Our research indicates that non-canonical Wnt signaling, activated by Wnt-5a ligand, regulates mitochondrial dynamics and/or preserves the MMP and prevents the mitochondrial fragmentation induced by Aβ oligomers and the exposure of Bcl-2, an anti-apoptotic mitochondrial protein, suggesting that Wnt components might be used to control mitochondrial dysfunction, such as the one observed in AD. The gene discussed is WNT5A; the disease is Alzheimer disease.