Atypical early neural responses to native and non-native language in infants at high likelihood for developing autism
Brain scans at 9 months show high-likelihood infants already miss the normal left-side jump for speech.
01Research in Context
What this study did
The team scanned 9-month-old babies while they listened to speech. Some babies had an older sibling with autism, so they were called "high-likelihood." The others had no family history.
The scan watched how each baby’s brain reacted to native and foreign words. The key question: would the left side of the brain light up the way it usually does for language?
What they found
High-likelihood babies showed weaker brain waves to every kind of speech. Their brains also failed to shift language work to the left side.
Typical-likelihood babies did the normal left-side jump. The gap was already clear before any child had a diagnosis.
How this fits with other research
Bassett-Gunter et al. (2017) saw the same risk group lose heart-rate interest in speech during the first year. The new study adds brain detail: the dip in attention lines up with a dip in left-side brain use.
Zhang et al. (2022) found over-connected local wires at 5 months in these babies. Wagner’s 9-month speech result suggests those messy wires may keep the left side from taking charge of language.
Gandhi et al. (2022) reviewed 17 papers and said no single brain-language picture exists for autism. This infant study helps explain why: the first step—left-side speech tuning—can already be off track.
Why it matters
You now have a 9-month red flag that lives inside the brain, not just in behavior. If you serve families with an older autistic child, share the finding that early speech responses can look different. Push for speech and parent-implemented language work before the first birthday. The window when the brain is still open is even earlier than we thought.
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02At a glance
03Original abstract
Language difficulties are common in autism spectrum disorder (ASD), a neurodevelopmental condition characterized by impairments in social communication as well as restricted and repetitive behaviors. Amongst infant siblings of children with an ASD diagnosis – who are at higher likelihood for developing ASD – a high proportion also show difficulties and delays in language acquisition. In this study, we used functional magnetic resonance imaging (fMRI) to examine differences in language processing in 9-month-old infants at high (HL) and typical (TL) familial likelihood for ASD. Infants were presented with native (English) and novel (Japanese) speech while sleeping naturally in the scanner. Whole-brain and a priori region-of-interest analyses were conducted to evaluate neural differences in language processing based on likelihood group and language condition. HL infants showed attenuated responses to speech in general, particularly in left temporal language areas, as well as a lack of neural discrimination between the native and novel languages compared to the TL group. Importantly, we also demonstrate that HL infants show distinctly atypical patterns of lateralization for speech processing, particularly during native speech processing, suggesting a failure to left-lateralize. Limitations: The sample size, particularly for the TL group, is relatively modest because of the challenges inherent to collecting auditory stimulus-evoked data from sleeping participants, as well as retention and follow-up difficulties posed by the COVID-19 pandemic. The groups were not matched on some demographic variables, but the present findings held even after accounting for these differences. To our knowledge, this is the first fMRI study to directly measure autism-associated atypicalities in native language uptake during infancy. These findings provide a better understanding of the neurodevelopmental underpinnings of language delay in ASD, which is a prerequisite step for developing earlier and more effective interventions for autistic children and HL siblings who experience language impairments. The online version contains supplementary material available at 10.1186/s13229-025-00640-w.
Molecular Autism, 2025 · doi:10.1186/s13229-025-00640-w