Autism spectrum research — NIH Funding Overview

Why this matters now

Autism prevalence estimates have continued to rise (CDC 2023 update: 1 in 36 8-year-olds), increasing pressure for research on early identification, services for adults, and underserved populations. Lifespan-focused funding has grown significantly relative to the historical pediatric concentration.

How NIH funds this area

Mechanisms include R01, P01, P50 (Autism Centers of Excellence), R21, and K-series career awards. The Autism Centers of Excellence (ACE) network is a flagship program at NICHD/NIMH. Data below covers all NIH awards mentioning autism in title, abstract, or terms.

Yearly NIH Awards for Autism spectrum research

Counts and total funding per fiscal year from NIH RePORTER. Recent fiscal years may understate final totals because of reporting lag.

Open the full interactive trends view for Autism spectrum research →

Top NIH Institutes (last 90 days)

Which NIH institutes funded the most Autism projects in the most recent 90-day window.

Common Activity Codes (last 90 days)

Which grant mechanisms (R01, R21, U01, P30, etc.) appeared most often for Autism in the recent period.

Most Active Institutions (last 90 days)

Universities and research organizations with the most Autism awards in the most recent 90-day window.

1. UNIVERSITY OF CALIFORNIA AT DAVIS — 10 awards
2. UNIVERSITY OF CALIFORNIA, SAN FRANCISCO — 10 awards
3. COLUMBIA UNIVERSITY HEALTH SCIENCES — 9 awards
4. MASSACHUSETTS GENERAL HOSPITAL — 8 awards
5. STANFORD UNIVERSITY — 6 awards
6. UNIV OF NORTH CAROLINA CHAPEL HILL — 5 awards
7. UNIVERSITY OF MARYLAND BALTIMORE — 5 awards
8. UT SOUTHWESTERN MEDICAL CENTER — 5 awards

Recently Awarded Autism spectrum research Grants

Twelve most recent awards mentioning Autism, drawn from NIH RePORTER. Click through to Find PIs for the full investigator search.

• Family caregivers in later life: A longitudinal study of well-being and mental health in families of adults with autism and developmental disabilities

  5R01AG080599-04
  Catherine Lord · UNIVERSITY OF CALIFORNIA LOS ANGELES, CA · $651,373 · awarded Apr 24, 2026 · R01

  Project Summary/Abstract This project aims to improve our ability to support the resilience of family caregivers of adults with autism and developmental disorders as the caregivers move into later life. Based on a 30 year longitudinal study that prospectively followed families from when their children were referred for possible autism or developmental delays, we will use a social convoy model to investigate trajectories of social connectedness and isolation over the next five years as they affect caregivers’ mental health and well-being. This model describes changes in social connectedness over time that may increase vulnerability or reduce the effects of caregiver burden. We examine additional interacting factors specifically related to family caregiver well-being and mental health in families with adult children with developmental disabilities. We will use questionnaires, app-based diaries, face to face interviews and exploratory measures of biological and cognitive aging over the course of 5 years during which our sample is in their 60’s, linked to rich behavioral data from the past 20-30 years. Our objective is to identify life milestones, such as retirement and the adult child’s moving out, as well as caregiver coping strategies that allow us to support well-being and mental health in family caregivers as they age.

• Mechanism of Par1c-mediated AMPA receptor trafficking and synaptic plasticity

  5F31NS143354-02
  Rebecca Shear · RUTGERS BIOMEDICAL AND HEALTH SCIENCES, NJ · $43,714 · awarded Apr 24, 2026 · F31

