Expression data from the neuron model of Alzheimer's disease (AD). Homo sapiens

To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment. One-way ANOVA was performed with the transcript clusters altered in PS1P117L cells compared with wild-type cells. Comparative analyses of PS1P117L cells and wild-type cells showed that the expression of genes involved in cellular assembly and organization, cellular function and maintenance, and tissue development were significantly altered. Overall design: Cholinergic neurons derived from human iPSCs established from normal subjects, in which a wild-type or mutant (PS1P117L) copy of the PSEN1 gene was introduced were used in this study, (n=3 for each group). RNA samples prepared from the cells were subjected to microarray analysis using the Affymetrix human Gene 1.0 ST platform (GPL6244).