To increase ATP levels from the mitochondrion, mitochondrial transcription factor A (TFAM) has been engineered in such a way that this engineered molecule passes readily across the cellular and mitochondrial membrane and causes selective genomic expression, which causes reduction in levels of Aβ in 3xTg-AD mice, increases levels of the transthyretin (a potent inhibitor of Aβ aggregate) and causes a reduction in levels of mitochondrial mutations [260]. This evidence concerns the gene TFAM and Alzheimer disease.