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

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. 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).