Preprint: Cntnap2 knockout mice show transient auditory brainstem changes and lasting startle hyperreactivity
A preprint from bioRxiv reports that mice lacking the ASD-associated gene Cntnap2 display early auditory brainstem abnormalities that partially resolve with age, while exaggerated startle responses persist — modelling sensory symptoms seen in autism spectrum disorder.
A preprint posted to bioRxiv (10.64898/2026.09.17.752490v1) examines how loss of Cntnap2 — a gene associated with auditory processing, language development, and autism spectrum disorder (ASD) — affects hearing and sensory reactivity in mice across development.
The study finds that Cntnap2 knockout animals display aberrant auditory brainstem responses (ABRs) and exaggerated acoustic startle reactions at early developmental time points. Notably, the auditory brainstem abnormalities are developmentally transient, partially resolving as the animals mature, which mirrors observations of delayed rather than permanently disrupted auditory development in some individuals diagnosed with ASD. However, startle hyperreactivity persists throughout the lifespan of the knockout animals, suggesting the two phenotypes have distinct underlying mechanisms and trajectories.
CNTNAP2 variants in humans have been associated with language impairment and ASD, and auditory hypersensitivity is a clinically recognised feature of the condition. This mouse model work characterises the developmental time course of sensory abnormalities and may inform the design of future studies testing interventions targeted at auditory or sensory processing in ASD-related conditions. As a preprint, these findings have not yet completed peer review.
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Primary sourcePreprint bioRxiv (Cold Spring Harbor Laboratory) · 2026-09-19Cntnap2 deletion in mice causes developmentally transient alterations in auditory processing and persistent startle hyperreactivity