NPSR1 and Alzheimer disease: These data indicate that the pathways that make C57BL/6J more susceptible to AD pathology could involve an upregulation in synaptic pruning, the microglial response, and myelination and a downregulation in neuropeptide receptor activity, while the pathways that make 5x‐CC006 more resistant to AD pathology could involve a less pronounced upregulation in synaptic pruning and microglial response as well as a downregulation in the neuroinflammatory response, neuron projection organization, and synapse maturation.