1. Bouelkhair M, Kacimi FE, Azzaoui FZ, Ramchoun M, Berrougui H, Boulbaroud S. Short-chain fatty acids, neuroinflammation, and autism spectrum disorders: A mechanistic systematic review. J Neuroimmunol;2026 (Mar 24);416:578914.

Autism spectrum disorder (ASD) is a complex neurodevelopmental condition characterized by social and communication deficits, repetitive behaviors, and cognitive alterations. Increasing evidence indicates that immune dysregulation, particularly neuroinflammation, is central to its pathophysiology. The gut-brain axis and microbial metabolites, especially short-chain fatty acids (SCFAs: butyrate, acetate, propionate), have emerged as potential modulators of these processes. SCFAs are absorbed from the gut and may modulate brain function via transporter-dependent mechanisms at the BBB, although evidence in ASD contexts remains limited, thereby allowing them to influence both peripheral and central immune responses. This qualitative systematic review included studies published between 2015 and 2025 addressing at least one of three links: (1) ASD and neuroinflammation, (2) ASD and SCFAs, and (3) SCFAs and neuroinflammation. Twenty studies met inclusion criteria and were analyzed. Findings indicate that SCFAs exert distinct effects: butyrate consistently shows neuroprotective and anti-inflammatory actions, acetate displays context-dependent dual effects, and propionate is mainly associated with detrimental outcomes, including social and cognitive impairments and elevated inflammatory markers. Overall, SCFAs may influence ASD pathophysiology through modulation of neuroinflammatory mechanisms, with effects depending on the specific SCFA, dosage, and context. Nutritional strategies that modulate SCFA production, such as dietary fiber enrichment, prebiotics, and probiotics, may offer feasible, non-invasive therapeutic approaches. However, clinical evidence remains limited and heterogeneous, highlighting the need for well-designed trials to determine optimal interventions targeting SCFAs in ASD.

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2. Chusak C, Pongpankhae P, Sukcharoen C, Suklaew PO, Adisakwattana S. Dietary behaviors, energy intake, and assessment of school lunch consumption in Thai children with autism. Sci Rep;2026 (Mar 29)

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3. Kowalczyk Z, Fadzil AHA, Ward I, Happé F, Stewart GR. ‘A New Pace of Life’: A Mixed-Methods Exploration of Retirement Plans, Preparations and Experiences in Middle-Aged and Older Autistic and Non-Autistic Adults. Autism;2026 (Mar 29):13623613261431925.

Retirement is a major life change affecting routines, finances and wellbeing. Autistic adults may face extra challenges during this transition due to employment barriers, limited support and planning difficulties. However, little is known about their retirement experiences compared to non-autistic adults. This mixed-methods study surveyed 517 adults from the United Kingdom (autistic n = 395), aged 40-90 years, about their retirement status, plans, experiences, employment history, income and financial security. Actual or expected retirement ages were similar across groups, but autistic adults were less likely to have made plans and more likely to have plans disrupted by financial, health or personal factors. They also reported lower rates of full-time work, reduced pensions and lower pre-retirement income. Many highlighted a lack of information about pensions and lifestyle planning. Concerns included isolation, loss of routine and financial worries, but some looked forward to more autonomy and time for self-care, leisure activities and interests. While there were many similarities between the autistic and non-autistic groups, our study found that autistic adults may reach retirement differently due to unique work histories, health needs and planning barriers. Tailored, accessible support is needed to help autistic adults plan for financial stability and meaningful post-retirement lives.Lay abstractRetirement is a major life change, but very little is known about how autistic adults experience this transition. This study explored retirement experiences/expectations of both autistic and non-autistic adults, finding that retirement happened or was expected to happen at similar ages across groups. However, autistic adults were less likely to plan for retirement and often had more difficulties with jobs, money, pensions and their health. Many felt unsure how to prepare for retirement and wanted clearer information. While some had concerns about isolation and changes to routine, others looked forward to more freedom and time for hobbies. The findings highlight the need for better support to help autistic people plan for retirement.

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4. Krzysztofik K. Temperamental Traits and Sensory Responsiveness in Children on the Autism Spectrum: The Moderating Role of Age. J Autism Dev Disord;2026 (Mar 28)

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5. Kuwabara H, Kojima M, Benner S, Otowa T, Watanabe T, Kuroda M, Owada K, Yassin W, Hamada J, Kano Y, Uno Y, Kushima I, Mori D, Arioka Y, Munesue T, Kasai K, Higashida H, Abe O, Takao H, Wakuda T, Kameno Y, Inoue J, Harada T, Yamauchi A, Ogawa N, Honda N, Kikuchi S, Seto M, Tomita H, Miyoshi N, Matsumoto M, Kawaguchi Y, Kanai K, Ikeda M, Nakamura I, Isomura S, Hirano Y, Onitsuka T, Takahashi N, Nakashima M, Saitsu H, Kondo K, Ikeda M, Iwata N, Shimada M, Sasaki T, Takei N, Ozaki N, Kosaka H, Okada T, Yamasue H. A key gene modulating oxytocin efficacy in autism: genome-wide discovery and verification in randomized controlled trials datasets. Mol Psychiatry;2026 (Mar 28)

