Autism spectrum disorders (ASD) are developmental disorders manifesting in early childhood resulting in language and social deficits in adulthood. Recent studies on mouse models for ASD based on highly penetrant genetic signals in patients have started to reveal aspects of the molecular and cellular underpinnings of ASD related phenotype in adulthood but little is known about their development. One of the most common genetic variations found in ASD is a deletion on chromosome 16p11.2 which creates cognitive/social/language impairment as well as seizures and hyperactivity. Mouse models of 16p11.2 have shown anatomical and functional alterations caused by the deletion which may be relevant to ASD. We will characterise the behaviours of this mouse model over the lifetime of the model that relate to the human clinical features of the deletion. Using the mouse models means that we can look more invasively and give predictive data regarding the brain regions involved in the development of the disorder. To achieve this objective we will use histology to identify neuronal networks involved in the phenotypes of the disorder. Using genetic, behavioural and electrophysiological recording techniques we will identify biomarkers for the development of the mouse phenotypes. A second aspect of our project will address the question of the generalisation of our findings to other genetic forms of ASD. To achieve this goal we will use another unrelated genetic mouse model for ASD, mice lacking the synaptic protein Neuroligin-3. Using the same approach to identify biological markers in the two mouse models we will be able to compare their developmental trajectories identify their markers that can be used for a large population of ASD mouse models.
Interagency Autism Coordinating Committee (IACC)
Autism Research Database (AFD)
