A transcriptomic characterization of immortalized hippocampal Ts16 cell lines to further elucidate the hippocampal dysfunction in Down Syndrome
Down Syndrome (DS, trisomy 21, T21) is caused by a triplication of human chromosome 21. The genetic disease affects roughly 1 in 700 births. While the majority of DS phenotypes vary in presence and severity by individual, all T21 individuals experience some level of cognitive disability that primarily impacts learning and memory processes. The ability of synapses, communication sites between neurons, to strengthen or weaken over time is known as synaptic plasticity. Synaptic plasticity allows for the brain to learn and store information. This process is dependent on the correct branching and growth of axons and dendrites in response to environmental cues. The trisomy 16 (Ts16) mouse model exhibits DS associated features but rarely survives gestation. The link between the hippocampus and synaptic plasticity has been extensively studied because the hippocampus is an important brain structure for learning and memory processes. The present study aims to characterize the transcriptome of an immortalized Ts16 hippocampal cell line by comparing it to that of a WT cell line. The identified differentially expressed genes largely suggest that there is a dysregulation of protein encoding genes regarding actin filament organization and regulation, lamellipodium function, and cell migration in the Ts16 cell line that ultimately prevents correct axonal and dendritic expansion in the hippocampus.
