Our group has recently proposed a hypothesis about the contribution of oxidative phosphorylation system dysfunction, through a decrease in de novo synthesis of pyrimidine nucleotides, to the pathogenesis of late-onset Alzheimer’s disease. Different individuals, carrying different genetic variants in mitochondrial DNA, will differ in their ability to oxidise coenzyme Q10 and synthesise pyrimidine novo nucleotides. In this hypothesis, we have also suggested different compounds that, favouring the oxidation of coenzyme Q10 or increasing the concentration of pyrimidine nucleotides, would improve the differentiation and function of neurons and would therefore be beneficial in preventing Alzheimer’s disease. Thus, the objective of this project is to confirm this hypothesis and the oxidative phosphorylation system as a therapeutic target in personalised preventive medicine. To carry out this project, we will use transmitochochondrial cell lines that share the nuclear genetic background and cultivation conditions, but differ in its genotype of mitochondrial DNA. These cybrid lines have the ability to differentiate to neurons.