In addition, it increased the amount of cells positive for the marker of neurogenesis doublecortin in the hippocampus and the density of the dendritic spine, and inhibited the levels of Bax- and Bcl-2-interacting mediator of cell death (Bim) proteins (pro-apoptotic members); the opposite is seen when cisplatin is administered alone, which despite presenting a considerable level of autophagy also induces an exaggerated increase in apoptosis, attenuating neurogenesis and synaptogenesis, explaining cognitive impairment [148]. The gene discussed is BAX; the disease is Cognitive impairment.