  Project Summary/Abstract The human brain is remarkably unique in its high capacity to learn and adapt to new environments, which has been attributed to the plasticity of synaptic connections. One form of synaptic plasticity, long-term potentiation (LTP), is associated with AMPA receptor trafficking to the surface of dynamic postsynaptic protrusions called dendritic spines. GluA2-deficient mice show enhanced LTP, supporting that regulation of synaptic surface GluA2 levels is important for LTP expression. However, the mechanism underlying GluA2 trafficking and how this translates to changes in synaptic plasticity is unclear. We have unexpectedly identified a significant increase in synaptic GluA2 in the hippocampi of forebrain-specific conditional knockout (cKO) of partitioning defective 1c (Par1c), also known as microtubule affinity-regulating kinase 1 (MARK1) mice. In addition, these mice exhibit reduced spine formation and impaired spatial learning. This suggests a potential role for Par1c in synaptic plasticity and cognitive functions through regulation of GluA2 trafficking. Importantly, genetic evidence supports that Par1c functions in higher level cognition. Single nucleotide polymorphisms (SNPs) in MARK1 have been associated with autism spectrum disorder (ASD) and bipolar disorder. Furthermore, MARK1 is highly expressed in forebrain pyramidal neurons and exhibits human-specific accelerated evolution, suggesting its importance in the development of cognition. However, the role of Par1c in AMPA receptor trafficking and synaptic plasticity remains unknown. Considering Par1c cKO mice show a significant increase in synaptic GluA2, we hypothesize that Par1c promotes synaptic plasticity by limiting GluA2 trafficking to the spine surface. When Par1c is knocked out, there will be increased synaptic incorporation of GluA2-containing AMPA receptors, leading to reduced spine density and impaired learning. Interestingly, unbiased phosphoproteomic analysis of Par1c cKO hippocampi revealed 7 of 17 significantly dysregulated proteins are associated with endocytic trafficking. Thus, Aim 1 will test the hypothesis that Par1c regulates GluA2 trafficking through phosphorylation of a potential novel target of Par1c identified through phosphoproteomic screen. Aim 2 will determine if synaptic plasticity induction requires Par1c activation using a novel, synaptic-targeted photoactivatable Par1c. The proposed work will elucidate the role of Par1c in regulating AMPA receptor trafficking and synaptic plasticity. Importantly, this project will train the applicant in multidisciplinary techniques including molecular biology, biochemical assays, FRET and FRAP imaging, primary neuronal cultures, and electrophysiology. It will also provide opportunities for the development of critical thinking, written and oral communication skills, and the execution of rigorous and reproducible science. The thorough mentorship and resources available to the applicant combined with her extensive and interdisciplinary neuroscience background will ensure her development into a successful, independent scientific professional.

• Microbiome Modulation of Visual System Development

  5F32EY035578-03
  David James · UNIVERSITY OF OREGON, OR · $81,580 · awarded Apr 24, 2026 · F32

  PROJECT SUMMARY Visual system dysfunction is a common and debilitating comorbidity for individuals diagnosed with a variety of neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD), schizophrenia, and attention deficit hyperactivity disorder. The microbiome is emerging as an important determinant of brain development, and recent research links these NDDs to intestinal dysbiosis, suggesting that a normal microbiome is a necessary component of typical brain neurodevelopment and function. To further connect these issues, microbial dysbiosis is also frequently associated with visual system dysfunction, yet practically nothing is known about the mechanisms by which the microbiota impacts visual system development. Therefore, a greater understanding of the dynamics between host and microbiome, including the specific cellular pathways and microbial products influencing neurodevelopment, is needed before effective treatments can be pursued. In this proposal, I will test the hypothesis that normal development of the visual system depends on sensing of specific secreted bacterial factors by specific cell types that mediate communication between the intestinal microbiome and the brain. To accomplish this, I will use the gnotobiotic zebrafish model to investigate how the microbiome interacts with intestinal cells and peripheral neurons to impact early visual neurodevelopment. This is a simple but powerful model system because it allows us to test the role that individual bacterial species and their byproducts play in neurodevelopment. I will use three approaches to determine the role specific host cell types and secreted bacterial products play in visual system development and its downstream behavioral output. Aim 1 tests the hypothesis that the microbiota is required for the normal development and function of a set of superficial interneurons involved in prey capture behavior. Aim 2 investigates the role of gut epithelial sensory cells and the vagus nerve in sensing bacterial products and relaying this information to promote visual system development. In Aim 3, I will identify the active product secreted from a gut bacterium that is sufficient to promote visual system development. These approaches allow an unbiased identification of the anatomical locations, cell types, and signaling pathways that relay microbial cues required for normal development of the visual system and its behavioral outputs. This work is significant because it lays the foundation for understanding mechanisms behind visual comorbidities associated with neurodevelopmental disorders like ASD, and ultimately serves to better inform intervention and treatment, and to one day prevent these complex NDDs and their associated comorbidities.

