The benefit of P110 treatment as an inhibitor of excessive (pathological) mitochondrial fission was determined using human neuroblastoma cell line SH-SY5Y cells treated with Aβ42 to induce Aβ-induced cytotoxicity, cells expressing a APP KM670/671NL double mutant, five different AD patient-derived fibroblasts and 5XFAD mouse model. The gene discussed is APP; the disease is neuroblastoma.