To resolve the contradiction with the accumulated data presented earlier in our review, the authors attribute the observed tendency to shift the balance of mitochondrial dynamics toward fusion in young animals to a compensatory mechanism in response to cellular stress and synaptic pathology induced by APOE4 expression and suggest that the decrease in mitochondrial fusion intensity observed in elderly patients with diagnosed AD and model animals is due to an inability to compensate for neurodegenerative changes [55,58,59]. This evidence concerns the gene APOE and Alzheimer disease.