• PCB Epigenomic Brain & Behavior Lasting Effects Study (PEBBLES)

  2R01ES029213-06A1
  Janine LaSalle · UNIVERSITY OF CALIFORNIA AT DAVIS, CA · $3,973,295 · awarded Apr 23, 2026 · R01

  The PCB Epigenomic Brain & Behavior Lasting Effects Study (PEBBLES) team of interdisciplinary environmental health scientists with expertise in neurodevelopmental genetics and epigenomics, toxicology, and epidemiology seeks to investigate specific gene x environment interactions responsible for the elusive male bias in neurodevelopmental disorders. Our research team has previously combined the multi-omic analyses of human placental and cord blood samples from the high-risk MARBLES pregnancy cohort with those of matched placenta and brain tissues derived from a mouse model of perinatal exposure to the same mixture of polychlorinated biphenyls (PCB) congeners detected in MARBLES mothers’ sera. We sought to understand if the fetal derived tissue of placenta was like the fetal brain in its molecular responses to PCBs. We identified sex- and dosage-specific differences in placental and fetal brain methylome and transcriptome in this mouse model of prenatal exposure to the PCB mixture, corresponding to male-specific social behavioral deficits. We further demonstrated that placenta and brain have a similar genome-wide signature of PCB exposure in a sex-specific manner, implicating epigenetic processes originating from sex chromosomal differences. Epigenome-wide analysis of cord blood or newborn blood from infants later diagnosed with autism demonstrated enrichment for X-linked genes. Does this striking sexual dimorphism in response to prenatal PCB exposure result from the presence of two X chromosomes in females that confer genetic and epigenetic resiliency? To address this question, we propose to test two inter-related mechanistic hypotheses involving specific X-linked genes Mecp2 and Xist in mouse models, and a chromosome-wide epigenetic erosion of these and other X-linked genes in human MARBLES mothers and offspring of both sexes. Bioinformatic and statistical analyses will integrate the multi-omic data sets with behavioral and molecular outcome measures and determine whether PCB-associated epigenetic differences in human newborns could be used to predict and prevent long-lasting adverse brain and behavioral outcomes in children.

• FMRP regulation of mitochondria and metabolism in human brain development

  3R01NS138268-02S1
  Xinyu Zhao · UNIVERSITY OF WISCONSIN-MADISON, WI · $74,640 · awarded Apr 23, 2026 · R01

  Same as parent

• Organization of neural coding and plasticity in L2/3 of mouse S1 cortex

  5R01NS092367-11
  Daniel Feldman · UNIVERSITY OF CALIFORNIA BERKELEY, CA · $465,071 · awarded Apr 22, 2026 · R01

  Summary Non-topographic, intermixed representations (salt-and-pepper maps) of sensory information are common in cerebral cortex, but how neural coding and plasticity are organized within them is unclear. We propose that salt-and-pepper maps contain distinct pyramidal (PYR) subnetworks with differential roles in coding stability and flexibility (including learning and attentional modulation). To test this, we study the whisker map in layer 2/3 of mouse somatosensory cortex (S1), where PYR cells tuned for the columnar whisker (CW) and for non- columnar (non-CW) whiskers are intermixed in each column. We recently discovered that non-CW tuned cells show marked tuning instability across days, while CW-tuned cells have stable tuning. This reveals that the L2/3 salt-and-pepper map has two components: a stable columnar map of CW-tuned cells, intermixed with non-CW tuned cells that are unstably tuned and have little columnar topography. We propose that CW- and non-CW tuned cells are distinct PYR subcircuits with different roles in coding and plasticity. This is a novel model of S1 circuit function. We predict that the CW network provides coding stability, while non-CW cells are the primary site for plasticity and learning. Based on preliminary data, we hypothesize that tuning instability in non-CW cells is internally driven, and acts to sample novel sensory codes which may then be stabilized by experience or reward. This is a novel hypothesis for how sensory maps balance stability and plasticity—by segregating these functions in different subcircuits. In Aim 1, we use longitudinal 2-photon calcium imaging to understand the nature and origins of tuning instability, and to test whether experience or reinforcement stabilizes whisker tuning. In Aim 2, we evaluate whether CW and non-CW networks represent distinct functional networks with different sensory coding and plasticity properties. We test our central hypothesis that non-CW cells are the primary locus of sensory plasticity and learning within the map. Aim 3 asks how attention modulates neural coding within intermixed maps. We developed a selective attention task in which mice use history-dependent cues to guide attention to a specific whisker to improve detection performance. Mice show robust spatial attention to cued whiskers. Attention lasts ~10 sec and is driven by recent pairing of whisker stimuli with reward. Preliminary data show that attention enhances whisker-evoked activity of PYR cells encoding the attended whisker in S1. This establishes S1 as a powerful site to study cortical mechanisms of attention. We will use 2-photon imaging and Neuropixels recording to study how attention modulates sensory coding in S1, including measuring the size and CW- or non-CW network specificity of the attentional spotlight. In a major effort, we use imaging and optogenetics to identify the control circuits for attention in S1, with initial focus on VIP interneurons. Together, these studies will reveal how plasticity and attentional modulation are organized within a canonical salt-and-pepper map.