Previous studies suggest that oxytocin has therapeutic potential for modulating core symptoms of autism spectrum disorder (ASD), although findings have been inconsistent. The unknown mechanisms underlying oxytocin’s effects and the substantial individual variability in treatment response impede the development of effective oxytocin-based therapies. In this study, we conducted a genome-wide association study (GWAS) using data from a randomized controlled trial (RCT) that examined the effects of a single dose oxytocin on behavioral and neural correlates of ASD. We further tested the association between the SNP identified in the GWAS and clinical efficacy in an independent, larger dataset comprising participants from three additional RCTs. In these trials, males with high-functioning ASD received repeated doses of oxytocin, and treatment response was assessed using the social reciprocity domain of the Autism Diagnostic Observation Schedule (ADOS), the common primary outcome across all three studies. The GWAS identified a significant association between oxytocin-induced improvements in medial prefrontal cortex activity during a social judgment task and the single nucleotide polymorphism (SNP) rs1871303 in the ryanodine receptor 2 (RYR2) gene (β = 2.37, t = 7.82, df = 72, P = 3.47 × 10⁻⁹). The validation analysis supported the association between this RYR2 SNP and individual variability in ADOS reciprocity improvement (β = 0.194, t = 2.30, df = 135, P = 0.023), with no significant association observed for placebo response (P > 0.1). To our knowledge, this is the first GWAS to investigate the pharmacogenomics of oxytocin efficacy in ASD. These findings highlight RYR2 as a key gene influencing oxytocin response, possibly through its role in calcium channel signaling and regulation of endogenous oxytocin release.

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6. Li R, Dybvik H, Feng D, Eng CM, Lee CH, Bartholomay KL, Zhang Y, Lightbody AA, Reiss AL. Atypical inter-brain synchrony and social communication deficits in girls with fragile X syndrome: Evidence from functional near-infrared spectroscopy hyperscanning. Eur Child Adolesc Psychiatry;2026 (Mar 28)

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7. Locke J, Williams NJ, Sridhar A, Shih W, Espeland C, Tagavi D, Bearss K. Study protocol for coaching and leadership in autism support settings: a cluster randomized controlled hybrid type 2 effectiveness-implementation trial. Implement Sci;2026 (Mar 28)

BACKGROUND: The increased prevalence of autism spectrum disorder creates a sense of urgency to improve outcomes for this population in publicly funded education systems, the primary setting in which autistic children receive behavioral health services in the United States. Important barriers to progress include a lack of feasible clinical interventions that address autistic children’s externalizing behaviors in schools and major challenges sustaining fidelity to newly implemented programs over time. This trial addresses these gaps by (1) testing the clinical effectiveness of the Research Units on Behavioral Interventions in Educational Settings (RUBIES) program relative to educator psychoeducation on externalizing behaviors of autistic children in public elementary schools, and (2) testing the effects of adding a leadership-focused organizational implementation strategy, Helping Educational Leaders Mobilize Evidence (HELM), to educator coaching in RUBIES on RUBIES sustainment. METHODS: In a cluster-randomized, hybrid type 2 effectiveness-implementation trial, schools will be randomized to one of 3 arms: 1) educator coaching in RUBIES and school participation in HELM; 2) educator coaching in RUBIES only; or 3) a control condition incorporating an active clinical comparator, educator psychoeducation. We will enroll 42 schools and 126 educators yoked to 126 elementary-aged autistic children. Depending on arm, educators will complete study instruments up to six times: 1) Spring semester prior to the year of school and student enrollment (implementation baseline; arms 1-2); 2) Fall semester Year 1 (clinical baseline; arms 1-3); 3) 16 weeks (arms 1-3); 4) 24 weeks (arms 1-3); 5) 52 weeks (arms 1-2); and 6) 76 weeks (arms 1-2). The primary clinical outcome compares arms 1 & 2 vs. 3 on change in autistic children’s externalizing behavior from clinical baseline to 24 weeks. The primary implementation outcome compares arms 1 vs. 2 on RUBIES sustainment, operationalized as educators’ average RUBIES fidelity at 52 and 76 weeks. DISCUSSION: Generating evidence for the clinical effectiveness of RUBIES addresses a significant gap in educator-delivered interventions to minimize highly prevalent externalizing behaviors among autistic children in public schools. Simultaneously, testing the effectiveness of HELM on sustainment of RUBIES will inform future efforts to successfully implement and sustain new innovations for autistic youth in public schools. NAME OF THE REGISTRY: Clinical Trials. TRIAL REGISTRATION: NCT07276750. Date of registration 12/10/25. URL of trial registry record https://clinicaltrials.gov/study/NCT07276750?cond=Autism&intr=RUBIES&rank=1.

