NAV3 and UNC5C are homologs and have been identified in C. elegans to have neuron outgrowth and guidance and are associated with AD in humans.(19, 20, 43, 44) Mechanistic studies on cell and animal models discovered that aberrant UNC5C might contribute to AD by activating death-associated protein kinase 1 (DAPK1) which is involved in AD pathogenesis with extensive involvement in aberrant tau, Aβ and neuronal apoptosis/autophagy.(20, 45) In addition, deleting UNC5C from netrin-1–depleted mice can mitigate AD pathologies and reduces cognitive disorders. The gene discussed is NTN1; the disease is cognitive disorder.