Neurexin-1 is a presynaptic cell adhesion molecule that binds to multiple postsynaptic ligands to mediate proper neuronal signaling at the synapse. Notably, large scale human genetic studies have placed the Neurexin-1 gene (NRXN1) as the most frequently deleted single gene mutation for schizophrenia (SCZ) and a high risk gene for autism, while also being implicated in multiple other neurodevelopmental disorders (NDD) such as bipolar, Tourette’s syndrome and intellectual disability. Past studies have shown that the loss of NRXN1, independent of genetic background, resulted in neurotransmission defects in mature human iPSC-derived glutamatergic neurons. Besides that, knockdown of NRXN1 showed a disruption in neuron-glial fate determination. However, up to date, no studies have examined the role of NRXN1 in early brain development. Here we utilized human pluripotent stem cell derived forebrain organoids differentiated from an isogenic line engineered to carry heterozygous loss of NRXN1 (isogenic-NRXN1 del), as well as schizophrenia and autism patients with heterozygous loss of NRXN1 (SCZ-, ASD-NRXN1 del) to study the functions of NRXN1 during forebrain development. Our single cell transcriptomic data showed most significant perturbations at the most mature time point in our analysis (3.5 months), compared to earlier time points (3 weeks and 2 months). However, in a genetic background dependent manner, we observed perturbed developmental trajectory of early cell types (such as neuroepithelial cells) and other maturing cell types in the SCZ-NRXN1 del forebrain organoids and dysregulation in pathways related to neuronal development and axonal projection in the ASD-NRXN1 del organoids. Moreover, we also observed variable dysregulations in overall spontaneous network activity in organoids across all genetic background, compared to controls, again displaying genetic background specific phenotypes. In this dissertation work we report findings and discuss the effects of NRXN1 in the cellular and molecular functions of brain development in specific disease backgrounds.