DOX affected the hippocampal mitochondrial respiration, leading to mitochondrial impairment by the formation of mitochondrial permeability transition pores [68], resulting in mitochondrial swelling, with the rupture of its membrane and the subsequent release of proapoptotic protein cytochrome c, which stimulated apoptotic protein caspase 3 [69], eventually leading to the neuronal cells’ apoptosis and cognitive impairment. Here, CASP3 is linked to Cognitive impairment.