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Updated: Mar 5, 2026

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Published on: July 6, 2022
Altered visual repetition suppression in Fragile X Syndrome: New evidence from ERPs and oscillatory activity
Simon Rigoulot1, Inga S Knoth2, Marc-Philippe Lafontaine3
1Departement de Psychologie, Université de Montréal, Montreal, Canada; Neuroscience of Early Development (NED), Montreal, Canada; Centre de Recherche en Neuropsychologie et Cognition (CERNEC), Montreal, Canada; Research Center of the CHU Ste-Justine Mother and Child University Hospital Center, Université de Montreal, Quebec, Canada; International Laboratory for Brain, Music and Sound Research (BRAMS), Montreal, Quebec, Canada.
Abstract:
Fragile X Syndrome (FXS) is a neurodevelopmental genetic disorder associated with cognitive and behavioural deficits. In particular, neuronal habituation processes have been shown to be altered in FXS patients. Yet, while such deficits have been primarily explored using auditory stimuli, less is known in the visual modality. Here, we investigated the putative alteration of repetition suppression using faces in FXS patients compared to controls that had the same age distribution. Electroencephalographic (EEG) signals were acquired while participants were presented with 18 different faces, each repeated ten times successively. The repetition suppression effect was probed by comparing the brain responses to the first and second presentation, based on task-evoked event-related potentials (ERP) as well as on task-induced oscillatory activity. We found different patterns of habituation for controls and patients both in ERP and oscillatory power. While the N170 was not affected by face repetition in controls, it was altered in FXS patients. Conversely, while a repetition suppression effect was observed in the theta band (4-8Hz) over frontal and parieto-occipital areas in controls, it was not seen in FXS patients. These results provide the first evidence for diminished ERP and oscillatory habituation effects in response to face repetitions in FXS. These findings extend previous observations of impairments in learning mechanisms and may be linked to deficits in the maturation processes of synapses caused by the mutation. The present study contributes to bridging the gap between animal models of synaptic plasticity dysfunctions and human research in FXS.
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