ARI’s Statement on Acetaminophen Use and Leucovorin Supplementation (9-22-25)
ARI awards grants to fund innovative research that holds realistic promise in impacting the lives of autistic people. In 2024, ARI awarded more than $700,000 in research grants.
We continue to focus on education while supporting research on genetics, neurology, co-occurring medical conditions, nutrition, sensory processing, severe and challenging behaviors, and adult and senior issues. Connecting investigators, professionals, parents, and autistic people worldwide is essential for effective advocacy.
View and print a pdf list of our 2024 Research Grant Recipients
2024 Robert L. Hendren Research Grant Award Winners
Dr. Robert Hendren
In honor of his many years of support for our work, serving as a member of ARI’s Scientific Advisory Board and Board of Directors, the top-scoring research grant proposals funded each year are now recognized as Robert L. Hendren Research Grant Award recipients.
2024 RECIPIENTS:
Philippe Campeau, MD, FCCMG
Marilena Griguoli, PhD
More Research Studies
2024
Excitation / Inhibition Imbalance as a Neural Marker of Language Impairment in Youth with Autism: Relation to Sex and Language Phenotype
Vardan Arutiunian, Ph.D.
Seattle Children’s Research Institute
Most individuals with autism have language impairment, varying in its severity (from nonverbal/minimally verbal to slightly impaired skills). Moreover, male and female individuals with autism have different profiles with respect to language/communication as well as general and domain-specific brain functioning. However, the interaction between language skills, sex difference, and neural mechanisms is largely unexplored. Given the importance of language for long-term education, social, and employment outcomes, there is an urgent need to explore neural mechanisms of language functioning in autistic males and females for understanding symptom trajectory, specificity of intervention targets, and improving objective markers for clinical trials. The main goal of the present project is to assess a set of novel EEG-based combinatory biomarkers of language impairment in autism. Using a large sample size (n > 350), this project will include a speech perception paradigm in EEG with formal behavioral assessment of language and communication in a group of sex-balanced youth with and without autism, varying in the language skills. The project addresses the excitation/inhibition imbalance hypothesis as a main neurophysiological factor contributing to language impairment in autism. The project will also explore additional conceptualization of neural functioning (novel neural metrics and innovative combinatory biomarkers) and their relation to language and communication skills in youth with autism.
Dissecting the Neuronal Consequences of Altered NuRD Complex Function in Autism
Philippe Campeau, M.D., FCCMG
CHU Sainte-Justine
Université de Montréal
NuRDopathies are frequent genetic diseases caused by mutations components of the chromatin-remodeling NuRD complex, such as CHD3, CHD4 and GATD2B. Clinical features include autism, intellectual disability and macrocephaly (a larger head). We have generated a mouse model with a Chd3 missense mutation which reproduces several clinical features, and MRIs show a larger brain. We have uncovered that a functional CHD3 protein is essential for the expression of certain genes previously associated with autism. We hypothesize that this is because CHD3 is important for unraveling DNA and permitting its transcription, which we will explore in mouse neurons. Secondly, to understand why certain areas of the brain are larger, we will be studying the number of cells of various types in specific regions, and their replication. We will correlate these findings with gene expression results to determine if altered expression of some genes are responsible for this abnormal brain overgrowth, and which mechanism (such as abnormal histone variant deposition) could explain this observation. We posit that by better understanding how CHD3 variants cause disease at the molecular and cellular level, we can also discover which signaling pathways need to be targeted for therapies.
Gut inflammation as a Pharmacological Target for Autism
Alessia Butera, PhD
Centro Nazionale per la Ricerca e la Valutazione Preclinica e Clinica dei Farmaci
National Center for Drug Research and Evaluation, Istituto Superiore di Sanità
We previously demonstrated, in the ASD mouse model of early immune activation (EIA), the presence of gut-inflammation. Blockade of innate cells and gut-experienced lymphocytes traffic by means of anti-α4β7 monoclonal antibody administration was able to inhibit the gut inflammation and rescue the mouse social responsiveness with expression of protective genes in hippocampus and prefrontal cortex. This suggests that ASD subjects with gut inflammation might benefit from anti-inflammatory treatments. The current project addresses two critical clinical needs: identifying pathogenetic biomarkers to stratify ASD individuals into subgroups for personalized therapy and evaluating the effectiveness of anti-inflammatory treatments. The project focuses on the involvement of the gut immune system microbiota interface in the pathogenesis of behavioral alterations. Specifically, we aim to assess the impact of oral anti-inflammatory treatment with a pH-sensitive preparation of mesalamine on behavioral alterations of the EIA mouse model of ASD characterized by the presence of intestinal inflammation. At the same time, based on the biomarkers identified in the model, a group of ASD subjects with or without GI symptoms will be divided into subgroups according to the biomarkers being studied. Through this project we expect to stratify ASD subjects and identify subgroups for whom intestinal anti-inflammatory treatment is effective in addressing behavioral disorders.
