDDs share some common features, including sleep disturbances, and may respond to common treatments. However, each of these NDDs has a distinct etiology, often associated with single-gene mutations or chromosomal deletions or other irregularities, along with other factors.

AS stems from maternal deletions in or lack of expression of a region of chromosome 15, which frequently include UBE3A mutations. Subtypes of AS emerge from different deletions, mutations, and translocations in this region. Sleep problems in AS include abnormal sleep–wake cycles, insomnia, nighttime epilepsy and breathing disorders. AS care may include sleep studies, reflux treatment, tonsillectomy and adenoidectomy (T&A), CPAP, improved sleep hygiene, and sleep and anti-seizure medications. Ongoing research is examining novel treatments with topoisomerase inhibitor drugs, antisense oligonucleotides, viral vector therapy, artificial transcription factors, and hematopoietic stem cell therapy.

RS is an X-linked NDD caused by pathogenic variants in the methyl-CpG-binding protein 2 gene (MECP2) in over 95% of cases. RS mainly affects girls and results in adverse effects on brain development and cognition, as well as in a spectrum of deficits in intellectual disability. Sleep disturbances are among the diagnostic criteria for RS and commonly accompany specific RS-associated genetic deletions and mutations. Some evidence suggests that individuals with RS have weaker modularity of brain states during sleep than the traditional spectral signatures seen in PSG. RS-related sleep disturbances often prove treatment-resistant and persist over the life course.

DGS is caused by a hemizygous deletion on one copy of chromosome 22 of about 46 protein-coding genes. DGS is associated with cardiac defects; immune deficiencies; craniofacial anomalies; increased risk for schizophrenia, ADHD, anxiety disorders, and ASD. Behavioral symptoms include sleep disturbances resulting from disruption of thalamocortical connectivity and aberrant impulse flow to somatosensory regions. These sleep problems are associated with worse behavioral, psychiatric, and physical health outcomes. Some sleep studies in individuals with DGS have involved wearable EEG devices and have characterized disturbances in NREM sleep associated with poor memory consolidation.

FXS is the most common cause of inherited intellectual disability and is associated with mutations in the FMR1 gene leading to epigenetic silencing. As FXS is an X-linked disorder, the syndrome tends to manifest with more severe symptoms in males. The variable FXS phenotype may involve joint laxity, recurrent otitis media, intellectual disability, ADHD, anxiety, hypersensitivity, perseverative behavior, irritability, aggression, ASD, seizures, and sleep problems, including apnea, insomnia, and daytime sleepiness. To date, no published studies have reported data on treatment for the associated sleep disorders.

PMS is associated with deletions in the 22q13.3 region or mutations in SHANK3. The variable PMS phenotype may involve developmental delays, intellectual disabilities, ASD, behavioral problems, neonatal hypotonia, seizures, decreased perspiration, vision problems, delayed or impaired language skills, and sleep difficulties, including delayed sleep onset, problems with sleep maintenance, parasomnias, and sleep apnea. Sleep problems in PMS may be more frequent at certain developmental stages and/or with particular genetic deletions or variants.

Combined analyses of phenotypes and genes can help researchers understand the mechanistic relationships among sleep, circadian dysfunction, and NDDs. Studies involving twins, other siblings, and other family members—ideally with large sample sizes—enable researchers to disentangle factors that contribute to NDD etiology, such as genetic, environmental, and maternal factors. PSG remains the best available way for researchers to characterize sleep in humans, but accelerometers and other devices can serve as pre-screeners and provide other useful data. Machine learning and AI approaches can help analyze sleep data and facilitate analysis integrating genetic and other data from electronic health records.

Key Themes and Opportunities:

• Future directions for research might include:
  • Improving objective home-based assessments of sleep using more user-friendly technologies like wearables and nearables;
  • Increasing the use of validated questionnaires;
  • Refining analyses of sleep states in rare NDDs;
  • Using current and novel animal models to study sleep in NDDs;
  • Expanding the study of NDDs and sleep beyond pediatric populations by incorporating adult participants and longitudinal data;
  • Using larger sample sizes and new study designs to differentiate further the characteristics of sleep disturbances across different NDDs, in different phenotypes within the same NDD and across the lifespan.

Animal Models of Neurodevelopmental Disorders

Several speakers discussed animal models of NDDs and demonstrated the utility of using organisms such as fruit flies (Drosophila), transparent zebrafish, and mice to study sleep disturbances associated with these disorders. Sleep is highly conserved across animal species. Animals sleep the most at early developmental stages, and REM sleep predominates sleep during these stages. NDDs are associated with motor and cognitive deficits, including sleep disturbances. However, it remains unclear whether sleep disturbances are a cause or consequence of NDDs—or both. Many workshop participants suggested a bidirectional causal relationship between sleep and NDDs but acknowledged that the nature of this relationship may differ across NDD types, subtypes, and individual cases.

