Title: Investigating the Synaptic Landscape of Trisomy 21 using human iPSCs
Abstract: Down syndrome (DS) or trisomy 21 (T21) is the most common genetic cause of intellectual disability. Deficits in synaptic formation, function, and maintenance have long been thought to play a major role in the characteristic intellectual impairment seen in DS. However, the biological mechanisms that govern these differences remain unclear. While DS mouse models have provided helpful insights into synapse biology, the etiology of DS–a complete triplication of human chromosome 21–is uniquely human and cannot be fully recapitulated by animal models. Therefore, human induced pluripotent stem cells (iPSCs) are an important resource in helping shed light on the biochemical and molecular regulators of T21-related synaptic differences. In an effort to fill this gap, our lab focused on developing a high-throughput analysis pipeline to accurately and rigorously quantify the synaptic density on iPSC-derived neurons. Equipped with this workflow, we have been able to efficiently and reliably characterize the effects of potential regulators of synapse development an maintenance to better understand how they may contribute to synaptic deficits, and ultimately intellectual disability, in T21.
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