Autism Spectrum Disorder is a neurodevelopmental disorder often characterised by social impairments and hypersensitivity to sensory stimuli. Neuroligin is a brain molecule and potential determinant of behavioural traits in people with Autism. C.elegans are roundworms used in biomedical research as a model for understanding many neurological diseases.

My study aims to test whether neuroligin-deficient C. elegans can effectively model the reactions of Autistic humans when exposed to a sensory stimulant. I hypothesized that when neuroligin-deficient C. elegans are exposed to a tapping mechanism, there will be a significant increase in distance compared to the N2(wild-type worms) since the neuroligin gene in Autistic humans plays a role in reacting to sensory sensitivity.

I age-synched all worms to standardize for different stages of their life cycle. I also tested two different ages to observe whether different ages would affect the worms’ sensitivity to tapping. I used an actuator to create a tapping movement in 30 second intervals and tracked the distance of the worms using a 1mm grid.

There was a (p<0.01) significant difference between the neurolgin-deficient worms when exposed to tapping versus without tapping; for both the older and younger worms. However, the younger neuroligin-deficient worms were more sensitive to the tapping stimulant in comparison to the older neuroligin-deficient worms.

When exposed to tapping, neuroligin-deficient worms modeled a similar reaction to humans with Autism, revealing that neuroligin-deficient C. elegans can effectively model the reactions of Autistic humans when exposed to a sensory stimulant.