Expression data from the neuron model of Alzheimer's disease (AD) with or without treatment of recombinant human mitochondrial transcriptional factor A (rhTFAM) protein

To delineate the mechanism by which 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 with rhTFAM treatment compared with those without the treatment. Comparative analyses of PS1P117L cells with or without rhTFAM treatment showed that the expression of genes involved in protein synthesis, gene expression, and cancer were significantly altered. From these microarray analyses, we found that the expression levels of the genes associated with neuritogenesis were decreased in PS1P117L neurons compared with those in the wild type, and that hTFAM significantly increased these gene expression. Cholinergic neurons derived from human iPSCs established from normal subjects, in which a mutant (PS1P117L) copy of the PSEN1 gene was introduced were used in this study, (n=3 for each group). PS1P117L neurons with or without recombinant hTFAM protein treatment. RNA samples prepared from the cells were subjected to microarray analysis using the Affymetrix human Gene 1.0 ST platform (GPL6244).