• Summer Undergraduate Research Program (NEUROSURP) in Neuroscience

  5R25NS105143-08
  Huaye Zhang · RUTGERS BIOMEDICAL AND HEALTH SCIENCES, NJ · $127,300 · awarded Apr 21, 2026 · R25

  Project Summary/Abstract The current proposal is to support a Summer Undergraduate Research Program in Neuroscience (NeuroSURP) mentored by Rutgers University research faculty. The program has three primary aims: (1) To increase student knowledge and appreciation of basic biological research by providing a closely-mentored, hands-on research experience; (2) To increase student knowledge and interest in pursuing careers in research through career development and educational activities; (3) To provide continued advice, support and guidance to program alumni to facilitate post-program career planning and implementation. Twelve undergraduates will be admitted to our program each year beginning 2024. Special consideration will be given to students from historically underrepresented minority and disadvantaged backgrounds including Black, Hispanic, Native American, Pacific Islander, or have physical or mental disabilities, or are from economically and/or socially disadvantaged backgrounds (collectively referred to as URM) that comprise a deep and diverse pool of potential future scientists. The research component of the proposed SURP involves hands-on experimentation in labs with active, nationally recognized and funded research programs in neuroscience with a focus on neurological disorders at Rutgers University. The infrastructure and general organization of the proposed program will be based on an existing program that has been in place for 27 years. Students will work on their own research projects under the close supervision of mentors in their host labs. The proposed SURP is designed to integrate student research experiences and mentoring with weekly meetings comprising training in neuroscience, oral and written presentations, critical reading of manuscripts, Responsible Conduct of Research as well as Rigor and Reproducibility including statistical analysis. In addition, there is a significant career development component during the weekly meetings in which PhD, MD/PhD and MD guest speakers discuss their career paths representing academic research, non-academic research as well as research- related careers. Each year students will present the results of their summer research projects in a symposium that is open to scientists on campus and members of the general public. In addition, the students submit a paper on their project in the format of a manuscript and receive feedback from MPIs. Finally, the Co-directors will maintain close contact with the alumni of our program as we have done for the past 27 years and will continue to provide them with advice and mentoring related to applying to graduate school and their careers. The mentors who will be supervising the students study neurological disorders including Alzheimer's, Parkinson's, multiple sclerosis, autism, traumatic brain injury, spinal cord injury, sensory loss, epilepsy, and stroke. The multidisciplinary research focus of the faculty mentors on the cellular, molecular, and genetic processes underlying developmental and degeneration of the nervous system has implications for the etiology, pathogenesis and progression of neurological disorders.

• Testing the accuracy of eye tracking as a screening tool for ASD in the general population

  4R37MH132924-04
  Karen Pierce · UNIVERSITY OF CALIFORNIA, SAN DIEGO, CA · $1,546,507 · awarded Apr 20, 2026 · R37

