Infant sensory gating and a developmental cascade to autistic traits and anxiety.
Schwarzlose Rebecca F
What this study means for families
This review suggests that problems with filtering sensory information in babies may lead to being overly sensitive to sounds, touch, and other sensations. This early sensory sensitivity might then contribute to developing autistic traits and anxiety later in life. The researchers propose that identifying these sensory differences early could help with screening and providing support during important developmental periods.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Research summary
This review proposes a developmental cascade model linking early sensory gating impairments to later autistic traits and anxiety. The model suggests that disruptions in inhibitory signaling during sensitive periods of infant neurodevelopment lead to sensory over-responsivity, which subsequently contributes to autistic traits, anxiety, and other psychiatric challenges. The review synthesizes evidence from both human and animal studies to support this developmental pathway. The authors highlight infant sensory responsivity as an important intermediate phenotype that could inform research approaches, screening protocols, and early supportive interventions.
This framework provides a mechanistic understanding of how early sensory processing differences may contribute to later developmental and psychiatric outcomes.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Key findings
- 1
Impaired sensory gating during sensitive periods of infant development may promote sensory over-responsivity, autistic traits, and anxiety
Confidence: moderateRelevance: Provides theoretical framework for understanding developmental pathways to autism and anxiety - 2
Infant sensory responsivity represents an important intermediate phenotype for research and intervention
Confidence: moderateRelevance: Suggests early sensory differences could be targets for screening and intervention
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Clinical implications
The proposed model suggests that early identification of sensory gating differences in infants could inform screening protocols and guide early supportive interventions. This framework may help clinicians understand how early sensory processing differences contribute to later autistic traits and anxiety symptoms.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Limitations
This is a theoretical review rather than an empirical study. The proposed developmental cascade model requires further empirical validation through longitudinal studies. No specific sample sizes or methodological details are provided as this synthesizes existing literature.
Summary by AutismInsights from published abstract. This is not a substitute for reading the original paper.
Original abstract
Disruptions to the infant sensory environment can have lasting effects on neural response properties and behavior in both humans and animals. Recent work has begun to highlight an additional factor in infant sensory experience: differences in inhibitory signaling and sensory gating. Converging work from human and animal studies has begun to implicate a developmental cascade by which impaired sensory gating during a sensitive period of neonatal neurodevelopment promotes a phenotype of sensory over-responsivity, autistic traits, anxiety, and other psychiatric challenges. In this Review, I propose a model for this developmental cascade and highlight how differences in infant sensory responsivity represent an important intermediate phenotype for research, screening, and supportive intervention.
Evidence Grade
moderate
Grade assigned by AutismInsights based on study type and published abstract.
Study Details
- Type
- Review
- Journal
- Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology
- Year
- 2026
- PMID
- 41094060
- DOI
- 10.1038/s41386-025-02253-6
MeSH Terms