Indeed, the evaluation of mitochondrial Fe metabolism and mitochondrial ROS demonstrated that suppressing mitoferrin-1 led to a decreased mitochondrial Fe content and a reduction in mitochondrial ROS levels in the CL2006 and GMC101 strains, suggesting that diminishing mitoferrin-1 expression may attenuate features inherent in the advancement of Alzheimer’s disease in C. elegans. This evidence concerns the gene SLC25A37 and early-onset autosomal dominant Alzheimer disease.