The symptoms of fragile X syndrome stem from the loss of a single protein, raising the possibility that reintroducing FMRP could counter the key problems that lead to disrupted signal processing and aberrant behaviors. Turner is proposing a new means to reintroduce a short active fragment of FMRP back into central neurons in the Fmrp1 knockout mouse model to assess its potential utility as a therapeutic strategy to restore circuit and behavioral function in fragile X syndrome.

Based on the critical role of silent synapses in developmental neurocircuit refinement, Oliver Schlüter aims to assess whether ASD-risk genes encoding proteins associated with glutamate receptor complexes play a common role in silent synapse development. Using three different ASD mouse models (Shank3, Syngap1 and Nlgn3 deficiency), Schlüter will assess whether alterations in silent synapse maturation represent a common mechanistic defect underlying the distinct phenotypic facets of ASDs.

Moses Chao will investigate how the oxytocin receptor transduces its signals in the brain to generate its physiological and behavioral effects, by exploring the signaling properties of the oxytocin receptor and its potential association with neurotrophin-related pathways. This project is directly relevant to understanding the mechanism of neuropeptides and their impact upon autism spectrum disorders, anxiety and social behavior.

The short-term goal and scope of this proposal is to eliminate head motion in MRI scans at the time of acquisition by developing new, patient-specific hardware that physically prevents the head from moving in the scanner. In the longer term, Jones aims to understand the neural representation of restricted interests and how shifts in restricted interests are represented in the brain of individuals with autism.

Sapiro will develop computational and machine-learning tools to allow gaze analysis and its integration with other video-recorded behaviors, from cameras embedded in standard phones/tablets/computers.

Polimanti will use genetic- and brain-imaging approaches to understand the relationship between positive selection for common ASD risk alleles and cognitive abilities in affected and unaffected individuals.

Panagiotakos and her lab will use the 16p11.2 mouse model to explore how alternations in calcium signaling influence the function of neural stem cells and contribute to disease phenotypes.

Ng and Chukoskie will objectively study movement behaviors and their relationship to physiological states in children with autism using low-cost, flexible movement and heart-rate sensors incorporated in wearable textiles.