  The field of ASD screening is at a crossroads: the sensitivity of the most popular screening tool is only 33%- 38%1,3, and pediatricians consistently refer only about a third of children who fail a screening tool for an evaluation4,5 - citing a lack of confidence in screening results as the primary reason for non-referral5. Within this context, it is not entirely surprising that the mean age of ASD diagnosis and eventual treatment remains at ~52 months6 - years beyond the disorder’s prenatal origins7, and beyond the age when it can be reliably diagnosed in many cases8. Clearly, new approaches need to be tested. Eye-tracking, which generates biologically-relevant, objective, and quantifiable metrics of social and non-social visual attention patterns, is a technology that holds considerable promise as a tool to dramatically change how screening is implemented. With the help of NIH funding, we developed 6 novel eye tracking tests that tap into key challenge areas for children with ASD including visual social attention, gaze shifting, and auditory social attention. Leveraging our large legacy eye tracking dataset collected from >2,000 toddlers spanning multiple diagnostic groups including ASD, non-ASD delay, and TD we determined optimal eye tracking metrics and cut-off values across for each test that result in very high specificity and PPV (~97% & ~90%) but modest sensitivity (~20% per test). Combining across all 6-tests however, dramatically improves sensitivity (~90%) and results in high classification accuracy (AUC .95). These findings, however, were demonstrated in a laboratory setting with utility in real-world clinical settings unknown. Thus, in AIM 1, we take the bold step of testing whether eye-tracking administered across 8,000 12, 18, & 24 month well-baby check-ups (from ~5,2000 unique toddlers) serving families from a wide range of racial, ethnic, and SES backrounds can improve ASD early screening when implemented by medical staff in pediatric offices. Toddlers who fail eye-tracking using resarcher defined criteria, and a percentage who pass, will be evaluated by a licensed psychologist blind to eye tracking scores, and diagnostic classification accuracy of eye-tracking computed. Relationships between eye tracking profiles and clinical phenotype will also be examined. In order to fully understand the accuracy of eye tracking as a screening tool, diagnostic outcomes of the entire screened cohort needs to be determined. Thus, in AIM 2 electronic health records (EHRs) will be leveraged to allow us to not only determine the true sensitivity, specificity, PPV and NPV of eye tracking for detecting ASD, but to also compare results to rates of ASD detection using the CSBS, a parent report screening tool used as standard of care in San Diego as part of our Get SET Early model9. State of-the-art bioinformatics will allow us to further determine if combining eye-tracking with parent report is superior relative to either approach alone. Statistical modeling will reveal whether or not factors such as age at screening, sex, race, ethnicity or SES impacts eye tracking scores. Finally in AIM 3, pediatricians and parents will rate their satisfaction with eye tracking.

• Neurodevelopmental mechanisms in 17q12 CNV disorders and autism

  5R01MH137004-03
  Eric Morrow · BROWN UNIVERSITY, RI · $786,292 · awarded Apr 17, 2026 · R01

  PROJECT SUMMARY Copy number variants (CNVs) are contiguous gene deletions or duplications that confer susceptibility to neuro- psychiatric and neurodevelopmental disorders (NDDs). Thereby, CNVs offer a powerful opportunity to investi- gate multigenic mechanisms in complex brain disease. Recent studies demonstrate that the 17q12 Deletion (17qDel) is among the strongest CNV risk factors for autism; however, the mechanisms of circuit dysgenesis caused by 17q12Dels remain poorly understood. The objective of this research is to define defective neurode- velopmental mechanisms caused by 17q12 CNVs, particularly 17q12Dels, which represent a high-penetrant, high-confidence risk factor for autism and related neurodevelopmental disorders (NDDs). To meet this objec- tive, we have generated unique experimental resources, including: a 17q12Del mouse; and human 17q12 CNV induced pluripotent stem cells (iPSCs) (with robust controls), from patients with 17q12Dels, as well as from pa- tients with reciprocal 17q12 duplications. Our central hypothesis is that the combinatorial haploinsufficiency of the genes within the interval, including the transcription factor Lhx1, a known regulator of Wnt signaling, dis- rupts multiple steps in brain and circuit development. Notably, we have discovered that 17q12Del mice exhibit a spectrum of anterior brain and craniofacial abnormalities. These phenotypes vary depending on the mouse genetic background, and are akin to, but milder than, the Lhx1-null mouse. The 17q12Del on the inbred C57BL/6N background displays greater phenotypic severity, including neonatal lethality, compared to 17q12Del mice on the outbred CD-1 background, that survive into adulthood with milder cortical and hippo- campal abnormalities. We will pursue the following Aims: 1) Define defective transcriptional mechanisms and molecular pathways in embryonic brain development in 17q12Del mice; 2) Define defective molecular path- ways and rescue strategies in patient-derived 17q12 CNV neurons; and 3) Define postnatal neurodevelopmen- tal and behavioral abnormalities in 17q12Del mice on diverse background genetics using MRI morphometry, molecular and behavioral studies. This research will have a sustained impact on the field given the high level of significance and innovation: 1) 17q12Dels represent an understudied, high-confidence autism locus; 2) the study of Wnt signaling will permit convergence of the 17q12Del mutation with other high-confidence autism genes; 3) we are testing proof-of-concept Wnt-related therapeutics; 4) methodologically, study of an autism- associated mutation on diverse, mouse genetic backgrounds provides an important, experimental paradigm for investigating phenotypic heterogeneity; and 5) we use an integrated translational approach, that involves a multidisciplinary team coordinating cross-species experiments, including in vivo rodent and in vitro human iPSC models, with clinical studies in patients. This research will permit bench-to-bedside and broadly-signifi- cant discoveries related to the diversity of phenotypes and treatment responses in neuropsychiatric disorders.

