The autism spectrum disorder (ASD) is a non-lethal neurodevelopmental disorder. The adult ASD patients carry a substantial comorbidity burden leading to a “premature aging” and a reduced life expectancy. Our main question was whether this “premature aging” is a mere consequence of initial neurodevelopmental deficits or due to a cumulative pathological process. We used ex vivo electrophysiology, optogenetics, chemogenetics, behavioural assessment and neuroanatomy to characterize the dysfunctions at different ages. We focused on identifying the onset of striatal dysfunctions in mouse models of ASD. We observed a worsening in motor dysfunctions in aged ASD animals. In addition, our preliminary data showed premature morphological alterations of striatal neurons inadult ASD. In addition, our results suggest that striatal interneurons could also be dysfunctional. These results open up a new field of investigation to better understand lifelong consequences of ASD in adults.
I am an associate professor at the University of Poitiers since 2017 and part of the LNEC ( laboratoire de neurosciences experimentales et cliniques (U-1084)). I obtained my PhD in 2011 (CEA) and I completed a postdoctoral stay at UCLA from 2011 to 2016 (project scientist from 2016-2017).I have been very interested in understanding the basal ganglia network in pathological conditions both during my thesis/post doc period (Huntington's disease) and currently (Autism Spectrum Disorders). I investigate the underlying mechanisms leading to a damageable phenotype in rodent transgenic model of the disease.
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