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The two cell-adhesion molecules, Neurexin-1 and Neuroligin-1, are essential for synapse function in neural networks. Interruptions to the function of these two proteins are associated with predestination for cognitive disorders, such as Autism spectrum disorder (ASD). In this paper, we study the effects of genetic missense mutations located on the cell interface between NRXN-1 and NLGN-1 on the development of neurodevelopmental disorders by identifying and determining the effects of mutations on bond strengths between NRXN-1 and NLGN-1 on the synaptic interface by building a computational platform. This was done by mapping all ASD-associated point mutations found in a web-based database on the computationally modeled structure of NRXN-1, then determining which mutations interact with NLGN-1. Then, the binding strength of the two proteins without the influence of the mutations was compared to the binding strength with the mutations so that the effects of the mutation were established. Based on our structural models and calculations of binding free energy, we found that these mutations can change the binding affinity of Neurexin-neuroligin interaction. Thus, we suggest that the changes in bond strength between Neurexin and Neuroligin at neural synapses can affect neural circuits, leading to autism-associated symptoms. [ABSTRACT FROM AUTHOR]