• Genetic discovery for neuropsychiatric traits in deep phenotype data: novel methods and applications

  1R01MH140223-01
  Iuliana Ionita · COLUMBIA UNIVERSITY HEALTH SCIENCES, NY · $534,191 · awarded Apr 17, 2026 · R01

  Summary One of the major problems in human genetics is understanding the genetic causes underlying complex phenotypes, including neuropsychiatric traits such as autism spectrum disorders, bipolar and schizophrenia. Despite tremendous work over the past few decades, it has been frustratingly difficult to get a good understanding of the underlying biological mechanisms in most cases. Nonetheless, large psychiatric genetic studies are beginning to deliver fundamental knowledge about genetic architecture, disease pathways and specific genetic loci for follow-up. Most psychiatric genetic studies to date have focused on individuals of European origin, leading to profound difference in genetic discoveries with limited transferability of results across populations, but also limiting our knowledge about disease pathophysiology in general. Recently, several large projects in neuropsychiatric genetics have focused on collecting and assembling genetic and deep phenotype data in admixed and populations of different geographic origins. Such projects include the Latin American Genomics Consortium (LAGC), the Genomics of Autism in Latino Ancestries (GALA), the Ancestral Population Network (APN), and PsycheMERGE. Most approaches for causal variant discovery fail to account for key complexities that arise in studies of varying geographic origin, including heterogeneity across populations in terms of effect sizes and linkage disequilibrium (LD) structure, and correlations across geographic origins. Furthermore, with meta-analyses with external LD from reference panels being commonly used in genome-wide association studies, certain types of inconsistencies are inevitable. Therefore, existing methods tend to have suboptimal power and can even produce invalid results, i.e., they prioritize non-causal variants. We propose to develop robust fine-mapping tools that model heterogeneity across populations and are robust to inconsistencies in the data. We also propose to leverage a possibly large number of genetically related traits available in electronic health record systems, including diagnoses, lab results and biomarkers with the goal to refine phenotypes and improve power of genetic association studies for psychiatric phenotypes. We further propose to apply these methods to the largest available collections of datasets from various geographic origins for autism, bipolar, schizophrenia and other neuropsychiatric traits, including data from several psychiatric genetics consortia and electronic health record systems. We believe that the proposed research is very timely and leverages modern datasets with the potential to substantially improve our understanding of the biological mechanisms underlying risk to neuropsychiatric diseases, including schizophrenia, autism and related disorders.

• A longitudinal study identifying psychological and service delivery targets to improve daily living skills and quality of life outcomes among autistic youth exiting high school