Sleep components emerge over the course of development. For instance, REM sleep characteristics—such as limb twitches, muscle atonia, hippocampal theta, rapid eye movements, and cortical activation—emerge gradually over the course of early development. Twitches during early-life REM sleep may promote sensorimotor plasticity and the construction of somatotopic maps. In rats, twitches appear to play a key role in the development of cerebellar-dependent internal models. Many of the studies of human sleep are corticocentric due to the prominence of the PSG in their analysis. Animal models enable researchers to look beneath the cortical surface and to characterize sleep features such as the emergence of the delta rhythm of quiet sleep in subcortical structures , e.g., how the GABAergic parafacial zone may function as the medullary slow-wave sleep-promoting center.

Drosophila models enable researchers to track the effects of sleeplessness on neurological development and behavior throughout life stages. With their small size and approximately 80-day lifespans, fruit flies can provide researchers with robust data over short time frames. By manipulating Drosophila genes, researchers can create animal models of sleep deprivation, of differing sensitivities to dopamine, and of sleep features associated with NDDs. Experiments with fruit flies at different early developmental stages show that juvenile sleep loss can result in long-lasting behavioral deficits and abnormal circuit development. However, the same experiments with sleep loss in mature flies have little or no effect and this finding was replicated in rodent models. Further experiments with flies have shown that disruptions of sleep-related genes homologous to those in humans can result in behavioral, circadian, memory, sleep, and social deficits.

NDD models with transparent fish species such as zebrafish, cavefish, and Danionella enable researchers to study sleep disruptions and associated synaptopathies by visualizing neural and muscle activity at the single-cell level via a technique called fluorescence-based PSG. As vertebrate brains share the same organization, neurotransmitters, and sleep and behavior centers, transparent fish are an appropriate animal model. Longitudinal studies of the brain synapses of live zebrafish have shown that sleep is critical to synaptic formation and pruning. Fish are highly amenable to gene editing, and 90% of human genes are conserved in the fish genome. Thus, researchers can introduce a specific human mutation into the fish genome to model an NDD, understand the impact of associated sleep disruptions, and evaluate the benefits of interventions.

Mouse models of NDD can establish construct validity by introducing known human mutations in the mouse. Alternatively, mouse models of NND can establish face validity through similar mouse and human phenotypes (e.g., similar behavioral, social, and anatomical markers in humans with ASD and the model organisms). Alternatively, spontaneous mutations in inbred mouse lines can result in phenotypes that are similar to human phenotypes. Finally, animal models can emulate human environmental exposures (e.g., to blue light from electronic devices). Mouse models allow for automated data collection via surgically implanted electrodes, which can gather data on wakefulness, NREM sleep, REM sleep, and other measures. These mouse models enable many different types of experimental designs, which obviously must account for differences between this model organism and humans (e.g., mice are nocturnal).

Key Themes and Opportunities:

• Animal models demonstrate that rapidly developing brain regions appear to be susceptible to early-life sleep loss.
• In humans, sleep phenotyping usually involves a snapshot in time. Animal models enable study of sleep phenotypes longitudinally, across all developmental stages, and even during fetal development.
• Animal models enable study of sleep in brain regions other than the neocortex. Although often considered the gold standard of sleep measurement, PSG gauges only some surface measures or proxy indicators of sleep and cannot characterize sleep activity in other likely critical brain regions.
• Future research efforts may develop therapies and characterize the mechanisms of gene-specific phenotypes. These detailed phenotypes would enable researchers to define disorder subtypes and their sleep characteristics, including the lasting impact of disrupted sleep on behavior, socialization, cognition, memory, and overall health.

Conclusion

NHLBI’s two-day workshop on NDDs and associated sleep disruptions provided ample evidence that NDDs seldom present in isolation and often involve co-occurring conditions and comorbidities, including other NDDs, anxiety disorders, gastrointestinal problems, a variety of sleep disorders, and seizures. Workshop participants considered the complex interrelationships between sleep and NDDs—notably how sleep disturbances may be a causal factor for many NDDs, a consequence of many NDDs, or both. Research has demonstrated some bidirectional effects between sleep and NDDs. For instance, sleep problems often exacerbate NDD symptoms, and vice versa—a vicious circle in which sleeplessness results in more severe NDD symptoms, behavioral problems, and hyperarousal that further compound sleep problems. Workshop participants agreed that more research is needed in many areas of inquiry to better understand sleep and neurodevelopment in neurotypically developing populations and in individuals with NDDs.

Overall Themes and Opportunities:

• NDDs disrupt the underpinnings of sleep in the brain, and better-quality, more regular and undisrupted sleep can decrease the frequency and severity of some NDD symptoms, such as seizures and behavioral problems. NDD-related sleep problems can originate early in development and tend to continue into adulthood without significant improvement. NDDs and sleep disturbances often seem to have a bidirectional relationship.
• NDDs share many features and symptoms, including sleep disturbances. Study of both their similarities and their heterogeneity is necessary to better understand their etiologies, natural history, outcomes, and phenotypes, as well as to inform clinical practice and novel treatments.
• Detailed study of specific NDD phenotypes and sub-phenotypes might improve the understanding of specific genetic etiologies. A genetics-first approach might suggest how disruptions of different pathways, genes, and circuits can yield similar symptoms but require distinct types of treatment. However, it is likely that most NDDs are polygenic in origin, so multiple factors, including environmental exposures, must inform consideration of these disorders.
• Many workshop participants recommended a holistic approach to treatment that addresses core NDD symptoms, co-occurring conditions, and sleep disturbances simultaneously. Clinicians could prioritize those interventions and medications that treat multiple symptoms and patient complaints to avoid overmedicating patients. Treatment plans should address the primary complaints of patients and their families and could include pharmacological, behavioral, environmental, and surgical strategies, as well as other intervention strategies.
• Cohort-based studies and large population data sets have the potential to illuminate the relationships among NDDs, sleep, genetics, environmental factors, co-occurring conditions, and other influences.
• Using fruit flies, rodents, transparent fish, and other organisms as models can provide researchers with more controllable experimental parameters, greater uniformity of genetic background, and increased accessibility to brain regions other than the cortex. Studies with model organisms may improve the understanding of NDDs, sleep disturbances, and the relationships between them.
• Improving understanding of typical neurodevelopment and non-disordered sleep will also improve understanding of NDDs and problem sleep.
• New technologies such as at-home actigraphs, EEG headbands, remote monitors and other wearable and nearable devices will enable less burdensome collection of sleep-related data in individuals with NDDs.
• Providing information to families facing problems with NDDs and sleep is crucial and can help initiate productive conversations with health care providers. Child health organizations, neurodevelopmental organizations, and patient advocacy groups can aid and guide these efforts.

Workshop Organizer

Lawrence Baizer, Ph.D. — Program Director, National Center on Sleep Disorders Research (NCSDR), Division of Lung Diseases (DLD), NHLBI

Workshop Co-Chairs and Moderators

Lawrence Baizer, Ph.D. — Program Director, NCSDR, DLD, NHLBI (Co-Chair)
Ashura (Shu) Buckley, M.D. — Director, Sleep and Neurodevelopment Service, Office of the Clinical Director, National Institute of Mental Health
Eliza Gordon-Lipkin, M.D. — Staff Clinician; Metabolism, Infection and Immunity Section; National Human Genome Research Institute
Cindy Lawler, Ph.D. — Chief; Genes, Environment, and Health Branch; Extramural Research and Training Division; National Institute of Environmental Health Sciences
Lucia Peixoto, Ph.D. — Associate Professor, Washington State University (Co-Chair)
Jared Saletin, Ph.D. — Associate Director, EP Bradley Hospital Sleep Research Laboratory, Brown University (Co-Chair)

Workshop Speakers

Jennifer Accardo, M.D., M.S.C.E. — Assistant Professor, Children’s Hospital of Richmond at VCU
Carrie Bearden, Ph.D. — Director, Center for the Assessment and Prevention of Prodromal States, UCLA
Geraldine Bliss, B.A., M.S. — Founder and President, CureSHANK
Mark Blumberg, Ph.D. — Chair, Department of Psychological and Brain Sciences, University of Iowa
Michelle Bridi, Ph.D. — Assistant Professor, Department of Neuroscience, West Virginia University School of Medicine
Maja Bućan, Ph.D. — Co-Director, Autism Spectrum Program of Excellence, Department of Genetics, Perelman School of Medicine, University of Pennsylvania
Daniel Combs, M.D. — Assistant Professor of Sleep Medicine, University of Arizona
Jessica Duis, M.D., M.S. — RareDiseaseDoc
Annette Estes, Ph.D. — Director, University of Washington Autism Center
Heather Joseph, D.O. — Assistant Professor of Psychiatry and Pediatrics, University of Pittsburgh
Walter Kaufmann, M.D., A.M. (Hon.) — Adjunct Professor, Department of Human Genetics, Emory University School of Medicine; Co-Director, Fragile X Syndrome Program, Boston Children’s Hospital
Matthew Kayser, M.D., Ph.D. — Assistant Professor of Psychiatry, Perelman School of Medicine, University of Pennsylvania
Kristen Lyall, Sc.D. — Associate Professor, Modifiable Risk Factors Program, A.J. Drexel Autism Institute, Drexel University
Beth Malow, M.D., M.S. — Director, Vanderbilt Sleep Division, Vanderbilt University Medical Center
Natasha Marrus, M.D., Ph.D. — Assistant Professor of Child Psychiatry, Washington University in St. Louis School of Medicine
Philippe Mourrain, Ph.D. — Associate Professor of Psychiatry and Behavioral Sciences, Stanford University
Dimitrios Mylonas, Ph.D. — Assistant Professor of Psychology, Harvard University
Kathleen Nadeau, Ph.D. — Founder, The Chesapeake Center
Renée Shellhaas, M.D., M.S. — David T. Blasingame Professor of Neurology, Washington University in St. Louis School of Medicine
Bernhard Suter, M.D. — Assistant Professor of Pediatrics, Baylor College of Medicine

Disclaimer
The findings, knowledge gaps, and opportunities described here represent a summary of individual opinions and ideas expressed during the workshop. The summary does not represent a consensus opinion or directive made to or by NHLBI or NIH.