Ecological Monitoring of Autonomic Nervous System Activity and Relationship with Social Communication and Gastrointestinal Symptoms in Autism Spectrum Disorder
Bradley Ferguson, PhD
University of Missouri
Research suggests that many individuals with autism spectrum disorder (ASD) experience gastrointestinal (GI) symptoms, which are linked to increased stress, anxiety, and social withdrawal. However, previous studies in these areas rely on parent report of symptoms and stress assessments conducted in laboratory settings which may not reflect real-world functioning. To address these issues, our team developed Core Autism, a smart watch application that objectively measures pulse rate variability (PRV), a measurement of stress, and actual verbal social communication in real time. This study will track 60 autistic participants aged 6-24 over three weeks to examine the relationship between GI symptoms, stress, and social interaction. Findings could inform future clinical trials and improve the quality of life for individuals with ASD.
Investigating the Interplay Between Oxytocin and Neuroinflammation in the Effects of Social Buffering in a Mouse Model of 22q11.2DS
Valentina Ferretti, PhD
Università degli Studi di Roma
Social buffering (SB) refers to the process by which the presence of a peer can mitigate the negative effects of stress. In this study, we will explore the impact of SB and intranasal oxytocin on socio-cognitive functions and stress response in LgDel/+ mice, a model of human 22q11.2DS, during adolescence and adulthood. Additionally, we will assess the potential effects of this protocol on the neuroimmune axis and synaptic plasticity.
By characterizing the SB paradigm and its underlying behavioral, synaptic, and neuroimmunological mechanisms, this research aims to provide critical insights into the development of non-invasive, personalized interventions for individuals with autism spectrum disorders.
Role of Septal Cholinergic Neurons in ASD Social Novelty Deficits
Marilena Griguoli, PhD
Institute of Molecular Biology and Pathology
European Brain Research Institute
The capacity to discriminate between familiar and novel items allows us to focus the attention on what is unknown, to promote exploratory behavior and facilitate learning, however the neuronal substrates underlying these skills are not known. Atypical habituation to familiar and aberrant exploration of novel stimuli have been related to the severity of autism spectrum disorders (ASD). Young ASD patients show prolonged attention and attachment to objects, but reduced interests to social stimuli. Moreover, ASD patients are hypo responsive to novel visual stimuli and exhibit a slower habituation to faces. Cholinergic neurons (ChAT) localized in the Medial Septum (MS), projecting to the hippocampus and releasing acetylcholine (ACh), may be crucial for the habituation to familiar stimuli and for the exploration of novel stimuli. This idea is supported by the fact that ChAT neurons increase their activity in response to novel stimuli. Moreover, we have recently shown that ChAT neurons silencing affects the capacity to discriminate between a familiar and a novel conspecific. Notably, dysfunctions in cholinergic signaling have been well documented in ASD. Based on these observations, this project aims to test the hypothesis that alterations in septo-hippocampal cholinergic pathway may underlie deficits in social novelty discrimination observed in ASD.
A Role for the Exposome in Understanding the Biology of Autism
Laura Hewitson, PhD
Johnson Center for
Child Health and Development
A number of environmental factors are associated with the development of autism spectrum disorder (ASD) although these have primarily been focused on maternal exposures. For example, taking medications during pregnancy, such as antidepressants, anticonvulsants, and even acetaminophen increase the risk of ASD. Exposure in utero and in early life to air pollution, particulate matter, and pesticides may also increase ASD risk. There have been few studies, however, to investigate cumulative environmental exposures and their potential impact on the severity of ASD in young children. The exposome is defined as the cumulative measure of environmental influences and associated biological responses throughout the lifespan, including exposures from the environment, diet, behavior and endogenous processes. The present study will examine the exposome in boys diagnosed with ASD compared to typically developing boys (n=100/group, aged 18 m-8 years). Using machine learning, we will analyze the impact of demographic, clinical, and behavioral variables on exposomic datasets to determine whether exposomic contaminants are associated with ASD and ASD severity. This will provide distinct exposure-derived biological effects that may identify molecular pathways particularly relevant to ASD symptomology, particularly immune and/or gastrointestinal function in ASD, both of which are known to be sensitive to environmental factors.
Linking Human Ancestry and Microbiome to Predict Autism Treatment Outcomes
Taichi A. Suzuki, PhD
College of Health Solutions, Biodesign Center for Health Through Microbiomes
Arizona State University Biodesign Institute B230C