  5R01MH133838-04
  BENJAMIN YERYS · CHILDREN'S HOSP OF PHILADELPHIA, PA · $791,853 · awarded Apr 17, 2026 · R01

  Approximately 1 million autistics will turn 18 in the next decade, many without the skills they need to achieve the quality-of-life that they and their families’ desire. Without effective supports, autistic youth struggle with daily living skills, regardless of their intellectual abilities. Daily living skills are fundamental to independence, paid employment, and better quality-of-life for autistic adults. Existing daily living skill interventions for this age group have only modest effects or show poor generalization to real world settings. Current treatments rely on explicit instruction of specific daily living skills (e.g., the steps for taking a shower), and they lack inclusion of mutable psychological factors that support the development and generalization of daily living skills. Treatments are further limited by inadequate knowledge of how social determinants of health (e.g., family income, community resources) contribute to daily living skills. Identification of mutable psychological factors and social determinants of health driving change in daily living skills for autistic youth exiting high school is a vital to improving public health. This knowledge will identify pivotal intervention and service delivery targets for improving daily living skills. Better executive function and self-determination skills are associated with more advanced daily living skills, and both factors improve with treatment in autism. Our central scientific premise is that interventions for daily living skills, and the service delivery systems that promote them, will be enhanced with greater knowledge of psychological and systemic factors that directly impact these skills. Further, enhanced daily living skills will result in downstream improvements in quality-of-life and productivity. This project will address gaps in our knowledge with a prospective longitudinal study that evaluates psychological factors that drive change in daily living skills during the time when autistic youth exit high school (AIM 1), as well as the impact of daily living skills on quality-of-life (AIM 2). We will also explore the influence of both individual- (e.g., family income) and neighborhood-level (childhood opportunity index) factors on daily living skills (AIM 3). Finally, there is a general need for large samples reflective of the autism population in the Mid-Atlantic region (i.e., IQ range, speaking/nonspeaking, sex, race, ethnicity). The proposed longitudinal study will contain 3 visits (T1: baseline, T2: +1 yr., T3: +2 yrs.; final N=170). Our recruitment strategy will ensure all participants have at least one timepoint pre- and post-high school exit. We predict: AIM 1, H1) executive function and self-determination will explain significant variance in concurrent daily living skills above covariates; AIM 1, H2a,b) executive functioning and self-determination at baseline will predict daily living skills at T3 and change in daily living skills over time above covariates; AIM 2, H3a,b) larger increases in daily living skills will predict better objective and subjective quality-of-life and better change in quality-of-life over time. In AIM 3, we explore both direct and indirect effects of social determinants of health. This project will generate critical knowledge for enhancing daily living skills interventions and delivery systems that will improve long-term outcomes for autistic adults and increase access to services.

• The Maternal Immune Axis Programs Fetal Corticogenesis

  1R01MH138484-01A1
  Yeong Shin Yim · UNIVERSITY OF PENNSYLVANIA, PA · $689,249 · awarded Apr 17, 2026 · R01

  Project Summary This project seeks to elucidate sex-specific mechanisms by which maternal immune activation (MIA) during pregnancy impacts cortical development and elevates the risk for neurodevelopmental disorders (NDDs), focusing specifically on the CXCR7 (Ackr3)/CXCL12 chemokine signaling axis. MIA, triggered by maternal infection or inflammation, is a known risk factor for conditions such as autism spectrum disorder and schizophrenia, with male offspring often showing increased vulnerability and differing symptom profiles compared to females. The molecular basis of these sex differences remains poorly understood, representing a critical knowledge gap in both developmental neurobiology and translational medicine. Aim 1 will investigate the physiological role of the CXCR7/CXCL12 axis in corticogenesis, examining how sex-specific regulation of CXCR7 affects neural progenitor cell (NPC) differentiation and migration. By employing Ackr3 knockout models and epigenetic profiling, we will determine how CXCR7 signaling is modulated in male and female NPCs, which may underlie differences in cortical organization between the sexes. Aim 2 will examine the pathophysiological role of CXCR7/CXCL12 in response to MIA, testing the hypothesis that MIA induces a male-specific upregulation of CXCR7 that leads to aberrant cortical development and behaviors associated with NDDs. We will use advanced molecular techniques to assess how CXCR7 activation in males contributes to cortical disorganization, precocious NPC maturation, and behavioral changes, as well as to evaluate the dependency of these effects on maternal IL-17 signaling. Together, these aims will provide mechanistic insights into how intrinsic sex differences interact with environmental factors like MIA to shape brain development and vulnerability to NDDs. This work is significant because it addresses an urgent need to understand how intrinsic sex differences and external maternal immune influences jointly shape neurodevelopmental trajectories. This research ultimately aims to bridge a gap in neurodevelopmental disorder research by providing a clearer understanding of how male and female brains respond differently to environmental stressors during critical periods of development, which may have lasting implications for public health and clinical care.

Related topics

• Mental health and psychiatric research