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8. Naviaux RK. The 3-Hit Metabolic Signaling Model for Autism Spectrum Disorder: A Summary. Autism Res;2026 (Mar 28):e70228.

Autism spectrum disorder (ASD) is a highly heritable yet environmentally sensitive neurodevelopmental condition whose biological heterogeneity has resisted a unifying causal explanation for over 100 years. The 3-hit metabolic signaling model proposes that ASD arises from abnormal persistence of an evolutionarily conserved stress-response program-the cell danger response (CDR)-during critical windows of neurodevelopment. In this framework, ASD emerges from the sequential interaction of: (1) inherited genetic or epigenetic variants that sensitize mitochondrial metabolism, intracellular calcium handling, and purinergic signaling to environmental change; (2) early prenatal or postnatal activation of the CDR by infection, immune dysregulation, metabolic disturbance, or environmental toxicant exposure; and (3) prolonged or recurrent exposure to CDR-activating triggers for 3-6 months from the late 1st trimester to 18-36 months of age. The CDR is initiated by extracellular ATP (eATP)-associated purinergic signaling and mitochondrial changes that are resource- and energy-intensive. Persistent or recurrent activation of the CDR during the critical neurodevelopmental window is proposed to sensitize developing cells to eATP-related signaling, leading to false alarms and a mixture of chemical, immune, and neurosensory under- and over-responsivity. More frequent cycles of CDR activation and recovery are proposed to cause cellular competition for key bioenergetic, mitochondrial, and metabolic resources needed to support the normal trajectory of child development. Phenylketonuria (PKU) provides a proof-of-principle example. Untreated PKU historically caused intellectual disability and autistic features, while universal newborn screening and early treatment interrupt this sequence and prevent or decrease these outcomes despite strong genetic predisposition. A 3‐hit developmental model for autism spectrum disorder is described. New methods in systems biology have identified a pattern of changes in mitochondrial function and metabolism that underlie the core symptoms of ASD. The metabolic features of the cell danger response (CDR), maintained by abnormalities in ATP‐related purinergic signaling, have emerged as a common denominator for each of the genetic and environmental causes of ASD studied to date. eng

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9. Sauer AK, Walsh JA, Curran D, Zohourian N, Stanton JE, Zabetakis I, Brown JAL, Grabrucker AM. Synaptic protein mutations in autism. Neurobiol Dis;2026 (Mar 26):107365.

Several genetic and non-genetic factors associated with the etiology of Autism Spectrum Disorder (ASD) have been identified, impacting directly or indirectly on the formation and function of synapses. Therefore, in recent years, synaptopathy has emerged as a central motif for a causative mechanism of ASD. Within synapses, many physically linked proteins or proteins found within the same signaling process have been associated with ASD and studied in in vitro systems and animal models. The results of this research support the crucial role of synaptic protein dysfunction in the development of ASD. The synaptic processes defined by critical proteins may be a point of convergence for many genetic and non-genetic factors. Therefore, this review will summarize key findings on the link between synaptic proteins and ASD from human genetic and animal studies and discuss the emerging synaptic biological processes directed by these proteins. The convergence of genetic and environmental risk factors impacting these processes will be highlighted to unify a theory in ASD research: A significant portion of ASD cases may in fact be explained by the dysregulation of essential synaptic proteins.

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10. Stacey N, Turtle B, Daly-Lynn J. An Investigation of Factors Affecting Bowel Movement Hygiene in Autistic Children. Occup Ther Int;2026;2026(1):e5464138.

Bowel movement hygiene is an essential life skill. Autistic children can have difficulties attaining this skill. There is limited research exploring postbowel movement hygiene (PBMH) and autism. This study explores factors of PBMH for autistic children. An online survey was developed, included open and closed questions, and distributed via Facebook groups. It was completed by N = 74 parents. Descriptive statistics and thematic analysis were used to analyze the data. Statistically significant correlations were found between variables related to the sensory and motor aspects of PBMH, scared of sitting on toilet and refusal to engage in PBMH (p ≤ 0.5). Four qualitative themes were identified: toilet paper, difficulties in reaching the bottom, health related factors, and successful strategies used by parents. Future research is needed to strengthen the validity of these findings and produce practice guidelines for occupational therapists working in this area.

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